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Farm Beef vs Store Beef – Real Food Fresh No AntiBiotics, No Hormones, No Presevatives, No Dyes, No Chemicals vs Mass Production

The Truth News — Sat, 03 Aug 2024 21:11:49 +0000

Grocery Store Meat Vs Farm Fresh Meat

A question many people have today is why is supermarket meat cheaper than meat you can purchase fresh from a farm. There are reasons to make the best choice for yourself and your family.

The meat you find in a grocery store is mass-produced. Its origins are more like a factory than a traditional farm. Operating with government subsidies, the purpose of these meat factories is to produce as much meat as possible.

This means poor quality control and poor meat quality. Factory-style farming means fewer nutrients in the meat. Mass-produced meat is also more likely to contain antibiotics and growth hormones. Factory-style farmingalso includes additives in animal feed. You do not want to pass these unhealthy substances on to your family by eating mass-produced meat.

While this type of farming itself is questionable, so is the overall quality of the meat. You do not know how long the meat is been in a processing and packaging facility, or the health and safety precautions that are taken at the facilities. In addition, you do not know if the meat has been transported to the store in a sanitary manner, how it has been handled at the store, or how long it has been available for sale. You are taking chances if you rely on the expiration dates.

You will not have these concerns when you buy farm fresh meat. You will have the healthiest, safest product. You are assured of excellent quality and excellent service. When you buy farm fresh meat, you are supporting local businesses and local farms. Also, you are creating sustainability for farms and farmers while protecting the environment.

The small extra cost is worth it. You are doing your part to sustain local businesses, and you are providing the very best for your family.

Farm Beef vs Store Beef

Real Food Fresh No AntiBiotics, No Hormones, No Presevatives, No Dyes, No Chemicals vs Mass Production

There is no doubt that beef is one of the most popular and widely consumed meats in the world. Whether you’re a steak lover or prefer burgers, beef is a staple in many diets. However, the quality of beef can vary greatly depending on where it’s sourced from. While store-bought beef may seem convenient and cost-effective, there are many benefits to choosing farm-fresh beef instead.

First and foremost, farm-fresh beef is often raised in a more humane and ethical manner than store-bought beef. Farmers who raise their own livestock typically have a smaller number of animals to care for, which allows them to provide individual attention and care to each animal. This can lead to healthier and happier cows, which ultimately results in better quality beef.

Additionally, farm-fresh beef is often raised using more sustainable and environmentally-friendly practices. Farmers who raise their own livestock typically have greater control over the feed and living conditions of their animals, which can lead to a more sustainable and eco-friendly operation.

Finally, farm-fresh beef is often more flavorful and nutritious than store-bought beef. This is because the animals are typically raised on a natural diet of grass and other vegetation, which can lead to a more complex and rich flavor profile. Additionally, farm-fresh beef is often lower in fat and higher in nutrients like Omega-3 fatty acids, which can be beneficial for overall health.

In conclusion, while store-bought beef may seem like the more convenient choice, there are many benefits to choosing farm-fresh beef instead. Not only is it often raised in a more ethical and sustainable manner, but it’s also more flavorful and nutritious. So next time you’re in the market for beef, consider choosing farm-fresh for a better overall experience. source

What’s Wrong with Beef from the Grocery Store?

The beef that you’re purchasing from the grocery store (you know, the kind on the styrofoam plates with the plastic wrap on top, or in the plastic tubes) is vastly different from the grass-fed meat you can purchase from a local farmer. The primary difference is in how the cow was raised. Your standard grocery store beef has been was raised on a feedlot.

When cattle is raised on a feedlot, they are provided a mostly grain-based diet. A grain-based diet causes health problems for cows because cows are ruminants: they are designed to digest grass, not corn and soy derivatives. Being on a grain-based diet greatly increases the risk of them carrying e. coli and other pathogens due the change of pH in their gut. Begin grain-fed also decreases the nutritional value of the meat.

Because of their poor diet and cramped living quarters, they’re prone to health problems, so they’re almost constantly on antibiotics. Many farmers routinely keep their cows on antibiotics which have caused problems with antibiotic resistant strains of bacteria.

You may be surprised to find there are a number of very undesireable ingredients that make their way into animal feed (read this startling article from the Environmental Health Perspectives journal, “What Do We Feed to Food-Production Animals? A Review of Animal Feed Ingredients and Their Potential Impacts on Human Health“). Animal feed can include: meat from animals of other species or meat from the same species, roadkill, meat from diseased animals, bits of feathers, hair, skin, hooves, blood, manure and other animal waste, plastics, drugs, chemicals, and unhealthy amounts of grain.

Remember the old adage, “You are what you eat.” Well, so is the cow…and you’re eating that cow…which means all of that garbage the cow ate is now going into you. That’s pretty gross!

So why do farmers feed animals grains and other undesireables if it creates diseased cows and meat with low nutrients and high levels of toxins? It all comes down to the bottom line. Farmers feed the cattle this diet because it fattens them up more quickly. Also, grain-based feed is cheap because the government subsidizes farmers who grow corn and soy. So, now you know why grain fed meat is cheaper: the farmers can raise them quickly and feed them cheaply.

The Wonders of Grass-Fed Beef

Must we all forgo juicy hamburgers and succulent steaks if we are to avoid these health pitfalls? Never fear my carnivorous friends, there is a very healthy alternative to grocery store meat, but it will take a little more work and money to get your hands on it. There are many benefits of finding a local farmer who raises grass-fed and grass-finished beef.

Grass-fed beef has been raised on what cows were designed to eat: grass! As such there are a plethora of health benefits in eating a grass-fed and grass-finished cow.

Though the meat tends to be lower in total fat, there is a greater concentration of omega-3 fatty acids. Grain-fed beef is virtually deplete of all omega-3s. Omega-3 fatty acids are essential for human health, but our body cannot synthesize them on our own. The standard American diet is quite deficient in omega-3’s. You eat Omega 3 fatty acids in algae, fish oil, grass-fed meat, and flax seed oil (though our bodies do not utilize the omega-3’s in flax seeds as well as in meat sources).
Grass-fed beef is the richest known source of conjugated linolic acid (CLA), which has been found to have many health benefits. CLA has anti-cancer properties and increases cardiovascular health. Grass-fed beef has approximately 300-500% more CLA than a cow that is fed half grains.
The meat your get from a grass-fed cow has much less chance of being infected with e. coli and other diseases.
A grass-fed cow is much higher in b vitamins, vitamin k and e, as well as essential trace minerals. In fact, many experts report that the bio-available (what your body can actually use) vitamins and minerals that are in meat vastly outweighs that which is found in fruits and vegetables.

The Real Difference Between Grass-Fed And Grain-Fed Beef

Grass fed beef is not the same as grain fed, and you might be surprised at the difference.

Grocery stores can be confusing places, and the meat department is no different. From free-range chicken to wild-caught salmon and everything in between, it can be hard to know which way to go. When it comes to grass-fed beef versus grain-fed, knowing the difference is also about understanding the food chain. Knowing which of these products are worth the investment will help you make the right decision for your dinner table.

Beef Industry Approaches

The traditional practice of the cattle industry to fatten livestock on a grain-based diet originated in the 1950s. Currently, About 80% of cattle in the United States are raised this way. As cattle become older, they become less efficient in converting feed to muscle or meat. Grain has more energy than a forage diet of grass or hay, and allows cattle to maintain higher growth rates. Feeding grain to cattle also concentrates their lives into a smaller area which frees up land for other uses.1

Grass-fed beef, which is the product of cows who spend their whole lives grazing on grass, can cost more money per pound. The cost lies behind the fact that it takes longer for grass-fed cattle to reach their processing weight on an all-grass diet. Raising beef this way, though more sustainable, is more expensive for the farmer.

An Alternative Worth Exploring

A grass-fed animal requires more time on feed to reach a target weight. As a result, the meat has less marbling. Grass-fed cattle are typically leaner with lower fat and calories. American grass-fed beef consumers are health conscious, enjoy variety, and seek a high-quality product. They associate grass-fed beef with being more natural and being of a higher quality. They also consider it to be better for the animal and their personal health.2 When raised in a feedlot, an animal experiences more stress. Animals that are stressed release hormones into the meat which results in it being less tender.

If you are interested in how an animal is raised before it is harvested, and consider the humane aspects of ranching to be important, choosing pasture-raised beef might be your best option. Not only that, but the sustainable farming methods surrounding grass-fed cattle, and a concern for natural resources, allow farmers to heal the land so future generations can use it.2

Grass Fed Nutritional Benefits

Grass-fed beef is higher in vitamins and antioxidants with double the amount of omega-3 fatty acids as grain-fed beef. What a cow eats can significantly affect the nutrient composition of its beef. This is particularly evident when it comes to fatty acid composition. Grass-fed beef usually contains less total fat than grain-fed beef, which means that gram for gram, grass-fed beef contains fewer calories. The composition of fatty acids within the meat is also different.

Grass-fed beef contains much less monounsaturated fat than grain-fed beef.
As far as omega-3 fatty acids are concerned, grass-fed is the clear winner. It contains up to five times more than grain-fed.
Grass-fed beef contains about twice as much conjugated linoleic acid (CLA) as grain-fed beef. CLA has been shown to improve functions in the body and is also considered to possess anti-carcinogenic, anti-obese, anti-diabetic, and anti-hypertensive properties. This means CLA can be effective in preventing lifestyle diseases or metabolic syndromes.3

In short, there are some significant differences in the composition and amount of fat and nutritional benefits in grass and grain-fed beef.

Tasting The Difference

Most of the cattle industry starts their cows on grass and then transitions them to corn or grain to bulk them up quickly. It’s essentially fast food for cows. And because it’s not their natural diet, many farmers rely on antibiotics to keep their herds healthy. Other additives go along with a grain-fed diet, including hormones that aid in accelerating the growth of the animal. If you are used to buying this more mainstream, widely available beef version, you are already used to the taste.

As far as grass-fed beef is concerned, some report that the meat is slightly more gamey than the ordinary offering. This isn’t necessarily bad, and when we use the word “gamey”, we are not tripping into venison territory. If you give it a chance, you will experience what a cleaner version of beef tastes like. And when you consider all of the health benefits that go along with this choice, you may find it more appealing. source

What’s Wrong with Beef from the Grocery Store?

Remember the old adage, “You are what you eat.” Well, so is the cow…and you’re eating that cow…which means all of that garbage the cow ate is now going into you. That’s pretty gross!

The Wonders of Grass-Fed Beef

Grass-fed beef has been raised on what cows were designed to eat: grass! As such there are a plethora of health benefits in eating a grass-fed and grass-finished cow.

Though the meat tends to be lower in total fat, there is a greater concentration of omega-3 fatty acids. Grain-fed beef is virtually deplete of all omega-3s. Omega-3 fatty acids are essential for human health, but our body cannot synthesize them on our own. The standard American diet is quite deficient in omega-3’s. You eat Omega 3 fatty acids in algae, fish oil, grass-fed meat, and flax seed oil (though our bodies do not utilize the omega-3’s in flax seeds as well as in meat sources).
Grass-fed beef is the richest known source of conjugated linolic acid (CLA), which has been found to have many health benefits. CLA has anti-cancer properties and increases cardiovascular health. Grass-fed beef has approximately 300-500% more CLA than a cow that is fed half grains.
The meat your get from a grass-fed cow has much less chance of being infected with e. coli and other diseases.
A grass-fed cow is much higher in b vitamins, vitamin k and e, as well as essential trace minerals. In fact, many experts report that the bio-available (what your body can actually use) vitamins and minerals that are in meat vastly outweighs that which is found in fruits and vegetables.

Things to Keep in Mind

You need to remember that organic does not mean grass-fed and -finished. Most organic beef is still, at a minimum, finished on a feedlot with organic feed.

When talking to farmers you need to verify that they are both grass-fed and grass-finished. A farmer can label their meat “grass-fed” even if they fatten the cow up with grain the last couple of months. You want to find a grass-finished cow for an optimal level of nutrients! When farmers finish their cows off with grain to quickly fatten them up the last few months of their life, there is a drastic reduction in vitamins and minerals.

Finally, I’ve heard some report that they had a bad experience with grass-fed beef. It just didn’t taste good. I’m sure there are less than optimal tasting grass-fed cows, just as there are grain-fed cows. But being the foody that I am, I can happily report my family and I have been exceedingly pleased with the taste of our grass-fed cow. We’ve been so happy with it we’re anxiously awaiting a pastured pig from the same farmer! source

Know what you’re buying. This picture has store beef(right), and farm beef(left). There is an obvious visible difference between the two but the differences don’t stop there!

1. You may notice the color difference in the picture. The store bought is pumped full of additives and preservatives, including propyl gallate, to protect against spoilage due to long term air exposure.

2. There isn’t a guarantee of where that beef came from, OR how many cows are in it.

Yes, it may have the USDA label on it but as long as that animal was packaged in the US, it can be called a Product of the USA.

And yes, the meat in the right package is not from one single cow, rather scraps from multiple cows. It may have come from Argentina, Canada, or Brazil.

3. The beef on the left is fresher, darker and is farm raised beef. It is filled with more nutrients & flavor. The ground is also from one cow and not just low quality scraps from multiple cows.

store beef(right), and farm beef(left)

Buy from a local farm

Scientists find link between mouthwash Erectile Dysfunction, High Blood Pressure & Gut Problems

The Truth News — Mon, 01 Jul 2024 03:32:30 +0000

Scientists find link between mouthwash Erectile Dysfunction, High Blood Pressure & Gut Problems

Scientists find link between mouthwash use and raised blood pressure

HOUSTON, U.S.: A balanced oral microbiome can contribute to good cardiovascular health by converting dietary nitrate into nitric oxide (NO), a signaling molecule that helps maintain normal blood pressure. Now, a new study has suggested that chlorhexidine, an antiseptic substance found in mouthwash, may kill NO-producing bacteria and raise systolic blood pressure.

The researchers used 16S rRNA gene sequencing and analysis to examine whether using chlorhexidine antiseptic mouthwash twice a day for one week would change the oral bacterial communities and blood pressure levels in 26 healthy individuals. They collected samples of the participants’ saliva and tongue scrapings and measured their blood pressure at baseline as well as seven, ten and 14 days later.

The results indicated that using chlorhexidine twice a day was associated with a significant increase in systolic blood pressure and that recovery from use resulted in an enhancement in nitrate-reducing bacteria on the tongue. Individuals with relatively high levels of bacterial nitrite reductases had lower resting systolic blood pressure.

“The demonstration that the presence of NO-producing bacteria in the oral cavity can help maintain normal blood pressure gives us another target to help the more than 100 million Americans living with high blood pressure,” said lead researcher Dr. Nathan S. Bryan, an adjunct professor in the Department of Molecular and Human Genetics at the Baylor College of Medicine in Houston. “Two out of three patients prescribed high blood pressure medication do not have their blood pressure adequately managed,” he added. “None of the [current] drugs for management of hypertension are targeted towards these NO-producing bacteria.”

According to Bryan, owing to the widespread nature of the molecule, oral bacteria may have other profound effects on human health besides regulating blood pressure. “We know one cannot be well without an adequate amount of NO circulating throughout the body. Yet, the very first thing over 200 million Americans do each day is use an antiseptic mouthwash, which destroys the ‘good bacteria’ that help to create the NO. These once thought good habits may be doing more harm than good,” he said.

The study, titled “Frequency of tongue cleaning impacts the human tongue microbiome composition and enterosalivary circulation of nitrate,” was published online on March 1, 2019, in Frontiers in Cellular and Infection Microbiology. source

Can mouthwash raise your blood pressure?

New research, published in the journal Frontiers in Cellular and Infection Microbiology, shows that an antiseptic compound found in mouthwash destroys “friendly” oral bacteria that help maintain normal blood pressure levels.

New research finds that mouthwash could destroy ‘friendly’ oral bacteria, which may have important consequences for a person’s cardiovascular health.

Scientists know that the bacteria in our guts influence overall health, but perhaps less obvious is the connection between oral bacteria and a variety of health conditions.

For instance, Medical News Today recently reported on a range of studies that linked gum disease and the buildup of certain bacteria in the mouth with Alzheimer’s disease, cardiovascular disease, and respiratory conditions.

Another recent article showed how a specific oral bacterium could speed up the progression of colorectal cancer and make the disease more aggressive.

These studies focused on bacteria that cause disease, but, just like our guts, our mouths also contain “friendly” bacteria, which are necessary for maintaining good health.

An oral microbiome with a good balance between these different kinds of bacteria can keep disease at bay. StudiesTrusted Source have found that when this balance is upset it “contributes to oral and whole-body systematic diseases” as diverse as inflammatory bowel disease, Alzheimer’s, rheumatoid arthritis, obesity, atherosclerosis, and diabetes.

New research points out that a balanced oral microbiome helps maintain good cardiovascular health by helping the conversion of dietary nitrateTrusted Source into nitric oxide (NO) — a signaling molecule that helps maintain normal blood pressure.

Worryingly, however, the new study shows that chlorhexidine, an antiseptic substance in mouthwash, may kill NO-producing bacteria, which in turn, may raise systolic blood pressure.

Nathan Bryan, Ph.D., from the Department of Molecular and Human Genetics at Baylor College of Medicine in Houston, TX, led the new research.

Mouthwash ‘may do more harm than good’

Bryan and colleagues used “16S rRNA gene sequencing and analysis” to examine whether using chlorhexidine antiseptic mouthwash twice a day for 1 week changed the oral bacterial communities and blood pressure levels in 26 healthy individuals.

After 1 week, the 26 study volunteers went back to their usual oral hygiene practices.

The researchers collected samples of the participants’ saliva and tongue scrapings and measured their blood pressure at four different points throughout the study: at baseline, then 7, 10, and 14 days later.

Bryan and colleagues report that “twice-daily chlorhexidine usage was associated with a significant increase in systolic blood pressure after 1 week of use and recovery from use resulted in an enrichment in nitrate-reducing bacteria on the tongue.”

“Two out of three patients prescribed high blood pressure medication do not have their blood pressure adequately managed,” he adds, and “this may provide an explanation as to why. None of the [current] drugs for management of hypertension are targeted towards these NO-producing bacteria.”

The researcher continues to explain the mechanisms underlying the findings, saying that NO “is one of the most important signaling molecules produced in the human body.”

Because of the “ubiquitous” nature of this molecule, “the systemic effects of orally produced bacteria may have other significant effects on human health beyond maintenance of blood pressure,” Bryan says. source

“We know one cannot be well without an adequate amount of NO circulating throughout the body. Yet, the very first thing over 200 million Americans do each day is use an antiseptic mouthwash, which destroys the ‘good bacteria’ that helps to create the NO. These once thought good habits may be doing more harm than good.”

Nathan Bryan, Ph.D.

Does mouthwash kill the mouth’s healthy bacteria?

WHETHER YOU’RE TRYING to get rid of garlic breath, prevent cavities or stave off gum disease, you may be concerned that swishing mouthwash will upset the balance of bacteria/”bugs” in your mouth and cause health issues.

The chance is very low, especially if you use it on a temporary basis. Mouthwash acts as a barrier, reducing the bacteria from attaching to the teeth. And, because it has such a short amount of contact with those bugs, there isn’t much concern that it could wreak havoc in your mouth. Read on for answers to more common questions about mouthwash and the mouth’s microbiome.

Is mouthwash safe to use?

Mouthwashes are cleared by the U.S. Food and Drug Administration, endorsed by the American Dental Association and, in general, safe to use. But keep in mind that they are used for prevention of oral health issues and will not treat those issues.

What is the microbiome in the mouth, and how does mouthwash affect it?

The microbiome is the balance of healthy and unhealthy bacteria in the mouth. Mouthwash can change the proportion, but there’s not much evidence to show this is cause for concern, especially when it’s used on a temporary basis.

What are benefits of mouthwash?

Mouthwash can help reduce the chance of getting gingivitis, which causes inflammation of the gums, the soft tissue around the teeth. Gingivitis can lead to worsening gum disease that ultimately involves losing jawbones around teeth (periodontitis).

Mouthwash also can be useful on a temporary basis to help prevent cavities for people wearing braces or who have recently had gum surgery and have difficulty brushing their teeth.

It’s important to emphasize that you need to use mouthwash before problems develop. Once you progress to gum disease or jawbone loss, or once bacteria become calcified (calculus), mouthwash won’t help.

What are some drawbacks of using mouthwash?

Sometimes mouthwash can stain teeth after a few weeks of use, because certain formulas attach to the tooth. In some people, the chemicals can affect taste.

Also, many mouthwashes contain alcohol and can be detrimental to people who are sensitive to alcohol. Mouthwashes with alcohol also should be avoided by children and pregnant people.

Is there a link between the oral microbiome and high blood pressure?

There is some correlation between oral hygiene and heart health. Patients with poor oral hygiene habits have a higher chance of developing cardiovascular complications when compared with patients with good oral hygiene habits. However, there could be other factors at play. For example, patients with poor oral hygiene habits may tend to have other habits that contribute to heart disease.

There also is some preliminary data that shows bacteria that’s usually found in the oral cavity also being found in the heart of a patient who suffered from heart complications. That’s indirect evidence that somehow oral bacteria may migrate, but it’s not strong evidence.

However, good oral hygiene is simple to achieve, costs very little, and there are many possible benefits. So, if there’s potential to improve your heart health by taking care of your teeth, you should brush and floss regularly and use mouthwash if you choose.

Is there a benefit to probiotic mouthwash?

The concept of probiotic mouthwashes is to supplement the user’s good bacteria. But currently, there’s no strong evidence to show that probiotic mouthwashes are better than standard mouthwashes.

How do I choose a mouthwash?

Choose a mouthwash tailored to what you’re trying to prevent. If you have gingivitis or some initial gum problems, choose one that targets gum inflammation. If you want to prevent decay from occurring, you could choose one that contains fluoride. Consult with your dentist about this.

If you’re pregnant, have children in the home or are susceptible to alcohol, choose one that’s alcohol-free.

Does mouthwash help with bad breath?

The causes of bad breath are gum disease, stomach issues, sleep problems, stress and specific types of bacteria in your mouth. Sometimes mouthwash helps. Sometimes it doesn’t. But it’s just a temporary fix. If you have chronic bad breath, you need to determine the root cause and address it.

How would I know if I have an imbalance of mouth bacteria?

It’s hard to know if the bacteria in your mouth are imbalanced unless you do a bacterial test, which looks at the profile in your saliva. It’s possible you may have symptoms. Some bacteria cause cavities and some cause gum disease. source

You might find it surprising, but there are important things you need to know about the potential harm caused by mouthwash. In this post, I’ll delve into the reasons why mouthwash can cause disease and suggest alternative ways to improve your oral health.

Check out my video on mouthwash to hear what I really think of it!

Did you know that mouthwash can…

Disrupt your gut microbiome
Reduce your body’s ability to make nitric oxide
Increase your risk for cardiovascular disease and diabetes
Increase systemic inflammation
Raise your blood pressure

These are all scientifically-proven facts. Let’s talk about how mouthwash can promote disease and what to do instead.

The Cascading Effect of a Disrupted Oral Microbiome

You’ve probably heard about the importance of the gut microbiome, and if you’ve been around RIFM more than a minute, you definitely have! Research shows that our microbiome is a major key to our health. I’ve discussed on the blog how poor gut health is directly related to chronic disease, cardiovascular disease, and mental health problems.

But crucial bacteria are not limited to just our gut. They also exist in our mouth, on our skin, in our sinuses, and even on our genitalia. Each of these areas has its own unique microbiome or bacterial colonies, and when they are in harmony and balance, they play a beneficial role in maintaining our overall health.

Did you know your gut microbiome is actually seeded by bacteria in your mouth? Maintaining a balanced pH and fostering a healthy bacteria population in your mouth directly influences your gut health.

Now that we know that a disruption in the oral microbiome can directly disrupt the gut microbiome, it’s clear to see how that seemingly innocent bottle of mouthwash on your bathroom counter could be very harmful to your health.

How Mouthwash Affects Nitric Oxide

Ever heard of nitric oxide? It’s the compound responsible for the functioning of medications like Viagra and nitroglycerin. Nitric oxide plays a pivotal role in dilating blood vessels, lowering blood pressure, preventing heart attacks, and promoting healthy sexual function. To ensure its presence in the arteries, it’s essential to consume nitrates found in foods like beets and leafy greens.

The surprising element in the nitric oxide story is that we need specific mouth bacteria to help release these nitrates from foods so that our body can absorb them. What could kill these good bacteria in the mouth, preventing this critical release of nitrates? You guessed it – mouthwash. So now we can see how mouthwash can also prevent the absorption of these critical nutrients from our food.

Without the right bacteria in the mouth – because of mouthwash – nitric oxide fails to reach your system, impacting brain function, blood pressure regulation, and other vital processes.

Oral Health Out of Balance: It’s Not Just About Pretty Teeth

One noticeable sign of imbalance in the mouth is the presence of tartar. If you frequently experience tartar buildup or scaling, it indicates the formation of a biofilm that harbors harmful bacteria in your mouth. This condition is linked to various oral problems, such as periodontal disease, gum recession, and cavities, all of which can have a significant impact on your overall oral health. But the effects of an imbalanced oral microbiome extend beyond just the mouth, affecting the entire body.

During my medical career, I’ve observed interesting connections between oral health and other conditions. It’s remarkable how often I encounter diabetic patients or individuals with severe gut issues who also have poor dentition and oral hygiene. New research is showing associations between periodontitis (chronic gum infections) and conditions like Alzheimer’s disease, along with other disease states. We are also seeing a link between the bacteria in your mouth and vascular health.

While I don’t recommend using mouthwash, I always recommend that my patients take their oral health seriously because of its intricate relationship with our overall well-being.

Ways to Promote Oral Health Without Using Mouthwash

There are several simple steps you can take to promote a healthy mouth and oral microbiome. If you’re experiencing things like gum inflammation, tartar buildup, foul-smelling breath, or a white tongue, it’s important to take some steps to address your oral health.

One effective technique is called oil pulling, which involves swishing coconut oil or olive oil in your mouth for about five minutes, twice a day. This practice helps combat harmful bacteria and promotes a healthier balance of microbes in the mouth.
Another option is to incorporate oral probiotics into your routine. These specially formulated probiotics are chewed so that they are lodged on the gums, contributing to a healthier balance of bacteria. Some toothpaste brands even offer probiotic-infused options, providing an additional way to support oral health. See below for the oral probiotic that my family uses.
There are new mouthwashes containing essential oils can be beneficial in controlling bacteria in both your mouth and gut. These mouthwashes have shown positive results in putting periodontal disease into remission, reducing tartar buildup, and enhancing overall oral health.

Beyond Fresh Breath: The Far-Reaching Effects of Imbalanced Oral Microbiome

As you can see, maintaining a healthy oral microbiome is vital for your overall well-being. The bacteria in your mouth have a significant impact on your gut health and can even affect processes like nitric oxide production, blood pressure regulation, blood sugar balance, sexual health, and brain function. Since mouthwash disrupts our microbiome, it’s easy to see how it could be very harmful to your health.

There are simple steps you can take to improve your oral health without relying on mouthwash. Prioritizing your oral health is a great place to start to improve your overall health trajectory and ensure that you get the most benefit from the nutritious foods that you eat. source

The role of dietary nitrate and the oral microbiome on blood pressure and vascular tone

Abstract

There is increasing evidence for the health benefits of dietary nitrates including lowering blood pressure and enhancing cardiovascular health. Although commensal oral bacteria play an important role in converting dietary nitrate to nitrite, very little is known about the potential role of these bacteria in blood pressure regulation and maintenance of vascular tone. The main purpose of this review is to present the current evidence on the involvement of the oral microbiome in mediating the beneficial effects of dietary nitrate on vascular function and to identify sources of inter-individual differences in bacterial composition. A systematic approach was used to identify the relevant articles published on PubMed and Web of Science in English from January 1950 until September 2019 examining the effects of dietary nitrate on oral microbiome composition and association with blood pressure and vascular tone. To date, only a limited number of studies have been conducted, with nine in human subjects and three in animals focusing mainly on blood pressure. In general, elimination of oral bacteria with use of a chlorhexidine-based antiseptic mouthwash reduced the conversion of nitrate to nitrite and was accompanied in some studies by an increase in blood pressure in normotensive subjects. In conclusion, our findings suggest that oral bacteria may play an important role in mediating the beneficial effects of nitrate-rich foods on blood pressure. Further human intervention studies assessing the potential effects of dietary nitrate on oral bacteria composition and relationship to real-time measures of vascular function are needed, particularly in individuals with hypertension and those at risk of developing CVD. source

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Over-the-counter mouthwash use, nitric oxide and hypertension risk

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Foods to help balance fatty liver

The Truth News — Sun, 23 Jun 2024 18:09:19 +0000

Foods to help balance fatty liver

1. What is fatty liver disease?

Fatty liver disease is a condition in which too many fat cells accumulate in the liver cells. Normally, there is still fat in the liver, but when the number of fat cells increases, accounting for more than 5% – 10% of the weight of the liver, it can be considered as fatty liver. Excess fat accumulation in the liver makes the liver more susceptible to damage, which can lead to hepatitis, cirrhosis, and liver failure.

There are many causes for a person to have fatty liver such as hepatitis C, metabolic diseases such as diabetes, thyroid disease. Fatty liver disease is classified into two groups:

Alcoholic fatty liver disease: With fatty liver disease caused by alcohol, the important treatment is to stop drinking alcohol, otherwise the disease will get worse. , which can lead to cirrhosis, even liver cancer.

Non-alcoholic fatty degeneration: Mainly due to metabolic disorders, and a small part due to viral hepatitis. In the case of fatty liver disease caused by metabolic disorders – excess energy, the important treatment measure is to change lifestyle. For example, an improper vegetarian diet can also lead to fatty liver disease. A vegetarian diet that is completely protein-free or a vegetarian but still drinking alcohol will not provide enough energy for the body, which will weaken the immune system.

Fatty liver is a common disease with an increasing incidence. Fatty liver disease, if not detected and treated early, can lead to hepatitis, cirrhosis, and even liver cancer. Therefore, it is best to prevent disease with foods that help balance fatty liver.

2. Fatty liver eat what?

Fatty liver disease if not detected and treated early can lead to hepatitis, cirrhosis, even liver cancer. So how should the diet and daily activities need to be changed to help improve the problem of fatty liver? The following are foods that help balance fatty liver:

Turmeric: Not only is turmeric a favorite spice often added to dishes, but turmeric also offers many great health benefits. Turmeric helps prevent and treat fatty liver disease through stimulating the digestion of fat in the body, reducing the amount of fat cells that accumulate in the liver. To effectively treat people with fatty liver, you can take half a teaspoon of turmeric powder mixed in a glass of hot water, wait until it cools and drink three glasses a day. You can also mix half a teaspoon of turmeric powder with a glass of warm milk.

Lemon: Lemon is a fruit rich in vitamin C, a very good natural antioxidant that helps the liver produce more glutathione and plays an important role in the detoxification process for the body. Recent studies have shown that lemons contain a compound called naringenin, which reduces liver inflammation associated with fatty liver disease. Drinking fresh lemon juice 2-3 times a day, continuously for a month or thinly sliced lemon in a bottle of water and drinking daily also helps improve fatty liver.

Apple juice: Apple juice and apple cider vinegar are among the best foods in treating fatty liver disease, promoting weight loss and helping to reduce fat accumulation in the liver. Mix a tablespoon of apple cider vinegar with a teaspoon of honey mixed in a glass of warm milk, drink every day before meals, continuously for many months will bring great results.

Green Tea: Green tea is packed with nutrients and is rich in antioxidants that are important for the body. Green tea not only supports brain function, is good for the stomach, kills bacteria, but also boosts fat burning in the body and reduces the risk of cancer. Therefore, drinking green tea water is one of the most effective measures in preventing fatty liver disease, especially for people with non-alcoholic fatty liver disease.

Dandelion: Dandelion is a very liver tonic herb, helps to activate better liver function and is used to treat fatty liver disease not caused by alcohol but related to obesity, because dandelion He has the effect of enhancing the metabolism of fat accumulated in the liver. Use dandelion by mixing a teaspoon of dandelion powder with hot water, let it cool for a few minutes before drinking. You can also add a little honey to enhance the taste. Drink one glass a day, divided into 2-3 times, continuously for several weeks. Note, dandelion should not be used by people with diabetes because it can cause unwanted side effects.

Papaya: Papaya fruit and papaya seeds have great fat burning benefits that accumulate in the liver. So papaya is very good to improve fatty liver.

Protein: Foods that provide protein such as lean meats, poultry, fish, seafood, eggs, soybeans, legumes are good for weight loss and weight maintenance. Milk and dairy products: Nutrient-rich but low-fat milk as well as healthy dairy products including fat-free or low-fat milk, yogurt and cheese should be added to your daily diet. people with fatty liver disease.

Other foods: Licorice can be mixed with warm water or used as a supplement to treat nonalcoholic fatty liver disease. Grapefruit juice contains powerful antioxidants that enhance liver function.

3. Lifestyle changes in fatty liver disease

In addition to paying attention to what fatty liver disease eats, lifestyle changes are also a measure to help balance fatty liver. Lifestyle change measures include:
Control and maintain ideal weight: Regular monitoring of weight as well as weight gain is essential in controlling fatty liver disease, helping to control fatty liver disease. Regulates excess fat accumulation in the liver. When you are overweight or obese, you need to actively lose weight to achieve your ideal weight.

Change your diet and eating habits to ensure liver health:

A healthy diet consists mainly of plants with fruits, vegetables, whole grains, and vegetable oils. Green vegetables and fruits will provide the body with many important vitamins and minerals, in which vitamins A and E work to prevent the accumulation of extra fat in the liver. This will support the liver to work better and prevent the liver from working too hard. Avoid fatty foods, fast foods, processed foods, and junk foods. Exercise regularly and regularly, for at least 30 minutes a day and at least 5 days a week. If you are new to exercise, you should start with gentle exercises, then gradually increase the intensity. Regular exercise helps to increase metabolism and burn excess fat in the body, helping to lose weight and maintain a healthy weight. In a nutshell, fatty liver disease means the accumulation of fat in the liver cells and makes the liver more susceptible to damage, which can lead to hepatitis, liver failure. Currently, there is no specific treatment for fatty liver disease that can only be reversed by changes in diet and daily activities. source

The BEST Drink for a Fatty Liver

https://goodshepherdmedia.net/wp-content/uploads/2024/06/Liver-Disease-Healing-Liver-with-Dandelion-Lemon.mp4

Some research suggests that dandelion may help prevent and treat nonalcoholic fatty liver disease (NAFLD). For example, a 2013 study found that dandelion leaf extract (DLE) improved insulin resistance and reduced lipid accumulation in the livers of mice fed a high-fat diet. DLE also suppressed total cholesterol, triglycerides, fasting glucose, and insulin levels in the serum.

Dandelion root tea is also believed by some to help detoxify the liver and relieve symptoms of liver disease. To make dandelion tea, you can steep one tablespoon of dandelion roots or flowers in five ounces of boiling water for 30 minutes, then strain or drink the mixture.

However, you should avoid dandelion tea if you are pregnant or breastfeeding, taking diuretics, or taking antibiotics like Cipro or Levaquin. Dandelion also has natural diuretic properties, so it may interfere with the action of lithium and similar medications. If you are being treated for liver or kidney issues, you should also avoid dandelion or dandelion tea unless your doctor says it’s okay.

Easy Liver Cleanse Recipe: Detox Naturally with Lemon and Olive Oil

You only need to look at simple liver cleanse recipes that combine the flavorful combination of lemon and olive oil. This cleansing method supports liver function and promotes general well-being by utilizing the natural detoxifying qualities of these herbs in a gentle yet effective way.

Olive oil and lemon are the main ingredients in the main cuisine of European restaurants. Many people say that the combination of lemon juice and olive oil can treat many diseases like gallbladder stones.

Furthermore, research has looked at the possible health benefits of the components in lemon juice and olive oil independently.

This article will talk about the fact that studies support the purported health benefits of combining lemon juice with olive oil.

We’ll also review the olive oil lemon juice liver cleanse recipe.

Discover the Mutual Impact of Olive Oil and Lemon on liver

There we will learn about the combination of lemon juice and olive oil. Lemon and olive oil make an extremely unique combination. It is open to all, committed, and productive for the skin, liver, and even blood flow.

Let’s first explore the two fruits independently: The ability of lemon to act as an acidifying agent is its power.

The human body can become acidified if its pH level is out of balance, which can have major negative effects on health. Hyperacidity is countered and the pH value is adjusted during alkalizing. Therefore, sick cells typically lose their strength as well as their breeding ground.

There are many liver cleansing recipes with lemon juice and olive oil. Because these are the most easily used liver detox. Lemon Liver detox works properly to clean liver stones and many other harmful small agents.

Olive oil and Lemon Juice Liver Cleanse Recipe

Ingredients:

1/2 cup of extra virgin olive oil
1/4 cup of freshly squeezed lemon juice
1-2 cloves of minced garlic

Instructions:

Before beginning the cleanse, fast for a minimum of 12 hours to enable your liver to get ready for detoxification.
In a bowl, thoroughly mix the olive oil, lemon juice, and minced garlic.
During one to two hours, take one tiny serving (about one to two tablespoons) of the olive oil mixture every fifteen minutes.
After you’ve finished the olive oil mixture, lie on your right side with your knees pulled up to your chest for half an hour.
Spend the rest of the evening sleeping so that the cleanse has time to work.

How do you know that this combination is best for you?

Some research shows that eating lemon juice and olive oil together has health benefits. Many claim that they can aid in weight loss, treat and prevent gallstones, and perform cleanses and detoxes.

Let’s look at each of these claims properly.

Cleansing and Detoxification Ideas

A fast internet search will bring up a variety of recipes claiming to use lemon juice, olive oil, or both to detox and cleanse. It is said that waste and toxins that have accumulated in your body over time are taken out by cleanses and detoxes.

On the other hand, research on the potential cleansing and detoxifying effects of lemon juice and olive oil does not seem to be very extensive.

When compared to those who consumed other plant oils, the researchers discovered that those who consumed olive oil during the study period had greater levels of HDL (good) cholesterol and lower levels of LDL (bad) cholesterol in their blood.

In this article, we will give you the natural liver detox recipe for your best hygiene.

However, the polyphenols and antioxidants in lemon juice and olive oil could be referred to as “cleansing” because they “clean up” or neutralize dangerous free radicals. Which otherwise damages cells and may be a factor in sickness and disease.

Lemon and olive oil are recommended as the best quick liver detox. The human body uses a variety of biological processes to get rid of pollutants and keep itself operating at its best.

I suggest eating a diet that is rich in fruits, vegetables, whole grains, legumes, nuts, seeds, and lean protein sources to support your body’s optimal functioning.

Weight Loss

Vitamin C is rich in lemon juice. 38.7 mg, or 43% of the Recommended Dietary Allowance (RDA) for men and 52% of the RDA for women, is present in a 3-ounce (100-gram) serving. Vitamin C plays a crucial role in the body’s synthesis of carnitine.

A substance called carnitine is responsible for moving fat molecules into cells so they may be broken down and used as an energy source. Thus, a low vitamin C consumption could result in less fat being broken down. For

weight loss, many quick liver detox drinks are also available in the market.

Health Benefits of using Liver oil and Lemon Cleanse

What health advantages are associated with gallbladder cleansing?

To prevent gallstones, certain supporters of alternative healthcare advise liver cleansing. They maintain that the liver releases the gallstones as a result of the liver cleaning.

The gallstones should then ideally pass via the stool. This would mean that the patient would have fewer gallstones left to produce uncomfortable symptoms and might be able to avoid surgery.

There are various kinds of liver cleanses. Alternative medicine practitioners provide many ” liver detox recipes” and traditional treatments online.

Olive oil and lemon juice. Using this method, you will fast for 12 hours during the day and then drink 4 tablespoons of olive oil and 1 tablespoon of lemon juice, eight times every 15 minutes, starting at 7 p.m.
Vegetables and apple juice. Using this method, all you consume till five o’clock in the evening is apple and vegetable juice. Every fifteen minutes after 5 p.m., ingest eight ounces of olive oil by consuming 18 milliliters (ml) of olive oil mixed with 9 ml of lemon juice.

In these points, we tell you about the easy liver detox remedy that you can use at home easily.

How might a liver cleanse cause side effects?

Depending on the “recipe” one follows, cleansing may have different adverse effects. For example, a lot of individuals cleanse their livers using olive oil. When consumed in excess, this may have a laxative effect.

The following symptoms are possible for some people to experience after a gallbladder cleanse:

Diarrhea vomiting nausea
Depending on the herbs or other things someone utilizes in their cleanse, there could be additional negative consequences.

Furthermore, a person may perform a gallbladder cleansing yet still not be able to get rid of their gallstones. To prevent their symptoms from getting worse or an infection in their gallbladder. They probably need to have surgery at that point.

How to liver cleanse at home?

To support your liver’s natural detoxification activities and enhance general well-being. Liver cleansing at home might be a quick and easy solution. A possible strategy is to consume fewer processed meals, alcoholic beverages, and added sugars while increasing your intake of foods high in fiber, such as fruits, vegetables, and whole grains.

Furthermore, drinking lots of water throughout the day to stay hydrated promotes liver function and the removal of toxins. Herbal teas that you can drink regularly, like milk thistle or dandelion root, are also well-known for their liver-cleansing qualities. Different liver detox tea recipes are also present on the internet.

How much olive oil for detox?

Depending on things like tolerance levels, individual health status, and particular detox procedures, there are differences in the suggested quantity of olive oil for detoxification. In general, it’s important to balance safety and efficacy while using olive oil in a detox program.

As part of a detox treatment, it is generally recommended to ingest 1-2 tablespoons of extra virgin olive oil daily.

The body’s natural detoxification processes are supported by this moderate amount of beneficial substances, which do not overburden the system. These components include antioxidants and monounsaturated fats.

Conclusion

Cleanse Your Liver

In addition to lifestyle changes, nutrition can have an impact on liver health. Check out these beverages that can aid in improving liver function.

Your liver plays many important roles in your physical health. It aids in digestion and metabolism and acts as a filter for the blood, breaking down harmful substances into waste that is expelled from the body through urine and stool.

According to the Mayo Clinic, symptoms of liver dysfunction include:

Skin and eyes that appear yellowish (jaundice)
Abdominal pain and swelling
Swelling in the legs and ankles
Itchy skin
Dark urine color
Pale stool color
Chronic fatigue
Nausea or vomiting
Loss of appetite
Tendency to bruise easily

Liver disease can be genetic. Other factors like viral infections, age, obesity, or excessive alcohol use may also cause liver damage or dysfunction. If left untreated, this damage can be fatal.

The good news is the liver is the only organ in the body with the ability to regenerate new cells and repair damaged ones. Repairing liver damage can be challenging; however, it is possible through consistent diet and lifestyle changes. These include:

Maintaining a healthy weight
Eating nutritious food and having a balanced diet
Getting regular exercise
Avoiding harmful additives and chemicals
Avoiding excessive or continued alcohol or illegal drug use (damage from alcohol abuse can cause irreversible cirrhosis of the liver)

Also, many beverages, such as water, tea, and grapefruit juice, can be beneficial for your overall health and may aid detoxification of the body and liver.

Water

Staying properly hydrated is an important factor in maintaining a healthy liver. Dehydration can greatly affect liver function, especially the ability to detoxify blood. On average, you should drink eight to ten glasses of water a day; those with health conditions may need to increase their water intake beyond the recommended amount.

Teas

There are a few natural teas that may assist in liver function. Several popular and possibly beneficial teas for liver health include:

Lemon Ginger Tea – reduces the risk of liver disease
Peppermint Tea – improves digestion and detoxifying functions of the liver
Green Tea – reduces the accumulation of lipids in the liver and contains antioxidants

Research the health effects and benefits of specific teas or discuss recommendations with your health care provider to ensure safe recommended use.

Grapefruit Juice

Grapefruit juice contains specific antioxidants that stimulate the liver and help filter and excrete chemicals from the body. Grapefruit also contains flavonoids naringin and naringenin, which have anti-inflammatory and antioxidant properties that may help protect the liver. However, it is recommended to not consume more than six ounces of grapefruit juice per day. Grapefruit juice also interacts with many prescription medications, so please check with your doctor or pharmacist and read your medication warning labels before adding it to your diet.

Turmeric Water

Turmeric is a commonly used supplement that may decrease inflammation and assist with liver repair, due to its ability to help flush out harmful toxins while decreasing fat buildup in the liver. For safe use, medical studies recommend mixing one to three grams of dried turmeric root in hot water each day for up to three months.

Lemon Water

Many citrus fruits, including lemon, can be added to water to help stimulate and flush out the liver. Lemons are high in nutrients like vitamin C and antioxidants. To help prevent liver disease, enjoy four to six tablespoons of lemon juice mixed with water each day.

Ginger Water

Ginger helps protect your liver and reduces inflammation in the body. It may also boost immunity and improve digestive health. The recommended consumption is less than four grams of ginger per day, mixed with warm or cold water.

As with any change in nutritional intake or supplement use, please use caution. Some people may experience unwanted results or side effects, and some herbs and foods may interact with certain medications. Also, the information presented above is based on adult studies and should not be used for children. Research any supplements and consult a health care professional before making abrupt changes to your diet or lifestyle. source

DRINK 1 CUP PER DAY to Remove Fat from Your Liver – Dr. Berg

Many people have a fatty liver and don’t even know it.

Today I want to help you better understand the liver and how to remove fat from the liver. The purpose of the liver is to break down toxins into harmless particles. A fatty liver can become heavy and enlarged. This can lead to fullness under the right rib cage and shoulder pain.

Important functions of the liver:

It makes bile
It helps convert thyroid hormones
It buffers excess sex hormones

Bile is made by the liver, and it helps you break down fat. A lack of bile can lead to a lot of various health problems. Bile is also very important to keep fat out of the liver. Anything you can do to help increase bile reserves will help you remove liver fat. You may even want to take purified bile salts. Keep in mind that the ketogenic diet and intermittent fasting can help remove fat from the liver. I believe this is essential if you have a fatty liver.

A great shake to keep fat off the liver: Ingredients (organic if possible):

2 cups kale (frozen)
1 cup blueberries (frozen)
1 cup water
1 cup plain whole-milk kefir (organic and grass-fed if possible)

Instructions: Blend all of the ingredients in a blender for a couple of minutes. Drink once a day in combination with a Healthy Keto diet and intermittent fasting.

Protective Effects of Lemon Juice on Alcohol-Induced Liver Injury in Mice

Abstract

Chronic excessive alcohol consumption (more than 40-80 g/day for males and more than 20-40 g/day for females) could induce serious liver injury. In this study, effects of lemon juice on chronic alcohol-induced liver injury in mice were evaluated. The serum biochemical profiles and hepatic lipid peroxidation levels, triacylglycerol (TG) contents, antioxidant enzyme activities, and histopathological changes were examined for evaluating the hepatoprotective effects of lemon juice in mice. In addition, the in vitro antioxidant capacities of lemon juice were determined. The results showed that lemon juice significantly inhibited alcohol-induced increase of alanine transaminase (ALT), aspartate transaminase (AST), hepatic TG, and lipid peroxidation levels in a dose-dependent manner. Histopathological changes induced by alcohol were also remarkably improved by lemon juice treatment. These findings suggest that lemon juice has protective effects on alcohol-induced liver injury in mice. The protective effects might be related to the antioxidant capacity of lemon juice because lemon juice showed in vitro antioxidant capacity.

PubMed Disclaimer

1. Introduction

Alcohol abuse and alcoholism could lead to serious health and socioeconomic problems worldwide. Chronic excessive alcohol consumption (more than 40–80 g/day for males and more than 20–40 g/day for females) could lead to several illnesses, such as gastrointestinal damage, pancreatitis, alcoholic liver disease, neurologic disorders, diabetes mellitus, and cancer [1, 2]. Among these diseases, alcoholic liver disease has attracted more attention due to its high morbidity and mortality. Alcoholic liver disease is a major type of chronic liver disease throughout the world and can progress to liver cirrhosis and liver cancer.

Chronic alcohol consumption can generate abundant reactive oxygen species (ROS), including superoxide anion radical (O₂^−•), hydroxyl radical (OH^•), and hydrogen peroxide (H₂O₂). The ROS can react with most cellular macromolecules and subsequently cause cellular damage [3]. Therefore, the excessive ROS induced by alcohol is regarded as an important factor in the development of alcohol-induced liver injury. Various enzymatic and nonenzymatic antioxidants are related to protecting cells against ROS. Antioxidant enzymes include catalase (CAT), superoxide dismutase (SOD), and glutathione peroxidase (GPx), and nonenzymatic antioxidants include glutathione (GSH), vitamin E, ascorbate, vitamin A, and ubiquinone [4]. Nonenzymatic antioxidants can be enhanced by antioxidant intake. In recent years, many natural products that have abundant antioxidants were reported to possess the effect of scavenging free radicals and protecting the liver from oxidative damage [4, 5].

Lemon is a popular fruit consumed as juice and contains high contents of vitamins and polyphenols (mainly flavonoids), such as hesperidin, eriocitrin, naringin, neohesperidin, rutin quercetin, chlorogenic acid, luteolin, and kaempferol [6]. The in vivo and in vitro experiments have shown that lemon has various health benefits, such as anticancer effect, antimicrobial effect, lipid-lowering effect, and protective effect against cardiovascular diseases [6]. In addition, lemon is used to treat liver ailments in tribal medicine [7]. However, effects of lemon juice on chronic alcohol-induced liver injury have not been reported in the literature. The objective of this study is to investigate the effects of lemon juice on chronic alcohol-induced liver injury in mice. In addition, the in vitro antioxidant capacities of lemon juice were evaluated. The results of this study could supply valuable information for the general public to reduce harm of alcohol consumption.

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2. Materials and Methods

2.1. Chemicals and Reagents

The compounds 6-hydroxy-2,5,7,8-tetramethylchromane-2-carboxylic acid (Trolox), 2,2′-azinobis(3-ethylbenzothiazoline-6-sulfonic acid) diammonium salt (ABTS), 2,4,6-tri(2-pyridyl)- S-triazine (TPTZ), quercetin, gallic acid, and Folin–Ciocalteu’s phenol reagent were purchased from Sigma-Aldrich (St. Louis, MO, USA). Assay kits for the determination of SOD, lipid peroxidation, CAT, and TG contents were purchased from Nanjing Jiancheng Bioengineering Institute (Nanjing, China). Other chemicals were of analytical grade.

2.2. Materials

Lemon was obtained from markets in Guangzhou, China. The fruit was cleaned with deionized water. The edible portion was weighed precisely and mixed with deionized water (1 : 1, m/v), and the mixture was ground into a homogenate with a homogenizer. Then, the homogenate was centrifuged at 5,000g for 10 min, and the supernatant was obtained. The supernatant was used for the measurement of antioxidant capacity, total phenolic contents (TPC), and total flavonoid contents (TFC) and for animal experiments. Moreover, in animal experiments, the original supernatant and the diluted supernatant (1 : 5 and 1 : 10, m/v) were used as the high, medium, and low dose, respectively. The lemon juice was freshly prepared before gavage every time.

2.3. Animal Study

Male C57BL/6 mice (20–25 g) were employed in this study. Thirty mice were randomly divided into 5 groups, each group containing 6 mice. They were maintained in a SPF laboratory animal room, which kept a 12 h light/dark cycle at 22 ± 0.5°C with 40%–60% relative humidity. The animal study was performed according to the “Principles of Laboratory Animal Care” and approved by the Institutional Animal Ethics Committee of Sun Yat-sen University. The model group was treated daily with ethanol and distilled water (10 mL/kg) at the same time; the lemon juice treatment groups were treated daily with different concentrations (high dose 1 : 1 (m/v), medium dose 1 : 5, and low dose 1 : 10) of lemon juice (10 mL/kg) and ethanol simultaneously; the control group was treated daily with isometric distilled water. The model group and the lemon juice treatment groups were given ethanol according to the following ways: 35% ethanol (v/v) at a dose of 3 g/kg body weight for 7 days, 40% ethanol (v/v) at a dose of 4 g/kg body weight for the next 7 days, and 52% ethanol (v/v) at a dose of 5 g/kg body weight on the 15th day [8]. All the intervention methods were intragastric administration. The blood and liver were collected from mice 9 h after the last ethanol administration. The blood sample was centrifuged at 4,000g for 10 min and the serum was collected. The obtained serums were stored at −22°C before determination. A piece of tissue was taken from liver and fixed in 4% paraformaldehyde, and then the remaining liver tissue was stored at −22°C until use.

2.4. Measurement of Biochemical Parameters in the Serum

The levels of ALT, AST, and TG in serum were determined by a Hitachi-7180 automated biochemistry analyzer (Hitachi, Japan) with the corresponding reagent kit.

2.5. Measurement of TG and Antioxidant Enzyme Activities in the Liver

The levels of TG, SOD, and CAT in liver tissue were measured using the commercial detection kits according to the manufacturer’s instructions.

2.6. Measurement of Lipid Peroxidation Levels in the Liver

The levels of lipid peroxidation in liver tissue were measured by thiobarbituric acid (TBA) method using the commercial detection kits according to the manufacturer’s instructions. The reference standard was malondialdehyde (MDA), and the results were expressed as nmol MDA equivalent/mg prot.

2.7. Liver Histopathological Assessment

The liver tissue fixed in 4% paraformaldehyde was embedded in paraffin, sectioned into 5 μm thickness, and stained with hematoxylin-eosin (H&E) for evaluation of histopathological changes. The histopathological changes of stained liver slices were observed under a bright-field microscope.

2.8. Ferric-Reducing Antioxidant Power (FRAP) Assay

The FRAP assay was performed based on the method described in the literature [9]. In brief, the FRAP reagent was prepared from 10 mmol/L TPTZ solution, 20 mmol/L iron(III) chloride solution, and 300 mmol/L sodium acetate buffer solution (pH 3.6) in a volume ratio of 1 : 1 : 10, respectively. 100 μL of the diluted sample was added to 3 mL of the FRAP reagent and the mixture was measured after 4 min at 593 nm. The standard curve was established using FeSO₄ solution, and the results were expressed as μmol Fe(II)/g dry weight of lemon.

2.9. Trolox Equivalent Antioxidant Capacity (TEAC) Assay

The TEAC assay was carried out according to the procedure in the literature [10]. Briefly, the ABTS^•+ stock solution was prepared from 2.45 mmol/L potassium persulfate and 7 mmol/L ABTS solution in a volume ratio of 1 : 1 and then placed in the dark for 16 h at room temperature. The ABTS^•+ working solution was prepared by diluting the stock solution, and the absorbance of ABTS^•+ working solution was 0.710 ± 0.05 at 734 nm. 100 μL of the diluted sample was mixed with 3.8 mL ABTS^•+ working solution, and the absorbance of the mixture was measured at 734 nm after 6 min, and the percent of inhibition of absorbance at 734 nm was calculated. The reference standard was Trolox, and the results were expressed as μmol Trolox/g dry weight of lemon.

2.10. Determination of TPC

TPC were measured according to the literature [11]. Briefly, 0.50 mL of the diluted sample was added to 2.5 mL of 0.2 mmol/L Folin–Ciocalteu reagent. After 4 min, 2 mL of saturated sodium carbonate solution was added. After incubation for 2 h at room temperature, the absorbance of the mixture was measured at 760 nm. The reference standard was gallic acid, and the results were expressed as mg gallic acid equivalent (GAE)/g dry weight of lemon.

2.11. Determination of TFC

TFC were measured according to the literature [12]. In brief, 0.50 mL of the sample was mixed with 1.5 mL of 95% ethanol (v/v), 0.1 mL of 10% aluminum chloride (w/v), 0.1 mL of 1 mol/L potassium acetate, and 2.8 mL of water. After incubation for 30 min at room temperature, the absorbance of the mixture was determined at 415 nm. The reference standard was quercetin, and the results were expressed as mg of quercetin equivalent (QE)/g dry weight of lemon.

2.12. Statistical Analysis

Statistical analysis was carried out by one-way analysis of variance (ANOVA) with post hoc LSD test using SPSS 13.0 software. p < 0.05 was regarded as significant.

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3. Results

3.1. Effects of Lemon Juice on the Levels of ALT and AST in Serum

As shown in Figure 1, the administration of alcohol led to a significant (p < 0.05) elevation of alanine transaminase (ALT) and aspartate transaminase (AST) levels in serum of the model group compared with that of the control group. The administration of low and medium concentration of lemon juice slightly prevented the elevation of serum level of AST, while a high dose of lemon juice significantly (p < 0.05) decreased it. At the same time, the prevention of the elevation of serum levels of ALT was observed significantly (p < 0.05) in medium and high concentration of lemon juice group and displayed a dose-effect relationship.

Figure 1

Effects of lemon juice on the levels of AST (a) and ALT (b) in serum of mice. Control: normal group; Model: alcohol group; LL: alcohol and low dose of lemon juice group; LM: alcohol and medium dose of lemon juice group; LH: alcohol and high dose of lemon juice group. ∗ means the levels of parameters in the model group were significantly (p < 0.05) different from those of the control group. # means the levels of parameters in the treatment group were significantly (p < 0.05) different from those of the model group.

3.2. Effects of Lemon Juice on the Levels of TG in Serum and Liver

Triacylglycerol (TG) content in serum was significantly (p < 0.05) increased in the model group compared with that in the control group (Figure 2(a)). Administration of lemon juice reduced the accumulation of TG in a dose-dependent manner, especially in high concentration of lemon juice group (p < 0.05). In addition, hepatic TG content was significantly (p < 0.05) increased in model group compared with that in the control group (Figure 2(b)). Administration of medium and high concentration of lemon juice significantly (p < 0.05) reduced the accumulation of hepatic TG in a dose-dependent manner.

Figure 2

Effects of lemon juice on TG contents in serum (a) and liver (b). Control: normal group; Model: alcohol group; LL: alcohol and low dose of lemon juice group; LM: alcohol and medium dose of lemon juice group; LH: alcohol and high dose of lemon juice group. ∗ means the levels of parameters in the model group were significantly (p < 0.05) different from those of the control group. # means the levels of the parameters in the treatment group were significantly (p < 0.05) different from those of the model group.

3.3. Effects of Lemon Juice on Liver Lipid Peroxidation Levels

The lipid peroxidation levels in liver tissue are shown in Figure 3. Compared with that of the control group, there was a significant (p < 0.05) increase in the lipid peroxidation level of the model group. The administration of lemon juice significantly (p < 0.05) decreased the level of lipid peroxidation in a dose-dependent manner.

Figure 3

Effects of lemon juice on hepatic lipid peroxidation level in mice. Control: normal group; Model: alcohol group; LL: alcohol and low dose of lemon juice group; LM: alcohol and medium dose of lemon juice group; LH: alcohol and high dose of lemon juice group. ∗ means the levels of the parameters in the model group were significantly (p < 0.05) different from those of the control group. # means the levels of the parameters in the treatment group were significantly (p < 0.05) different from those of the model group.

3.4. Effects of Lemon Juice on Liver Antioxidant Enzyme Activities

Figure 4 represents the results of hepatic antioxidant enzyme activities in five groups. The SOD level in the liver increased significantly (p < 0.05) in the model group compared with that in the control group. The CAT level in the liver decreased only slightly (p > 0.05) in the model group compared with the control group in this study. However, treatment with lemon juice significantly (p < 0.05) decreased the levels of SOD and CAT compared with those of the model group. In addition, all the biochemical parameters are summarized in Table 1.

Figure 4

Effects of lemon juice on the activities of SOD (a) and CAT (b) in liver. Control: normal group; Model: alcohol group; LL: alcohol and low dose of lemon juice group; LM: alcohol and medium dose of lemon juice group; LH: alcohol and high dose of lemon juice group. ∗ means the levels of the parameters in the model group were significantly (p < 0.05) different from those of the control group. # means the levels of the parameters in the treatment group were significantly (p < 0.05) different from those of the model group.

Table 1

Effects of lemon juice on the levels of several biochemical parameters.

Parameters	Control	Model	LL	LM	LH
AST (U/L)	103 ± 10.45	136.53 ± 19.94^∗	117.88 ± 15.37	113.5 ± 7.7	98.85 ± 10.94^#
ALT (U/L)	40.5 ± 3.89	54.32 ± 4.76^∗	54.05 ± 7.18	41.32 ± 6.25^#	34.68 ± 2.71^#
Serum TG (nmol/L)	0.4 ± 0.06	1.01 ± 0.12^∗	1.09 ± 0.04	1.03 ± 0.05	0.82 ± 0.08^#
Liver TG (mmol/g prot)	0.07 ± 0.01	0.1 ± 0.02^∗	0.09 ± 0.01	0.07 ± 0.01^#	0.06 ± 0.01^#
Lipid peroxidation (nmol MDA equivalent/mg prot)	0.64 ± 0.14	1.26 ± 0.22^∗	0.88 ± 0.12^#	0.84 ± 0.15^#	0.72 ± 0.13^#
SOD (U/mg prot)	89.6 ± 3.42	97.51 ± 3.96^∗	85.27 ± 5.57^#	83 ± 9.28^#	81.03 ± 6.65^#
CAT (U/mg prot)	6.55 ± 0.41	6.29 ± 0.39	5.55 ± 0.64^#	5.47 ± 0.28^#	5.17 ± 0.51^#

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Note. Control: normal group; Model: alcohol group; LL: alcohol and low dose of lemon juice group; LM: alcohol and medium dose of lemon juice group; LH: alcohol and high dose of lemon juice group. ∗ means the levels of the parameters in the model group were significantly (p < 0.05) different from that of the control group. # means the levels of the parameters in the treatment group were significantly (p < 0.05) different from that of the model group.

3.5. Histopathological Evaluation

Histopathology assessment of the liver was carried out for all groups (Figure 5). There was no pathological abnormality observed in the liver of the control group with preserved cytoplasm and distinct nucleus as shown in Figure 5(a). In Figure 5(b), it was observed in the model group that ethanol induced necrosis changes and substantial small fat droplets changes in liver section. However, livers of mice in all lemon juice treated groups showed noticeable recovery from ethanol induced liver damage with fewer small fat droplets changes and hepatocytes necrosis features.

Figure 5

The photomicrographs of liver sections taken from mice. (a) Normal group; (b) alcohol group; (c) alcohol and low dose of lemon juice group; (d) alcohol and medium dose of lemon juice group; (e) alcohol and high dose of lemon juice group. Arrow indicates a condition of small fat droplets changes, and the circle indicates hepatocytes necrosis, which mainly occurs in alcohol model group.

3.6. The In Vitro Antioxidant Activity, Total Phenolic Contents (TPC), and Total Flavonoid Contents (TFC) of Lemon Juice

The in vitro antioxidant activities of lemon were evaluated using ferric-reducing antioxidant power (FRAP) and Trolox equivalent antioxidant capacity (TEAC) assays. The FRAP and TEAC values were 50.82 ± 2.70 μmol Fe(II)/g dry weight (DW) and 19.88 ± 0.66 μmol Trolox/g DW, respectively. The total phenolic contents (TPC) and total flavonoid contents (TFC) of lemon were 6.21 ± 0.28 mg GAE/g DW and 0.30 ± 0.03 mg QE/g DW, respectively.

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4. Discussion

Alcohol use disorder causes substantial diseases, and the liver is the most adversely affected organ. In the present study, the effects of lemon juice on chronic alcohol-induced liver injury in mice were investigated. Ethanol induced impairment of liver in mice was evidenced by increased AST and ALT levels. Treatment with lemon juice lowered the increased levels of AST and ALT in serum. The return of the activities of aminotransferases (AST or ALT) in serum to normal indicates the regeneration of hepatocytes and the healing of hepatic parenchyma; therefore, lemon juice had a protective effect on alcohol-induced liver injury. The results were in agreement with previous reports that showed lemon possessing a hepatoprotective effect on liver injury induced by carbon tetrachloride and acute exercise [7, 13]. In addition, the chronic alcohol-induced liver damage was further confirmed by liver histopathological changes in the present study, and treatment with lemon juice also remarkably improved the liver histopathological changes, which further confirmed the hepatoprotective activity of lemon juice on alcohol-induced liver injury in mice.

Various factors and mechanisms are associated with the pathological progress of alcohol-induced liver injury, and oxidative stress was one of them [3]. ROS is one kind of prooxidants including hydroxyl radical, superoxide radical, and hydrogen peroxide, which are frequently generated spontaneously during metabolism. Normally produced ROS is rapidly eliminated by the antioxidant defense system. The antioxidant defense system is able to scavenge ROS and terminate chain reaction of free radicals in vivo. Alcoholic exposure can result in excessive accumulation of ROS and contribute to cellular damage. Excessive accumulation of ROS could cause lipid peroxidation of hepatocytes, which was regarded as the primary mechanism concerned with chronic alcohol-induced liver damage [8]. MDA, the product of lipid peroxidation induced by ROS, also accumulates in the alcohol-damaged liver and represents a good estimation of the total oxidative stress [3]. In the present study, alcohol significantly augmented lipid peroxidation levels, which was similar to the previous study that showed increased lipid peroxidation in alcoholic patients [14]. Treatment with lemon juice reduced the level of lipid peroxidation to a normal level, which showed a significant protective effect of lemon juice against alcohol-induced oxidative stress.

Liver steatosis is the earliest disease of the liver on account of chronic ethanol consumption, with the characteristic of fat accumulation. It is generally accepted that, in the development of hepatic steatosis, ethanol exposure increases the ratio of reduced nicotinamide adenine dinucleotide/oxidized nicotinamide adenine dinucleotide in hepatocytes, which disturb mitochondrial fatty acid β-oxidation and induce steatosis further [15]. In this study, alcohol-induced occurrence of hepatic steatosis was confirmed by increased hepatic TG contents and histopathological changes. Treatment with lemon juice significantly lowered the hepatic TG contents and improved the damaged histopathological changes. In particular, the mice given high dose of lemon juice had almost completely recovered to normal.

The antioxidant enzymes, such as SOD and CAT, represent the defense response system to excessive ROS. SOD catalyzes the dismutation of two superoxide anions to hydrogen peroxide and oxygen, and then CAT degrades two hydrogen peroxide molecules to water and oxygen [16]. SOD is also considered as front line among antioxidant enzymes in defense against free radicals. In the literature, the effects of alcohol treatment on the levels of SOD/CAT are controversial. SOD showed an increase, no changes, or a decrease, depending on the model, diet, duration, and amount of alcohol consumption [17–19]. In addition, it was reported that CAT activity decreased upon chronic ethanol consumption in a study [20]. However, another study showed that CAT activity was increased in rat liver [18]. In our study, the alcohol treatment significantly increased the activity of SOD and slightly decreased the activity of CAT, while treatment with lemon juice decreased the activities of SOD and CAT. The increased activity of SOD reflects the activation of the compensatory mechanism which might be an attempt to counteract free radicals in the liver [21]. The treatment with lemon juice prevented ROS accumulation, and the compensatory effects were not available in the liver. Therefore, lemon juice decreased the activities of SOD and CAT. The results were similar to the report of Gasparotto et al. [22]. In addition, the in vitro antioxidant experiment of lemon also showed that lemon had medium in vitro antioxidant capacities, which contribute to the explanation of the in vivo free radical scavenging effect of lemon.

Lemon contains numerous beneficial bioactive compositions, including phenolic compounds (mainly flavonoids), vitamins, carotenoids, essential oils, minerals, and dietary fiber [6]. The hepatoprotective effect of lemon may be attributable to the presence of vitamins, flavonoids, essential oils, and pectin. Vitamin C, a water-soluble antioxidant in lemon, is in a unique position to scavenge aqueous peroxyl radicals and react with free radicals, thus preventing oxidative damage including lipid peroxidation [14]. Sometimes, vitamin C could exert prooxidative effects at low concentrations and in the existence of transition metal ions [23], which might aggravate oxidative stress. However, it is difficult for vitamin C to have prooxidative effects in vivo due to the presence of NADPH-dependent recycling systems and glutathione [24]. In addition, there were some literatures reporting that vitamin C supplementation alone could reduce oxidative stress induced by ethanol, and the hepatoprotective effect of vitamin C treatment was more effective than silymarin, quercetin, and thiamine [25, 26]. Flavonoids, a class of secondary plant phenolics, can interact with hydroxyl radicals, chelate metal catalysts, and inhibit oxidases [27]. In previous studies, lemon flavonoid was shown to possess a hepatoprotective effect on liver damage induced by carbon tetrachloride and acute exercise, and the mechanism of the protective effect was related to the antioxidant capacity [7, 13]. Lemon essential oils and pectin were found to have protective effects on stomach and intestine barrier function [28, 29]. Ethanol exposure can injure the defensive intestinal barrier and increase the permeability of the small intestine, which lead to bacterial endotoxins leakage [25]. The bacterial endotoxins leakage is an important factor in the pathogenesis of alcohol-induced liver injury [30]. Therefore, the lemon essential oils and pectin might protect the intestine barrier function, thus indirectly protecting against alcohol-induced liver injury.

In this study, lemon juice revealed a protective effect on chronic alcohol-induced liver injury. Due to the fact that lemon contains a variety of bioactive ingredients, the hepatoprotective effect might be the result of joint action of multiple mechanisms, and it is difficult to clarify the specific mechanism of effect. The medium in vitro antioxidant capacities of lemon and reduced in vivo MDA levels indicated that lemon might reduce the oxidative stress induced by ethanol, thus exerting hepatoprotective effects. This study has found that lemon juice has a strong hepatoprotective effect, which provides valuable information for the general public to reduce harm of alcohol consumption. In the future, active components in lemon juice should be separated and identified, and the mechanism of action of the purified compound should be explored, including the action on the small intestine.

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5. Conclusions

Chronic alcohol consumption could induce liver injury. Lemon juice is readily available as a widely consumed beverage. In this study, we found that treatment with lemon juice exerted hepatoprotective effects on alcohol-induced liver injury in mice through decreasing the levels of serum ALT and AST as well as hepatic TG and lipid peroxidation. In addition, the in vitro antioxidant experiment of lemon showed that lemon had medium in vitro antioxidant capacities. Therefore, we speculate that the hepatoprotective effects might be related to the antioxidant capacities of lemon juice. The results showed that lemon juice might be a potential dietary supplement for the prevention and treatment of liver injury related to chronic alcohol consumption.

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Acknowledgments

This work was supported by the National Natural Science Foundation of China (no. 81372976), Key Project of Guangdong Provincial Science and Technology Program (no. 2014B020205002), and the Hundred-Talents Scheme of Sun Yat-sen University.

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Conflicts of Interest

The authors declare that there are no conflicts of interest regarding the publication of this paper.

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Authors’ Contributions

Tong Zhou and Yu-Jie Zhang contributed equally to this work.

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Prevention of the Pro-Aggressive Effects of Ethanol-Intoxicated Mice by Schisandrin B.

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Exercise Affects the Formation and Recovery of Alcoholic Liver Disease through the IL-6-p47^phox Oxidative-Stress Axis.

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References

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Taraxacum official (dandelion) leaf extract alleviates high-fat diet-induced nonalcoholic fatty liver

Abstract

The purpose of this study is to determine the protective effect of Taraxacum official (dandelion) leaf extract (DLE) on high-fat-diet (HFD)-induced hepatic steatosis, and elucidate the molecular mechanisms behind its effects. To determine the hepatoprotective effect of DLE, we fed C57BL/6 mice with normal chow diet (NCD), high-fat diet (HFD), HFD supplemented with 2g/kg DLE DLE (DL), and HFD supplemented with 5 g/kg DLE (DH). We found that the HFD supplemented by DLE dramatically reduced hepatic lipid accumulation compared to HFD alone. Body and liver weights of the DL and DH groups were significantly lesser than those of the HFD group, and DLE supplementation dramatically suppressed triglyceride (TG), total cholesterol (TC), insulin, fasting glucose level in serum, and Homeostatic Model Assessment Insulin Resistance (HOMA-IR) induced by HFD. In addition, DLE treatment significantly increased activation of adenosine monophosphate (AMP)-activated protein kinase (AMPK) in liver and muscle protein. DLE significantly suppressed lipid accumulation in the liver, reduced insulin resistance, and lipid in HFD-fed C57BL/6 mice via the AMPK pathway. These results indicate that the DLE may represent a promising approach for the prevention and treatment of obesity-related nonalcoholic fatty liver disease.

Keywords: AMPK; Fatty liver; High-fat diet; Insulin resistance; Taraxacum official (dandelion).

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Dandelion Polysaccharides Ameliorate High-Fat-Diet-Induced Atherosclerosis in Mice through Antioxidant and Anti-Inflammatory Capabilities.

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Dandelion (Taraxacum Genus): A Review of Chemical Constituents and Pharmacological Effects.

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Protective Effects of Taraxacum officinale L. (Dandelion) Root Extract in Experimental Acute on Chronic Liver Failure

Abstract

Background: Taraxacum officinale (TO) or dandelion has been frequently used to prevent or treat different liver diseases because of its rich composition in phytochemicals with demonstrated effect against hepatic injuries. This study aimed to investigate the possible preventing effect of ethanolic TO root extract (TOERE) on a rat experimental acute on chronic liver failure (ACLF) model. Methods: Chronic liver failure (CLF) was induced by human serum albumin, and ACLF was induced in CLF by D-galactosamine and lipopolysaccharide (D-Gal-LPS). Five groups (n = 5) of male Wistar rats (200–250 g) were used: ACLF, ACLF-silymarin (200 mg/kg b.w./day), three ACLF-TO administered in three doses (200 mg, 100 mg, 50 mg/kg b.w./day). Results: The in vivo results showed that treatment with TOERE administered in three chosen doses before ACLF induction reduced serum liver injury markers (AST, ALT, ALP, GGT, total bilirubin), renal tests (creatinine, urea), and oxidative stress tests (TOS, OSI, MDA, NO, 3NT). Histopathologically, TOERE diminished the level of liver tissue injury and 3NT immunoexpression. Conclusions: This paper indicated oxidative stress reduction as possible mechanisms for the hepatoprotective effect of TOERE in ACLF and provided evidence for the preventive treatment.

Keywords: acute on chronic liver failure, hepatoprotective, oxidative stress, Taraxacum officinale, 3-nitrotyrosine

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1. Introduction

Liver diseases are one of the major health problems in the world and became a general health care problem due to the high morbidity rate. They are associated with several risk factors such as inadequate nutrition, metabolic diseases, viral infection, ethanol, and drug use. Liver injury may trigger the onset of liver failure, a common medical condition with very high mortality [1]. Liver failure can progress as acute liver failure (ALF), as acute on chronic liver failure (ACLF), or as acute decompensation of end-stage liver disease [2]. ALF is defined as a severe liver injury in the absence of pre-existing liver disease. According to the World Gastroenterology Organization ACLF is defined as “a syndrome in patients with chronic liver disease with or without previously diagnosed cirrhosis, characterized by acute hepatic decompensation resulting in liver failure (jaundice and prolongation of the international normalized ratio) and one or more extrahepatic organ failures, associated with increased mortality up to three months” [2,3]. The prevalence of ACLF ranges from 24% to 40%, and it usually occurs in young or middle-aged patients [4] and it is potentially reversible [2].

The exact mechanism of ACLF is not fully elucidated but based on what was found the pathophysiology was described using a four-stage model: precipitating event, hepatic injury due to precipitating event, response to injury, and failure of other organs [4,5]. The precipitating event can be triggered by one or more factors, identified or unidentified, like infections, alcohol, gastrointestinal bleeding, reactivation of viral hepatitis B (HBV), superinfection with hepatitis A or E virus, acute episodes of autoimmune hepatitis, Wilson’s disease, or vascular liver disease [2,6,7]. During the propagation phase, the number of proinflammatory mediators increases, a systemic inflammatory response syndrome and a vascular endothelial dysfunction will be activated, with progression to organs failure. At the same time, liver macrophages release anti-inflammatory cytokines that will initiate a compensatory anti-inflammatory response syndrome, leading to an acquired immunodeficiency, a “paralysis of the immune response” [4,8]. Measurement of oxidative stress, inflammation, necrosis, and apoptosis biomarkers can define the risk profile of ACLF [4,8]. The presence of multiple organ failure is a requirement for the diagnosis of ACLF, and the number of affected systems has a prognostic value. The kidneys are the most commonly affected organs [2,3].

Thus, the therapy for chronic hepatic diseases needs to develop new prophylactic agents to prevent ACLF. With the extended studies upon the use of medicinal plants, phytotherapy became an important support for the treatment of many diseases. The use of medicinal plants in the treatment of liver diseases has a long history worldwide because many phytochemicals have hepatoprotective activity [1,9,10]. Only a few of the ethnomedicinal effects have been scientifically validated [11]. Considering that in ACLF inflammation and oxidative stress are important pathogenetic mechanisms, the herbal medicines that have anti-inflammatory and antioxidant effects could be a promising source of bioactive compounds [12].

The Taraxacum officinale F. H. Wigg. (TO) (dandelion) species belong to the Asteraceae family, includes 30–57 varieties, and are widely distributed in the warm-temperate zones of the Northern Hemisphere [13,14,15]. It is a plant used in folk medicine from ancient times as anti-inflammatory, antioxidant, diuretic, choleretic, laxative, and hepatoprotective. Because the phytochemical components may define the medicinal value of a plant, their identification and effects mechanism in disease prevention and treatment is a necessity [11]. Furthermore, it has to be considered that the chemical composition of the TO extracts depends on both the extraction protocol and the solvents used (ethanol, acetone, water, or methanol) [16], but also on which part of the plant has been used (whole plant, roots, stem, leaves, flowers).

TO is also frequently used in different food products, and dietary supplements [17]. These plants were found to be rich in polyphenolic compounds, vitamins, inositol, lecithin, and minerals, and to exhibit antioxidant, anti-inflammatory, antiallergic, anti-hyperglycemic, hypolipidemic, and anticoagulant activities [9,18,19], to protect against hepatic injuries, but the mechanisms of action are still incompletely investigated [20].

It was demonstrated that TO root extract may protect against some toxic hepatic injury [11,13,21,22], but there are no studies on the potential hepatoprotective effect of this extract in ACLF. Therefore, our study aimed to extend the characterization of the ethanolic TO root extract (TOERE) and evaluate the potential use as a preventive hepatoprotective agent in a rat d-galactosamine and lipopolysaccharide (D-Gal-LPS)-induced rat ACLF model.

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2. Materials and Methods

2.1. Chemicals

Phenolic compounds Sigma (St. Louis, MO, USA), Roth (Karlsruhe, Germany), Dalton (Toronto, ON, Canada); phytosterols Sigma (St. Louis, MO, USA); Folin–Ciocâlteu reagent, sulfanylamide (SULF), N- (1-Naphthyl) ethylenediamine dihydrochloric acid (NEDD), vanadium chloride (III) (VCl3), methanol, diethyl ether, xylenol orange [o-cresosulfonphthalein-3,3-bis (sodium methyliminodiacetate)], orthodianisidinedihydrochloric acid (3-3′-dimethoxybenzidine), ferrous ammonium sulfate, hydrogen peroxide (H2O2), sulfuric acid, hydrochloric acid, glycerol, trichloroacetic acid (TCA), ethylenediaminetetra-acetic acid, sodium dodecal, sulfate butylated hydroxytoluene, thiobarbituric acid, 1,1,3,3-tetraethoxypropane, 2,4-dinitrophenylhydrazine (DNPH), 5,5’-dithionitrobis 2-nitrobenzoic acid (DTNB), 1,1-diphenyl-2-picrilhydrazyl (DPPH), o-phthalaldehyde Merck (Darmstadt, Germany); Trolox (6-hydroxy-2,5,7,8-tetramethylchroman-2-carboxylic acid) Alfa-Aesar (Karlsruhe, Germany); Freund’s adjuvant, d-galactosamine (D-Gal) and lipopolysaccharide (LPS) from Merck and Sigma-Aldrich (Taufkirchen, Germany); Human serum albumin (HSA) (Octapharma GmbH, Austria). All chemicals were of analytical grade. Aspartate aminotransferase, alanine aminotransferase, total bilirubin, alkaline phosphatase, gamma glutamate transferase, creatinine, and urea kits were purchased from Spinreact (Sant Esteve de Bas, Spain). ELISA kit for 3-nitrotyrosine (KA0445-ABNOVA EMBLEM, Heidelberg, Germany) and primary antibody to 3-Nitrotyrosine for immunohistochemistry (Code ALX-804-505-C050, Enzo Life Sciences) were also used.

2.2. Plant Material

Fresh T. officinale F.H. Wigg. roots from the Alexandru Borza Botanical Garden “Babes-Bolyai” University of Cluj-Napoca, Romania, were purchased in June 2020, deposited in “Alexandru Borza” Botanical Garden Herbarium (Voucher CL:669002), and plant extract was prepared as previously described [23]. The roots were dried in a shaded place, grounded in a coffee grinder (Argis, RC-21, Electroarges SA, Curtea de Arges, Romania) for 5 min, and then the powder was screened through a 200 μm Retsch sieve [24]. Fifty grams were weighed and extracted with 70% ethanol, twice for 30 min using the UltraTurrax extraction apparatus (T 18; IKA Labortechnik, Staufen, Germany) at room temperature. The samples were then centrifuged at 4000 rpm for 30 min, and the supernatant was recovered, and filtered through a 0.45 μm micropore membrane (PTFE, Waters, Milford, MA, USA). The solvent was evaporated at 40 °C using a rotary evaporator (Hei-VAP, Heidolph Instruments GmbH & Co., Schwabach, Germany). Further, the obtained extracts were lyophilized (Advantage 2.0, SP Scientific, Warminster, PA, USA) [24]. The extract powder was stored at room temperature in airtight bottles. The extraction yield was 15.2% (w/w).

2.3. Phytochemical Analysis

Identification and Quantification of Polyphenolic Compounds by HPLC-DAD-ESI MS

The phenolic compounds of the T. officinale extracts were determined as previously described [23,24] with some modifications. Prior to LC analysis, the lyophilized extract was dissolved in MeOH. Chlorogenic acid was used for phenolic acid quantification, and results were expressed as mg chlorogenic acid equiv./g of dry plant material (mg CA/g d.w.) [25].

2.4. Animals and Experimental Design

The experiments were carried out on adult male Albino Wistar rats (strain Crl: WI), weighing 200–250 g, bred in the Animal Facility of Iuliu Hațieganu University of Medicine and Pharmacy, Cluj-Napoca as previously described [23]. Animals were randomly divided into 6 groups (n = 5): Control group with no disease and no treatment, acute on chronic liver failure (ACLF) group, ACLF with Silymarin pretreatment (ACLF-SYL) group (200 mg/kg b.w./day) [26], ACLF groups with TOERE pretreatment in three doses, respectively ACLF-TO200 (200 mg dry plant material/kg b.w./day), ACLF–TO100 (100 mg dry plant material/kg b.w./day), and ACLF-TO50 (50mg dry plant material/kg b.w./day). The daily dose of TOERE has been dissolved in corn oil (1ml/day/animal). All the procedures performed on laboratory animals, comply with the Directive 2010/63/EU, and Romanian national law 43/2014 for animal protection used for scientific purposes. The project was approved by the Veterinary Sanitary Direction and Food Safety Cluj-Napoca as previously described (no. 19/ 13.12.2016) [23].

The ACLF rat model was induced by human serum albumin (HSA), d-galactosamine (D-Gal), and lipopolysaccharide (LPS) as previously described [27,28]. Silymarin (SYL) or TO have been administrated per os (p.o.) by gavage for 7 days. The ACLF group was pretreated for 7 days with physiological saline (1 mL/day/animal). After completing the treatments, on day 8 in the ACLF, ACLF-TO200, ACLF-TO100, ACLF–TO50, and ACLF-SYL groups ACLF was induced by the intraperitoneal injection (i.p.) of d-galactosamine (D-Gal) (400 mg/kg b.w.) and lipopolysaccharide (LPS) (100 μg/kg b.w.) [27,29]. Six hours after ACLF induction the rats were anesthetized with ketamine (60 mg/kg b.w.) and xylazine (15 mg/kg b.w.), blood was withdrawn by retro-orbital puncture, serum was separated by centrifugation, and stored at −80 °C until use. At the end of the experiment, under general anesthesia animals were killed by cervical dislocation and liver biopsy was harvested from each animal. The experiments were performed in triplicate.

2.5. Biochemical Serum Analysis

The hepatic injury was evaluated with conventional serum liver markers: serum aspartate aminotransferase (AST), alanine aminotransferase (ALT), total bilirubin (BT), alkaline phosphatase (ALP), and gamma glutamate transferase (GGT) as previously described [23]. Oxidative stress associated with liver injury was evaluated by measuring serum total oxidative status (TOS), total antioxidant reactivity (TAR), oxidative stress index (OSI), malondialdehyde (MDA), total thiols (SH), total nitrites, and nitrates (NOx) and 3-nitrotyrosine (3NT) levels as previously described [23,30,31]. Renal failure induced by ACLF was diagnosed with creatinine and urea.

2.6. Histological Assessment

For the histological analysis two liver fragments were collected from the left lateral and right medial lobes [32], fixed in 10% phosphate-buffered formalin for 24 h, and routinely processed and embedded in paraffin wax. From each tissue fragment, two serial sections of 3 µm were stained with hematoxylin and eosin (H&E). The hepatic parenchyma was histologically assessed for intralobular and periportal degeneration/necrosis, portal inflammation, and fibrosis, and the Histological Activity Index (HAI) was calculated [33,34].

2.7. Immunohistochemical Analysis of 3-Nitrotyrosine

For the immunohistochemical analysis of 3NT, the paraffin sections were dewaxed in xylene, followed by rehydration in decreasing the concentration of alcohol. Sodium citrate buffer (pH = 6) was used for epitope retrieval and endogenous peroxidase was blocked with peroxidase for 5 min. The primary mouse monoclonal [clone 39B6] antibody to 3NT was diluted in 1% PBS-BSA (bovine serum albumin) at 1:200, and maintained overnight at 4 °C in a humid chamber, followed by placing the secondary antibody. The reaction was visualized using 3,3’-diaminobenzidine. Finally, the sections were counterstained with Mayer’s hematoxylin. The positive reaction was given by the brown labeling of the hepatocytes. Immunopositivity for 3NT was evaluated and scored, as follows: grade 0, no staining; grade 1, positive staining in less than 10% of hepatocytes/10 high power fields; grade 2, positive staining in more than 10% but less than 50% of hepatocytes/10 high power fields; grade 3, positive staining of more than 50% of hepatocytes/10 high power fields [35].

The sections were independently examined by two pathologists (MT and CT) using a light Olympus BX-41 microscope, and a multi-head microscope Zeiss Axio Scope A1 (Carl Zeiss Microscopy GmbH, Germany). When there was a divergence of opinion, an agreed diagnosis was reached by a simultaneous evaluation in a multi-head microscope Zeiss Axio Scope A1 (Carl Zeiss Microscopy GmbH, Germany). The photomicrographs were taken using an Olympus SP 350 digital camera and Stream Basic imaging software (Olympus Corporation, Tokyo, Japan).

2.8. Statistical Analysis

All results were expressed as mean ± standard deviation (SD) whenever data were normally distributed. Comparisons between the different experimental groups were performed using the one-way ANOVA test and the post hoc Bonferroni–Holm test. The correlations analysis was performed with the Pearson test. Values of p < 0.05 were considered statistically significant. The analysis was performed using IBM SPSS Statistics, version 20 (SPSS Inc. Chicago, IL, USA).

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3. Results

3.1. Phytochemical Analysis

In our study, HPLC-DAD-ESI MS identified significant concentrations of hydroxybenzoic, caffeic, and chicoric acids (Figure 1, Table 1).

Figure 1

Chromatogram obtained by HPLC-DAD-ESI MS analysis of a Taraxacum officinale root extract at 340 nm. For peak assignments, see Table 1.

Table 1

Identification and quantification of Taraxacum officinale root extract polyphenols from hydroxybenzoic and hydroxycinnamic acids groups.

No	Retention Time R_t (min)	UV λ_max (nm)	[M+H]⁺ (m/z)	Tentative Identification	Concentration * mg CA/ g TOERE
1	2.95	270	138	Hydroxybenzoic acid	3.65 ± 0.15
2	13.62	320	181, 163	Caffeic acid	1.09 ± 0.02
3	14.19	322	475, 312	Chicoric acid	1.95 ± 0.15
4	15.50	322	369	Feruloylquinic acid	0.6 ± 0.08
5	19.93	322	516, 181,163	Dicaffeoylquinic acid	0.53 ± 0.04
6	20.12	322	516, 181,163	Dicaffeoylquinic acid isomer	0.4 ± 0.03

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* mg CA/g TOERE-chlorogenic acid equiv. mg/g Taraxacum officinale ethanolic root extract. Values are the mean ± SD (n = 3).

3.2. Biochemical Serum Analysis

The hepatic injury was evaluated by measuring liver markers (AST, ALT, ALP, GGT, TB) [36] (Table 2). ACLF induction by D-Gal-LPS caused a severe increase of the liver markers than in Control animals (p < 0.001). Administration for a week of three different doses of TOERE or SYL in ACLF animals significantly prevented severe ACLF-induced increase of the AST, ALT, ALP, GGT, and TB (p < 0.001). Furthermore, the TOERE effect was dose-dependent, with the 100 mg TOERE/kg b.w./day concentration having the best inhibitory effect. In ACLF-TO200 and ACLF-TO100 groups TOERE hepatoprotective effects were better than in ACLF-SYL animals (p < 0.01) (Table 2).

Table 2

Liver and renal screening tests of the study groups.

Groups	AST (U/L)	ALT (U/L)	TB (mg/dL)	ALP (mg/dL)	GGT (mg/dL)	Urea (mg/dL)	CR (mg/dL)
ACLF-TO200	81.12 ^a ± 5.27	71.64 ^a,b,c ± 11.32	2.27 ^a,b,c ± 0.37	328.45 ^a,b ± 14.72	60.42 ^a,b,c ± 9.20	67.14 ^a,b,c ± 4.21	1.75 ^a,b ± 0.21
ACLF-TO100	82.14 ^a,b,c ± 4.20	54.08 ^b,c ± 12.37	1.30 ^b,c ± 0.27	310.38 ^a,b,c ± 11.19	49.97 ^b,c ± 8.37	78.93 ^a,b ± 5.18	1.78 ^a,b ± 0.14
ACLF-TO50	84.24 ^a,b,c ± 8.06	144.93 ^a,b,c ± 19.79	2.02 ^a,b ± 0.51	329.61 ^a,b ± 37.89	107.34 ^a,b,c ± 18.33	110.30 ^a,b,c ± 7.89	2.15 ^a,b ± 0.40
ACLF-SYL	126.37 ^a,b ± 6.58	111.67 ^a,b ± 13.04	2.44 ^a,b ± 0.13	332.59 ^a ± 29.20	74.51 ^a,b ± 9.86	81.25 ^a,b ± 12.15	2.02 ^a,b ± 0.29
ACLF	222.65 ^a,c ± 11.08	174.08 ^a,c ± 15.16	3.74 ^a,c ± 0.53	358.94 ^a,c ± 13.55	117.71 ^a,c ± 15.47	255.49 ^a,c ± 19.48	3.53 ^a,c ± 0.28
Control	35.04 ± 6.63	47.55 ± 10.08	1.01 ± 0.11	263.75 ± 15.20	44.31 ± 4.58	39.16 ± 2.71	0.57 ± 0.04

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Results are expressed as mean ± SD. Values are expressed as mean ± SD (n = 5). ^a p ˂ 0.05, versus Control; ^b p ˂ 0.05, versus ACLF; ^c p ˂ 0.05, versus SYL. AST—aspartate aminotransferase; ALT—alanine aminotransferase; TB—total bilirubin; ALP—alkaline phosphatase; GGT—gamma-glutamyltransferase; CR—creatinine; ACLF-TO200- acute on chronic liver failure pretreated with 200 mg TOERE/kg b.w./day; ACLF-TO100—acute on chronic liver failure pretreated with 100mg TOERE/kg b.w./day; ACLF-TO50—acute on chronic liver failure pretreated with 50 mg TOERE/kg b.w./day; ACLF-SYL—acute on chronic liver failure pretreated with 200 mg silymarin/kg b.w./d; ACLF—acute on chronic liver failure; Control—negative control.

Considering that in ACLF kidneys are the most affected organs, in a study of a plant with possible hepatoprotective use in ACLF it is also important to determine the nephroprotective activity. ACLF induction by D-Gal- LPS caused a severe increase of creatinine and urea (p < 0.001). Renal dysfunction tests were positively correlated with the liver markers (r = 0.6–0.9) in ACLF animals. The treatments of ACLF rats with TOERE or SYL caused a smaller increase of serum creatinine and urea after ACLF induction (p < 0.001). SYL effect was comparable to that from ACLF-TO200 and ACLF-TO100 groups, but better than that from ACLF-TO50 animals (Table 2).

In our study systemic oxidative stress was also evaluated. Compared to the control, serum TOS, OSI, and MDA were elevated in ACLF animals (p < 0.001. The treatment with TOERE or SYL reduced TOS, OSI and MDA increase after ACLF induction (p < 0.01). TOERE effect on the oxidative stress was dose-dependent, the higher concentration having the best antioxidant effect (Table 3).

Table 3

Oxidative stress tests of the study groups.

Groups	TOS (µM H₂O₂/L)	TAR (mM TROLOX/L)	OSI	MDA (nM/L)	NOx (µM/L)	3NT (nmol/L)	SH (mM GSH/L)
ACLF-TO200	30.61 ^a,b,c ± 6.85	1.088 ± 0.001	31.57 ^a,b,c ± 6.13	3.05 ^a,b,c ± 0.28	21.92 ^b,c ± 3.74	769.36 ^a,b,c ± 78.46	0.48 ^a,b ± 0.03
ACLF-TO100	35.50 ^a,b,c ± 7.27	1.089 ± 0.001	31.17 ^a,b,c ± 4.84	3.67 ^b ± 0.59	25.76 ^a,b,c ± 4.50	768.66 ^a,b,c ± 69.75	0.48 ^a,b ± 0.08
ACLF-TO50	40.45 ^a,b,c ± 8.46	1.089 ± 0.001	31.82 ^a,b,c ± 9.39	3.95 ^a,b ± 0.47	30.52 ^a,b,c ± 7.60	820.20 ^a,b,c ± 48.43	0.48 ^a,b ± 0.02
ACLF-SYL	36.41 ^a,b ± 7.75	1.092 ± 0.003	37.03 ^a,b ± 8.27	3.83 ^a,b ± 0.34	36.56 ^a,b ± 6.76	971.07 ^a,b ± 68.34	0.52 ^a,b ± 0.02
ACLF	47.98 ^a,c ± 7.95	1.089 ± 0.001	40.40 ^a,c ± 8.60	5.37 ^a,c ± 0.08	51.49 ^a,c ± 7.32	1053.99 ^a,c ± 91.15	0.40 ^a,c ± 0.03
Control	21.18 ± 1.72	1.089 ± 0.001	21.59 ± 4.61	3.57 ± 0.36	19.98 ± 1.99	480.45 ± 56.62	0.59 ± 0.01

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Results are expressed as mean ± SD. ^a p ˂ 0.05, versus Control; ^b p ˂ 0.05, versus ACLF; ^c p ˂ 0.05, versus SYL. TOS—total oxidative status; TAR—total antioxidant reactivity; OSI—oxidative stress index; NOx—nitric oxide; 3NT—3-nitrotyrosine; MDA—malondialdehyde; SH—total thiols; ACLF-TO200—acute on chronic liver failure pretreated with 200 mg TOERE/kg b.w./day; ACLF-TO100—acute on chronic liver failure pretreated with 100 mg TOERE/kg b.w./day; ACLF-TO50—acute on chronic liver failure pretreated with 50 mg TOERE/kg b.w./day; ACLF-SYL—acute on chronic liver failure pretreated with 200 mg silymarin/kg b.w./d; ACLFacute on chronic liver failure; Control—negative control.

In ACLF rats NOx and 3NT were also increased (p < 0.001). TOERE pretreatments prevented NOx and 3NT elevation (p < 0.001) after ACLF induction in a dose-dependent way, with a higher concentration having a better inhibitory activity. SYL was also a good inhibitor of NO production and peroxidation in ACLF animals (p < 0.001), but the effect was smaller than that of TOERE (Table 3).

Additionally, serum antioxidative activity was evaluated by measuring TAR and SH. TAR was not influenced by ACLF induction (p > 0.05). A depletion in the level of SH was observed in ACLF rats (p < 0.01), and the treatment with TO or SYL prevent SH reduction (p < 0.05) after ACLF induction. SYL has a better effect than TO on SH (Table 3).

3.3. Histological Assessment

In the livers of the Control group, no significant structural changes were observed (Figure 2a).

Figure 2

Photomicrographs of the liver tissues from the control and experimental animals. H&E stain: (a). Control; (b). ACLF; (c). ACLF-SYL; (d). ACLF-TO200; (e). ACLF-TO100; (f). ACLF-TO50; Bar = 50 µm (a–c,f) and 20 µm (d,e). ACLF—acute on chronic liver failure; ACLF-SYL—acute on chronic liver failure pretreated with 200 mg silymarin/kg b.w./d; ACLF-TO200—acute on chronic liver failure pretreated with 200 mg TOERE/kg b.w./day; ACLF-TO100—acute on chronic liver failure pretreated with 100 mg TOERE/kg b.w./day; ACLF-TO50—acute on chronic liver failure pretreated with 50 mg TOERE/kg b.w./day.

The highest histological scores were identified in the livers of the ACLF group (p < 0.001) (Table 4). The changes were represented by congestion, hemorrhages, multifocal to coalescing areas of coagulative necrosis, randomly distributed within the hepatic lobules or centered on periportal regions and associated with severe and mixed inflammatory infiltrates. The portal spaces were also affected and expanded by fibrosis, bile duct hyperplasia, and large numbers of inflammatory cells, predominated by small lymphocytes and macrophages (Figure 2b). The microscopical examination of the livers from the group ACLF-SYL group (Figure 2c) revealed the lowest histological scores if compared to ACLF, ACLF-TO200, ACLF-TO100, and ACLF-TO50 (p < 0,001). Compared to the untreated ACLF group, in ACLF-TO200 (Figure 2d), ACLF-TO100 (Figure 2e), and ACLF-TO50 (Figure 2f) animals, the hepatic injuries were significantly reduced by the TOERE pretreatments (p < 0.001), with no important differences between different TOERE doses (p > 0.05). Liver necroinflammatory scores and serum liver tests were positively correlated.

Table 4

Histological and IHC scores of the liver biopsies.

Groups	Portal Inflammation	Periportal Degeneration/ Necrosis	Intralobular Degeneration/ Necrosis	Fibrosis	HAI	3NT
ACLF-TO200	1.60 ^a,b,c ± 0.89	2.20 ^a,b,c ± 0.10	1.00 ^a,b,c ± 0.01	1.20 ^a,c ± 0.10	5.80 ^a,c ± 1.92	1.40 ^a,b,c ± 0.55
ACLF-TO100	2.20 ^a,b,c ± 0.10	2.60 ^a,b,c ± 0.89	1.40 ^a,b,c ± 0.89	1.00 ^a,c ± 0.10	7.20 ^a,b,c ± 1.10	1.40 ^a,b,c ± 0.55
ACLF-TO50	2.60 ^a,b,c ± 0.89	2.20 ^a,b,c ± 1.10	2.20 ^a,b,c ± 1.10	1.00 ^a,c ± 0.10	8.00 ^a,b,c ± 1.41	1.80 ^a,b,c ± 0.45
ACLF-SYL	1.00 ^a,b ± 0.00	0.60 ^a,b ± 0.55	0.80 ^a,b ± 0.45	0.40 ^a,b ± 0.55	2.80 ^a,b ± 0.45	1.20 ^a,b ± 0.45
ACLF	3.60 ^a,c ± 0.55	4.80 ^a,c ± 0.84	3.60 ^a,b ± 0.55	1.00 ^a,b ± 0.10	12.80 ^a,b ± 1.64	2.40 ^a,b ± 0.55
Control	0.40 ± 0.55	0.00 ± 0.00	0.00 ± 0.00	0.00 ± 0.00	0.20 ± 0.45	0.00 ± 0.00

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Results are expressed as mean ± SD. ^a p ˂ 0.05, versus Control; ^b p ˂ 0.05, versus ACLF; ^c p ˂ 0.05, versus SYL; ACLF-TO200—acute on chronic liver failure pretreated with 200 mg TOERE/kg b.w./day; ACLF-TO100—acute on chronic liver failure pretreated with 100mg TOERE/kg b.w./day; ACLF-TO50—acute on chronic liver failure pretreated with 50 mg TOERE/kg b.w./day; ACLF-SYL—acute on chronic liver failure pretreated with 200 mg silymarin/kg b.w./d; ACLF—acute on chronic liver failure; Control—negative control; HAI—histological activity index; 3NT—3-nitrotyrosine.

3.4. 3-Nitrityrosine Evaluation

3-NT immunoexpression was negative in the livers of the control group (Figure 3a). A marked hepatocellular immunoexpression of 3-NT with a diffuse or mediolobular pattern was found in all liver samples from the ACLF group (Figure 3b) (p < 0.01). In the group ACLF-SYL, the 3-NT expression was reduced compared to the ACLF group (p < 0.01), being mainly limited to hepatocytes near the portal spaces (Figure 3c) (Table 4).

Figure 3

Immunohistochemical expression of 3-nitrotyrosine (3-NT) in liver tissues from the control and experimental animals: (a). Control; (b). ACLF; (c). ACLF-SYL; (d). ACLF-TO200; (e). ACLF-TO100; (f). ACLF-TO50; Bar = 50 μm (a) and 20 μm (b–f). ACLF-TO200—acute on chronic liver failure pretreated with 200 mg TOERE/kg b.w./day; ACLF-TO100—acute on chronic liver failure pretreated with 100 mg TOERE/kg b.w./day; ACLF-TO50—acute on chronic liver failure pretreated with 50 mg TOERE/kg b.w./day; ACLF-SYL—acute on chronic liver failure pretreated with 200 mg silymarin/kg b.w./d.

As compared to the ACLF group, the expression of 3NT was lower in liver biopsies from TOERE treated animals, particularly in the ACLF-TO200 (Figure 3d) and ACLF-TO100 (Figure 3e) (p < 0.01) groups. The expression of 3NT in the ACLF-TO50 group (Figure 3f) was higher compared to the other treated groups. SYL effect on 3NT expression was better than that of TOERE (p < 0.05) (Table 4).

The correlation between the histological scores and biochemical tests were also analyzed. In ACLF, ACLF-TO200, ACLF-TO100, ACLF-TO50, and ACLF-SYL groups all histopathological scores were positively correlated with liver, renal, and oxidative stress markers.

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4. Discussion

In the current study, D-Gal-LPS-induced ACLF in rats with HAS-induced chronic liver failure triggered an immune-mediated liver injury with pathological serum liver marker tests and histological liver changes. The liver injuries were also associated with renal failure and systemic oxidative stress. A seven days pretreatment with TOERE reduced ACLF induced liver injury. The protecting effect of TOERE can be attributed, at least in part, to the reduction of the oxidative stress associated with immune liver injury in D-Gal-LPS-induced ACLF. Depending on the dose, the hepatoprotective effect of TOERE was similar or lower than that of SYL, an already used hepatoprotective drug.

By analyzing the TOERE extract, other studies identified sesquiterpenes, various triterpenes, phenolic compounds, and phytosterols. Our previous phytochemical analysis [23] showed that the tested TO root extract had a lower TPC than in Aremu et al.’s analysis of TO root extract (1.14 ± 0.01 mg/100 GAE/mg extract) and TO leaf extract (4.35 ± 0.15 mg GAE/mg extract) [37], but higher than in the TO aerial part extract (15.50 mg GAE/g d.w.) [38].

The HPLC-DAD-ESI MS analysis of our TO root extract identified, caffeic acid, chicoric acid, as previously described [23], plus feruloylquinic acid, dicaffeoylquinic acid, and dicaffeoylquinic acid isomer. All these compounds have anti-inflammatory and antioxidant properties [11,23,39,40,41]. The antioxidant activity of the TOERE measured by DPPH and FRAP tests was proved in our previous study [23].

Because the chemical composition correlates with the pharmacological effects, TO extracts from different plant parts had different activities. Several studies demonstrated that the TO roots extract reduces alcohol-induced oxidative stress, TO leaf extract alleviates high-fat diet-induced nonalcoholic fatty liver, and TO flower extract can scavenge reactive oxygen species [22]. Similar to other studies [16,42,43], and based on the evidence of the phytochemical analysis results, our TO root extract can be considered a good natural antioxidant candidate. These results encouraged us to continue by testing the in vivo hepatoprotective and antioxidant effects of TOERE in an experimental ACLF.

For ACLF experimental model, first HAS administration in rats caused an immune liver injury and fibrosis, and then LPS stimulated liver macrophages leading to hepatic necro-inflammatory change. D-Gal, an amino sugar metabolized selectively by the hepatocytes, in a few hours potentiated the hepatotoxic effect of LPS by inhibiting mRNA and protein synthesis, leading to acute hepatitis [28]. The hepatoprotective effect of the TOERE was evaluated by using serum liver markers and liver histological analysis [2,3]. AST and ALT elevation reflects generalized damage to hepatocytes, TB increase reflects liver metabolism, ALP and GGT elevation reflects cholestasis [20,43,44]. In ACLF rats, liver markers were consistent with hepatocytes injury, cholestasis and, lower liver metabolism, demonstrating that an ACLF model was successfully induced [27]. The preliminary tests evaluating the TOERE effect on negative control animals indicated that the product had no significant activity on the healthy liver and oxidative stress (see supplemental data). In ACLF TO pretreatment reduced liver markers, suggesting that TOERE may prevent severe ACLF and by that to reduce the mortality due to ACLF. ACLF-TO100 group had the best hepatoprotective effect. In a previous study, we also evaluated in the TO root extract some phytosterols with anti-inflammatory and antioxidative properties [23]. It was demonstrated that due to their structural similarity with cholesterol, phytosterols are prone to be oxidized and transformed into oxyphytosterols [45,46,47], and from antioxidants to become pro-oxidants. By lowering the dose of TO from 200 to 100mg dry plant material/kg b.w./day, phytosterol reduction may be involved in the better hepatoprotective effect of ACLF-TO100 than of ACLF-TO200.

Liver injury diagnosed by serum liver tests was further confirmed by histopathological characteristics. In a normal liver, there is a hypoimmune response, and in chronic liver inflammation there is a high cellular recruitment, extended tissue damage, and the repair process leads to tissue remodeling, fibrosis, and liver dysfunction [41,48,49]. Fibrosis represents a key characteristic of progression towards liver cirrhosis and hepatic failure. In the present work liver biopsy of the ACLF animals showed extended necro-inflammatory changes, fibrosis, and bile ducts hyperplasia. In ACLF rats, like previously observed, histopathological scores increased due to the ongoing inflammation activation and the direct cytotoxic effect of cell death products [50]. Pretreatment with our TOERE in ACLF had hepatoprotective activity by reducing liver necro-inflammatory changes, with no important effect on liver fibrosis.

Under physiological conditions, free radicals are scavenged by antioxidant mechanisms. If there is an excess of free radicals or if there is a deficiency of antioxidants, oxidative stress will build up and will cause oxidative damage of lipids, proteins, and DNA [2,43,49]. In D-Gal-LPS-induced ACLF, immune-induced liver injury triggered an important liver inflammatory response and systemic oxidative stress, with high serum TOS and OSI, along with increased production of MDA, NOx, and 3NT.

Many studies correlated the hepatoprotective activity of the medicinal plant extracts with the antioxidant compounds from these plants [51]. Moreover, other experimental studies demonstrated that the polyphenolic compounds isolated from TO extracts had a hepatoprotective effect by reducing oxidative stress through direct free radical scavenging activity, metal ions chelation, and regeneration of the membrane-bound antioxidants [40,49]. In the present work, TOERE decreased serum TOS, OSI, and MDA levels in a dose-dependent way. MDA reduction was relevant because recently lipid peroxidation was considered a vital process in chronic liver diseases [44]. TOERE did not affect TAR, and SH was just slightly increased, indicating that this extract reduced systemic oxidative stress mainly by scavenging the oxidants and less by increasing the antioxidant capacity.

In mammals there are three NO synthase (NOS) isoenzymes that are involved in NO synthesis: neuronal (nNOS/NOS-1), inducible (iNOS/NOS-2), and endothelial (eNOS/NOS-3). Inflammatory stimuli up-regulate iNOS, and excessively generate NO induces nitrosative and oxidative damage. In liver injury, NO can be produced by hepatocytes, Kupffer cells, hepatic stellate cells (HSCs), and hepatic sinusoidal endothelial cells. It was observed that NO may have a dichotomous effect on liver disease, respectively in chronic liver diseases NO can promote HSC apoptosis, but in acute liver diseases, NO may increase liver damage. In LPS-treated rats, the marked hepatocellular immunoexpression of 3NT indicated that the iNOS-ROS cycle augments liver injury [52]. In this study, we found that liver 3NT was down-regulated following treatment with TOERE, suggesting that TOERE may reduce liver inflammatory responses and oxidative stress by reducing NO production through the inhibition of iNOS gene expression. These properties of TOERE may be explained by the high content of antioxidant phytochemicals.

Only iNOS and eNOS were highly expressed in acute liver failure (ALF) liver tissue, causing plasma NO elevation, and in humans increased plasma NO levels were correlated to the clinical severity of ALF [52]. In D-Gal-LPS-induced ACLF elevation of serum NOx and 3NT confirmed excessive NO synthesis due to the severe liver injury and inflammation. The treatment with TOERE reduced the serum NOx and 3NT, indirectly indicating that TOERE had a significant inhibitory effect on systemic NO production.

Because systemic oxidative stress markers reduction was correlated with serum liver markers and liver histopathological scores improvement, we concluded that TOERE lowered liver injury by reducing oxidative stress. Like in other studies [10], it was found that the antioxidant effect of TOERE was dose-dependent, the higher extract concentration had better antioxidant activity due to the high concentration of antioxidant ingredients.

According to the World Gastroenterology Organization ACLF is characterized by acute liver failure and one or more extrahepatic organ failure because in ACLF liver inflammation may trigger systemic inflammation. The kidneys are the most commonly affected organs and renal failure range from acute kidney injury (AKI) to acute-on-chronic kidney failure [2,3]. Therefore, acute kidney injury (AKI) was tested as a major criterion in ACLF severity grading [53]. In ACLF two subgroups of secondary renal dysfunctions with different pathophysiology and prognosis can be associated. One is the hepatorenal syndrome-acute kidney injury (HRS-AKI), a reduction of kidney function without parenchymal damage caused by prerenal insults such as hypovolemia. The other one is the non–HRS-AKI, induced by a renal insult such as inflammatory tubular injury in sepsis, bile acid nephropathy, and drug-induced tubular damage [54]. In ACLF liver protein synthesis lowers and may cause complications like coagulopathy, hemodynamic instability, jaundice, hepatic encephalopathy, hepatorenal syndrome, and sepsis [50]. At the same time, the systemic inflammatory response may also cause an inflammatory kidney injury with anon–HRS-AKI. Moreover, in experimental ACLF proinflammatory cytokines and LPS can cause directly renal tubular injury with cell apoptosis. Intrahepatic cholestasis from ACLF with increased serum bilirubin and bile acids may induce renal injury due to the direct renal toxicity and by tubular obstruction [54]. In our study, in ACLF animals creatinine and urea reached AKI levels, and there was a positive correlation between serum creatinine and urea, liver biopsy scores, and serum liver test. TOERE and SYL pretreatments reduced serum creatinine and urea in a dose-dependent way, indicating that in ACLF animals TOERE hepatoprotective activity is associated with a nephroprotective effect.

Lately, SYL has been used as a hepatoprotective agent due to its antioxidant and anti-inflammatory effects [55]. A finding of the study was that in experimental ACLF TO roots extract effects on serum liver markers were better than those of SYL, and SYL caused a higher reduction of the liver histological scores and 3NT immunoexpression. These differences suggested that TOERE better prevented acute liver injury and SYL reduces more the chronic response to liver injury. Even when SYL can reduce oxidative stress by scavenging ROS, by inhibiting ROS production [56], and by activating antioxidant enzymes [55], in our study it had a lower systemic antioxidant activity than TOERE.

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5. Conclusions

This report highlights the hepatoprotective and nephroprotective effects of an ethanolic TO root extract on D-Gal-LPS-induced ACLF. The mechanism proposed is the antioxidant activity of the bioactive components of the TOERE. These findings suggest for the first time that TOERE may be a potential preventive therapeutic agent for the severe liver and renal inflammatory injury associated with ACLF. These observations are important considering that ACLF has a high mortality rate. Further studies and clinical trials are required to fully elucidate the beneficial effects of TO root extract supplementation to prevent ACLF.

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Author Contributions

Conceptualization, I.O.P. and A.E.P.; methodology, T.A., R.M.P., L.V., and A.U.; software, R.M.P. and A.U.; validation, I.O.P., A.E.P., and R.O.; formal analysis, D.T. and C.T.; investigation, T.A., R.M.P., L.V., A.U, and C.T.; resources, I.O.P. and M.T.; writing—original draft preparation, I.O.P., A.E.P., R.M.P., and M.T. All authors have read and agreed to the published version of the manuscript.

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Funding

This research received no external funding.

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Institutional Review Board Statement

The study was approved by the Institutional Review Board (or Ethics Committee) of “Iuliu Hațieganu University of Medicine and Pharmacy”, Cluj-Napoca (no. 19/ 13.12.2016).

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Informed Consent Statement

Not applicable.

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Data Availability Statement

Not applicable.

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Conflicts of Interest

The authors declare no conflict of interest.

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Footnotes

Publisher’s Note: MDPI stays neutral with regard to jurisdictional claims in published maps and institutional affiliations.

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The Benefits of a Lactobacillus to Your Health

The Truth News — Sat, 15 Jun 2024 09:07:52 +0000

The Benefits of a Lactobacillus to Your Health

Lactobacillus is a type of bacteria of which Lactobacillus gasseri is one type. You can find these ‘friendly’ Lactobacillus bacteria naturally in the human gut, urinary tract, and genital system. We can also get these helpful bacteria from certain foods and from dietary supplements called probiotics.

In general, Lactobacillus helps the body to break down food, absorb nutrients, and fight disease-causing organisms. Lactobacillus is also useful for preventing and treating diarrhea. Specifically, it is helpful for fighting diarrhea related to antibiotics use (1).

In this article, we’ll look more closely at probiotics and outline some health benefits of taking a Lactobacillus gasseri probiotic.

What are Probiotics?

Every human being is born with a certain ‘gut flora’. This flora consists of beneficial microorganisms, like bacteria, that you inherit for your mother. After birth, other helpful flora begins to ‘colonize’ your body. Although this may sound like some sort of alien invasion, it isn’t.

These beneficial or ‘friendly’ bacteria perform a number of roles in your body including immune system support, synthesizing certain vitamins, and converting fiber into acids (2).

So, probiotics are live microorganisms that are good for your health. Taking probiotics as a dietary supplement can help you boost your gut flora, the healthy bacteria in your gut (3). When taken in the correct amounts, your gut is healthier, and so are you!

Specific Health Benefits of Lactobacillus Gasseri

Lactobacillus gasseri is a probiotic which is useful for a number of health conditions. In addition to its general contribution to digestive and gut health, Lactobacillus gasseri probiotic is helpful for a number of other health conditions:

Weight Loss

According to some research, Lactobacillus gasseri couple possibly encourage weight loss and reduce abdominal fat. A British Journal of Nutrition study published in 2013 surveyed 210 obese adults.

These people were either given milk enriched with Lactobacillus gasseri or a placebo (milk without Lactobacillus gasseri). In the end, the Lactobacillus group saw an 8.5% reduction in abdominal fat compared to the placebo group after 12 weeks (4).

Vaginal Health

Lactobacillus gasseri probiotic also promotes vaginal health by preventing bacterial vaginosis. However, it is most effective when taken as a suppository. What’s more, studies suggest that Lactobacillus gasseri probiotic may also decrease menstrual pain in women (5).

Cholesterol

In one study, participants received a product containing Lactobacillus gasseri and insulin. This product helped reduced total blood cholesterol, LDL (low-density cholesterol), lipoproteins, and triglycerides in both men and women with high cholesterol (8).

Boosts Immunity

Heat-killed Lactobacillus gasseri has been shown to boost immunity in elderly adults by increasing the number of T cells (9).

Allergies

In one study involved participants with an allergy to Japanese cedar, heat-killed Lactobacillus gasseri improved their nasal symptoms and enhanced their immune response (10).

Fatigue

When university athletes were given Lactobacillus gasseri probiotic after strenuous exercise, they experienced less resting fatigue. On top of that, Lactobacillus gasseri probiotic also elevated their moods (11).

Summary

Lactobacillus bacteria are friendly microorganisms that are native to the human gut. They help with a number of normal processes and help keep us healthy. Generally speaking, Lactobacillus helps you break down food, absorb nutrients, and fight certain unhealthy microorganisms. What’s more, it also supports your immune system support and helps your body synthesize certain vitamins. When our gut flora is out of balance, our health can suffer.

In addition to balancing gut flora, taking Lactobacillus gasseri probiotic is beneficial for a number of other reasons. It is frequently used for treating and preventing diarrhea, especially diarrhea caused by antibiotics. Furthermore, it boosts vaginal health in women and eases menstrual pain in women with endometriosis.

References

9 Ways Lactobacillus Acidophilus Can Benefit Your Health

L. acidophilus is a beneficial bacteria found in your intestines that helps protect against various illnesses. To boost levels, consume fermented goods or take supplements.

Probiotics are becoming popular food supplements.

Interestingly, each probiotic can have different effects on your body.

Lactobacillus acidophilus is one of the most common types of probiotics and can be found in fermented foods, yogurt and supplements.

What Is Lactobacillus Acidophilus?

Lactobacillus acidophilus is a type of bacteria found in your intestines.

It’s a member of the Lactobacillus genus of bacteria, and it plays an important role in human health (1Trusted Source).

Its name gives an indication of what it produces — lactic acid. It does this by producing an enzyme called lactase. Lactase breaks down lactose, a sugar found in milk, into lactic acid.

Lactobacillus acidophilus is also sometimes referred to as L. acidophilus or simply acidophilus.

Lactobacilli, particularly L. acidophilus, are often used as probiotics.

The World Health Organization defines probiotics as “live micro-organisms which, when administered in adequate amounts, confer a health beneﬁt on the host” (2Trusted Source).

Unfortunately, food manufacturers have overused the word “probiotic,” applying it to bacteria that haven’t been scientifically proven to have any specific health benefits.

This has led the European Food Safety Authority to ban the word “probiotic” on all foods in the EU.

L. acidophilus has been extensively studied as a probiotic, and evidence has shown that it may provide a number of health benefits. However, there are many different strains of L. acidophilus, and they can each have different effects on your body (3Trusted Source).

In addition to probiotic supplements, L. acidophilus can be found naturally in a number of fermented foods, including sauerkraut, miso and tempeh.

Also, it’s added to other foods like cheese and yogurt as a probiotic.

Below are 9 ways in which Lactobacillus acidophilus may benefit your health

1. It May Help Reduce Cholesterol

High cholesterol levels may increase the risk of heart disease. This is especially true for “bad” LDL cholesterol.

Fortunately, studies suggest that certain probiotics can help reduce cholesterol levels and that L. acidophilus may be more effective than other types of probiotics (4Trusted Source, 5Trusted Source).

Some of these studies have examined probiotics on their own, while others have used milk drinks fermented by probiotics.

One study found that taking L. acidophilus and another probiotic for six weeks significantly lowered total and LDL cholesterol, but also “good” HDL cholesterol (6Trusted Source).

A similar six-week study found that L. acidophilus on its own had no effect (7Trusted Source).

However, there is evidence that combining L. acidophilus with prebiotics, or indigestible carbs that help good bacteria grow, can help increase HDL cholesterol and lower blood sugar.

This has been demonstrated in studies using probiotics and prebiotics, both as supplements and in fermented milk drinks (8Trusted Source).

Furthermore, a number of other studies have shown that yogurt supplemented with L. acidophilus helped reduce cholesterol levels by up to 7% more than ordinary yogurt (9Trusted Source, 10Trusted Source, 11Trusted Source, 12Trusted Source).

This suggests that L. acidophilus — not another ingredient in the yogurt — was responsible for the beneficial effect.

SUMMARY:L. acidophilus consumed on its own, in milk or yogurt or in combination with prebiotics may help lower cholesterol.

2. It May Prevent and Reduce Diarrhea

Diarrhea affects people for a number of reasons, including bacterial infections.

It can be dangerous if it lasts a long time, as it results in fluid loss and, in some cases, dehydration.

A number of studies have shown that probiotics like L. acidophilus may help prevent and reduce diarrhea that’s associated with various diseases (13Trusted Source).

Evidence on the ability of L. acidophilus to treat acute diarrhea in children is mixed. Some studies have shown a beneficial effect, while others have shown no effect (14Trusted Source, 15Trusted Source).

One meta-analysis involving more than 300 children found that L. acidophilus helped reduce diarrhea, but only in hospitalized children (16Trusted Source).

What’s more, when consumed in combination with another probiotic, L. acidophilus may help reduce diarrhea caused by radiotherapy in adult cancer patients (17Trusted Source).

Similarly, it may help reduce diarrhea associated with antibiotics and a common infection called Clostridium difficile, or C. diff (18Trusted Source).

Diarrhea is also common in people who travel to different countries and are exposed to new foods and environments.

A review of 12 studies found that probiotics are effective at preventing traveler’s diarrhea and that Lactobacillus acidophilus, in combination with another probiotic, was most effective at doing so (19Trusted Source).

SUMMARY:When consumed in combination with other probiotics, L. acidophilus may help prevent and treat diarrhea.

3. It Can Improve Symptoms of Irritable Bowel Syndrome

Irritable bowel syndrome (IBS) affects up to one in five people in certain countries. Its symptoms include abdominal pain, bloating and unusual bowel movements (20Trusted Source).

While little is known about the cause of IBS, some research suggests it might be caused by certain types of bacteria in the intestines (21Trusted Source).

Therefore, a number of studies have examined whether probiotics can help improve its symptoms.

In a study in 60 people with functional bowel disorders including IBS, taking a combination of L. acidophilus and another probiotic for one to two months improved bloating (22Trusted Source).

A similar study found that L. acidophilus alone also reduced abdominal pain in IBS patients (23Trusted Source).

On the other hand, a study that examined a mixture of L. acidophilus and other probiotics found that it had no effect IBS symptoms (24Trusted Source).

This might be explained by another study suggesting that taking a low dose of single-strain probiotics for a short duration may improve IBS symptoms the most.

Specifically, the study indicates that the best way to take probiotics for IBS is to use single-strain probiotics, rather than a mix, for less than eight weeks, as well as a dose of less than 10 billion colony-forming units (CFUs) per day (25Trusted Source).

However, it’s important to choose a probiotic supplement that has been scientifically proven to benefit IBS.

SUMMARY:L. acidophilus probiotics may improve symptoms of IBS, such as abdominal pain and bloating.

4. It Can Help Treat and Prevent Vaginal Infections

Vaginosis and vulvovaginal candidiasis are common types of vaginal infections.

There is good evidence that L. acidophilus can help treat and prevent such infections.

Lactobacilli are typically the most common bacteria in the vagina. They produce lactic acid, which prevents the growth of other harmful bacteria (26Trusted Source).

However, in cases of certain vaginal disorders, other species of bacteria begin to outnumber lactobacilli (27Trusted Source, 28Trusted Source).

A number of studies have found taking L. acidophilus as a probiotic supplement can prevent and treat vaginal infections by increasing lactobacilli in the vagina (29Trusted Source, 30Trusted Source).

Nevertheless, other studies have found no effect (31Trusted Source, 32Trusted Source).

Eating yogurt that contains L. acidophilus may also prevent vaginal infections. Yet, both of the studies that examined this were quite small and would need to be replicated on a larger scale before any conclusions could be made (33Trusted Source, 34Trusted Source).

SUMMARY:L. acidophilus as a probiotic supplement may be useful in preventing vaginal disorders, such as vaginosis and vulvovaginal candidiasis.

5. It May Promote Weight Loss

The bacteria in your intestines help control food digestion and a number of other bodily processes.

Therefore, they influence your weight.

There is some evidence that probiotics may help you lose weight, especially when multiple species are consumed together. However, the evidence on L. acidophilus alone is unclear (35Trusted Source).

A recent study that combined the results of 17 human studies and over 60 animal studies found that some lactobacilli species led to weight loss, while others may have contributed to weight gain (36Trusted Source).

It suggested that L. acidophilus was one of the species that led to weight gain. However, most of the studies were conducted in farm animals, not humans.

Furthermore, some of these older studies used probiotics that were originally thought to be L. acidophilus, but have since been identified as different species (37Trusted Source).

Therefore, the evidence on L. acidophilus affecting weight is unclear, and more rigorous studies are needed.

SUMMARY:Probiotics may be effective for weight loss, but more research is needed to determine whether L. acidophilus, in particular, has a significant effect on weight in humans.

6. It May Help Prevent and Reduce Cold and Flu Symptoms

Healthy bacteria like L. acidophilus can boost the immune system and thus help reduce the risk of viral infections.

In fact, some studies have suggested that probiotics may prevent and improve symptoms of the common cold (38Trusted Source, 39Trusted Source).

A few of these studies examined how effectively L. acidophilus treated colds in children.

In one study in 326 children, six months of daily L. acidophilus probiotics reduced fever by 53%, coughing by 41%, antibiotic use by 68% and days absent from school by 32% (40Trusted Source).

The same study found that combining L. acidophilus with another probiotic was even more effective (40Trusted Source).

A similar study on L. acidophilus and another probiotic also found similar positive results for reducing cold symptoms in children (41Trusted Source).

SUMMARY:L. acidophilus on its own and in combination with other probiotics may reduce cold symptoms, especially in children.

7. It May Help Prevent and Reduce Allergy Symptoms

Allergies are common and can cause symptoms such as a runny nose or itchy eyes.

Fortunately, some evidence suggests that certain probiotics can reduce the symptoms of some allergies (42Trusted Source).

One study showed that consuming a fermented milk drink containing L. acidophilus improved symptoms of Japanese cedar pollen allergy (43Trusted Source).

Similarly, taking L. acidophilus for four months reduced nasal swelling and other symptoms in children with perennial allergic rhinitis, a disorder that causes hay fever-like symptoms throughout the year (44Trusted Source).

A larger study in 47 children found similar results. It showed that taking a combination of L. acidophilus and another probiotic reduced runny nose, nasal blocking and other symptoms of pollen allergy (45Trusted Source).

Interestingly, the probiotics reduced the amount of an antibody called immunoglobulin A, which is involved in these allergic reactions, in the intestines.

SUMMARY:L. acidophilus probiotics can reduce the symptoms of certain allergies.

8. It May Help Prevent and Reduce Symptoms of Eczema

Eczema is a condition in which the skin becomes inflamed, resulting in itchiness and pain. The most common form is called atopic dermatitis.

Evidence suggests that probiotics can reduce the symptoms of this inflammatory condition in both adults and children (46Trusted Source).

One study found that giving a mix of L. acidophilus and other probiotics to pregnant women and their infants during the first three months of life reduced the prevalence of eczema by 22% by the time the infants reached one year of age (47Trusted Source).

A similar study found that L. acidophilus, in combination with traditional medical therapy, significantly improved atopic dermatitis symptoms in children (48Trusted Source).

However, not all studies have shown positive effects. A large study in 231 newborn children given L. acidophilus for the first six months of life found no beneficial effect in cases of atopic dermatosis (49Trusted Source). In fact, it increased sensitivity to allergens.

SUMMARY:Some studies have shown that L. acidophilus probiotics can help reduce the prevalence and symptoms of eczema, while other studies show no benefit.

9. It’s Good for Your Gut Health

Your gut is lined with trillions of bacteria that play an important role in your health.

Generally, lactobacilli are very good for gut health.

They produce lactic acid, which may prevent harmful bacteria from colonizing the intestines. They also ensure the lining of the intestines stays intact (50Trusted Source).

L. acidophilus can increase the amounts of other healthy bacteria in the gut, including other lactobacilli and Bifidobacteria.

It can also increase levels of short-chain fatty acids, such as butyrate, which promote gut health (51Trusted Source).

Another study carefully examined the effects of L. acidophilus on the gut. It found that taking it as a probiotic increased the expression of genes in the intestines that are involved in immune response (52Trusted Source).

These results suggest that L. acidophilus may support a healthy immune system.

A separate study examined how the combination of L. acidophilus and a prebiotic affected human gut health.

It found that the combined supplement increased the amounts of lactobacilli and Bifidobacteria in the intestines, as well as branched-chain fatty acids, which are an important part of a healthy gut (53Trusted Source).

SUMMARY:L. acidophilus can support gut health by increasing the amounts of healthy bacteria in the intestines.

How to Reap the Most from L. Acidophilus

L. acidophilus is a normal bacteria in healthy intestines, but you can reap a number of health benefits by taking it as a supplement or consuming foods that contain it.

L. acidophilus can be consumed in probiotic supplements, either on its own or in combination with other probiotics or prebiotics.

However, it’s also found in a number of foods, particularly fermented foods.

The best food sources of L. acidophilus are:

Yogurt: Yogurt is typically made from bacteria such as L. bulgaricus and S. thermophilus. Some yogurts also contain L. acidophilus, but only those that list it in the ingredients and state “live and active cultures.”
Kefir: Kefir is made of “grains” of bacteria and yeast, which can be added to milk or water to produce a healthy fermented drink. The types of bacteria and yeast in kefir can vary, but it commonly contains L. acidophilus, among others.
Miso: Miso is a paste originating from Japan that is made by fermenting soybeans. Although the primary microbe in miso is a fungus called Aspergillus oryzae, miso can also contain many bacteria, including L. acidophilus.
Tempeh: Tempeh is another food made from fermented soybeans. It can contain a number of different microorganisms, including L. acidophilus.
Cheese: Different varieties of cheese are produced by using different bacteria. L. acidophilus is not commonly used as a cheese starter culture, but a number of studies have examined the effects of adding it as a probiotic (54Trusted Source).
Sauerkraut: Sauerkraut is a fermented food made from cabbage. Most of the bacteria in sauerkraut are Lactobacillus species, including L. acidophilus (55Trusted Source).

Other than food, the best way to get L. acidophilus is directly through supplements.

A number of L. acidophilus probiotic supplements are available, either on their own or in combination with other probiotics. Aim for a probiotic with at least one billion CFUs per serving.

If taking a probiotic, it’s usually best to do so with a meal, ideally breakfast.

If you are new to probiotics, try taking them once daily for a week or two and then assess how you feel before continuing.

SUMMARY:L. acidophilus can be taken as a probiotic supplement, but it’s also found in high quantities in a number of fermented foods.

The Bottom Line

L. acidophilus is a probotic bacteria that’s normally found in your intestines and crucial to health.

Due to its ability to produce lactic acid and interact with your immune system, it may help prevent and treat symptoms of various diseases.

In order to increase L. acidophilus in your intestines, eat fermented foods, including those listed above.

Alternatively, L. acidophilus supplements can be beneficial, especially if you suffer from one of the disorders mentioned in this article.

Whether it’s obtained through foods or supplements, L. acidophilus can provide health benefits for everyone.\

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How To: Culture Lactobacillus (LAB) for Horticultural use

Generally when it comes to bacteria and microbes we’d be referring to the aerobic type you’d hope to produce in a Compost Tea (AACT) system, the reason being that the presence of anaerobic bacteria in these systems are nearly always ‘bad news’. However there are useful anaerobes out there and it is very much worth looking in to putting them to use in your horticultural endeavours!!

Enter Lactobacillus….

Lactobacillus is a facultive anaerobe that we are generally interested in for it’s ability to ferment a wide variety of things. It is this process that makes Lactobacillus or LAB the cornerstone of a range of processes the savvy gardener will find extremely useful. I’ll mention more about that later in this piece and in further blogs, but lets show you how to culture your own Lactobacillus first….

Step 1 – Rice wash

Technically you can use any reasonable carbohydrate source (preferably not simple sugars) but in this instance we’ll go with a Rice wash – I will be trying other more exciting things in the future, but until then….. Well the title says it all really, wash some rice and collect the water. This milky wash will now contain some of the starches from the rice and provide a food source for your bacteria.

Step 2 – Collect your initial culture

Place your rice wash in a suitable vessel (a jar…) and protect the neck with some kind of net to stop anything random getting in. Ideally you’ll want to place this outside, in a garden, on a balcony ect away from the elements but open to the air. This will allow the bacteria to go to work on the wash. A day or so should be fine. You will notice a change in the wash as the bacteria start to work, it will start to smell slightly sour and three distinct layers should be visible. You now need to collect the middle of these layers – the best way is with a siphon, but a syringe or whatever you have to hand will work – just try not to disrupt the layers.

Step 3 – Feed the LAB

Now it’s time to culture just the LAB that are present and nothing else. To do this we add milk to the liquid we collected at about 10:1, so for every 10ml of liquid you want to add 100ml of milk – You can use pretty much any milk as it’s the LAB in the wash we are culturing, however the least adulterated milk you can get your hands on the better. It’s probably worth saying you can’t use a lactose free milk for fairly obvious reasons….Finally we want to store this in an anaerobic state, so you have a few options – Ideally you can use a container with an airlock – the same as homebrewers use (or make one), you could use a bottle or jar and release the pressure every so often (not the best plan) or as I have use a heavy lid with a seal so any gas can escape but will then re-seal (not ideal to be honest….go buy some airlocks, you’ll want them for further projects!)

Step 4 – Prep & Store the LAB

After about a week you should notice a distinct change – You’ll have a layer of curds and a liquid layer – whey. It’s this liquid layer we want. Nothing too stressful here, just use a sieve and collect the liquid in a vessel – The curds can be put on the compost or whatever, it will be a great addition. Again your brew should smell sour (actually quite pleasant if you’re in to sour beers at all….) but not rancid, if it is bin it. OK, now you have your liquid you have 2 options, store it in the fridge where it will keep for about a week or mix it with Molasses to stabilise the culture where it will keep for 6 months or more. To stabilise mix the culture 1:1 with molasses, so 1 litre culture to 1 Litre of Molasses gives you 2 Litres…..it’s worth airlocking this too until the mix stabilises.

What’s the point?

Excellent question :o) The more mundane uses for LAB include using it as an odour neutraliser if you happen to keep chickens etc – Mix 30ml per litre of water and spray around the coop to reduce the smell – Unblock drains – 15ml per litre and let it go to work over night and many more! For your growing needs however mix 30ml or so with every litre of your plant’s water. The microbes will help cycle the nutrients in the soil making them more available to the plant! Add your LAB to compost – 30ml per litre and damp down every time you add to the pile or as you’re layering up. The Lactobacillus will speed up decomposition and start to cycle the nutrients! Finally (and more excitingly), I mentioned earlier that LAB is the cornerstone of further processes that are highly beneficial to a gardener. For instance LAB can be used for Bokashi composting, no more need to buy bran for your indoor composting! If you’ve never heard of Bokashi, I’ll cover it at some point. LAB can also be used to ferment plant material, for instance if you already add seaweed meal to your feeding regime, imagine if you could ‘pre-digest’ the nutrients held within the seaweed – making the non soluble elements readily available at application….with LAB you can. If you’re a gardener familiar with the process of rotting comfrey or nettles in a bucket to annoy your plot mates, why not use LAB to break down the vegetable matter without the smell, and more importantly, without the risk of culturing the bad anaerobic bacteria. Using these principles it’s basically possible to make your own organic liquid plant food for free and without losing friends or neighbours….. The last point for this post is probably my favourite – With LAB it’s possible to create your own fish fertiliser (Fish hydrolysate) this in conjunction with your nettle/seaweed/comfrey/grass brews will give you the perfect base for making your own liquid organic fertiliser…. …that’s not bad for a little milk and help from a bacterium.

Foot notes – There should really be a sequence of pictures to go with this post, but frankly they weren’t up to scratch. If anything needs clearing up drop me an email or comment below. – N.D source

LACTIC ACID BACTERIA: GARDEN AND SOIL BENEFITS(click Here)

Lactobacillus spp. for Gastrointestinal Health: Current and Future Perspectives

Abstract

In recent decades, probiotic bacteria have become increasingly popular as a result of mounting scientific evidence to indicate their beneficial role in modulating human health. Although there is strong evidence associating various Lactobacillus probiotics to various health benefits, further research is needed, in particular to determine the various mechanisms by which probiotics may exert these effects and indeed to gauge inter-individual value one can expect from consuming these products. One must take into consideration the differences in individual and combination strains, and conditions which create difficulty in making direct comparisons. The aim of this paper is to review the current understanding of the means by which Lactobacillus species stand to benefit our gastrointestinal health.

Keywords: lactobacillus, probiotic, microbiota, gastrointestinal barrier, inflammation

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Introduction

Ilya Ilyich Mechnikov (Elie Metchnikoff), a Nobel Laureate for his work on macrophage phagocytosis, is credited as the first to propose that the gut microbiota could be manipulated to benefit the host. Mechnikov believed that putrefactive activity of microbes in the intestine produced toxic substances that were damaging to the nervous and vascular systems and caused humans to age. He had observed that Bulgarian peasants consumed large quantities of yogurt and had a long life expectancy. He also observed that natural fermentation of food by lactic acid-producing bacteria prevented the growth of putrefactive organisms. In his book, titled ‘The Prolongation of Life’, he concludes that: “as lactic fermentation serves so well to arrest putrefaction in general, why should it not be used for the same purpose within the digestive tube?” (1). Although Mechnikov’s concept of aging by “intestinal auto-intoxication” has no scientific basis today, Mechnikov’s theories remain influential and have contributed to the commonly held opinion that Lactobacilli display important functional characteristics that contribute to gut health.

Lactobacillus is a genus of rod-shaped, gram-positive, non-spore-forming, facultative anaerobic bacteria of the phylum ‘Firmicutes’ (2, 3). Lactobacilli metabolise carbohydrates to produce lactic acid making them the largest genus within the lactic acid bacteria (LAB) group. As of March 2020 the 261 species of the Lactobacillacae were reclassified into 25 genera (including 23 novel genera) due to their extremely high genotypic, phenotypic and ecological diversity (4). For the purpose of this review, ‘Lactobacillus’ will refer to those species previously classified as Lactobacillus. Traditionally, Lactobacillus species may be divided into three groups based on their metabolism. The obligate homofermentative group which ferment carbohydrates to produce lactic acid as the main by-product (e.g. L. acidophilus and L. salivarius), the facultatively heterofermentative group which, under certain conditions or with certain substrates, ferment carbohydrates to produce lactic acid, ethanol/acetic acid and carbon dioxide as by-products (e.g. L. casei and L. plantarum) and the obligately heterofermentative group which always ferment carbohydrates to produce lactic acid, ethanol/acetic acid and carbon dioxide as by-products (e.g. L. reuteri and L. fermentum) (5).

Lactobacilli have colonised multiple areas of the human body, most notably the digestive tract including the oral cavity, and the female genital tract (6). The association between Lactobacilli and humans is a mutualistic relationship, with Lactobacillus species offering the host aid in digestion of certain dietary substrates, as well as protection from pathogens, in return for accommodation and nutrients (7). Lactobacillus species possess qualities that are commercially desirable both as health supplements and as tools in the food technology sector. The main uses for Lactobacilli are in the manufacturing process of fermented dairy, meat, or vegetable foods and sourdough breads, and they are also widely used as probiotics i.e., live micro-organisms that, when administered in adequate amounts, confer a health benefit on the host (8, 9). Lactobacilli have been granted a ‘generally recognised as safe’ (GRAS) status from the U.S. Food and Drug Administration (USFDA) and ‘qualified presumption of safety’ (QPS) status from the European Food Safety Authority (EFSA) thus making their use in food manufacture relatively straightforward. Due to their economic importance, Lactobacilli are highly studied and, relative to other bacterial genus’, are well characterised in terms of genomics and also their interactions with humans in terms of both health and disease. These features make Lactobacillus species ideal probiotic candidates.

Considering the widespread media attention that the microbiota have attracted in recent years with many news outlets covering this link between microbes and health it is little wonder that the commercial probiotic market is worth approximately $54 billion USD worldwide (10). For a list including some of the most common Lactobacillus strains found in probiotic products and their sources see George Kerry et al. (11). Although the strain L. rhamnosus GG is one of the most heavily studied, L. acidophilus is the most commonly used in commercial products. For an in-depth review of common commercial Lactobacillus strains see the chapter by Tang and Zhao in the book ‘Lactic Acid Bacteria: Omics and Functional Evaluation’ (12).

In 2002 a joint Food and Agriculture Organisation (FAO) and WHO working group released guidelines for the evaluation of probiotics in food (8). The minimum requirements include: assessment of strain identity (genus, species, strain), in vitro tests to show probiotic effects (e.g. resistance to gastric acidity, digestive enzymes and bile acid, and anti-microbial activity against pathogens), safety assessment to prove that the probiotic product is safe for consumption and without contamination, and finally in vivo studies to authenticate the purported health claims of the product (13). In Europe, the EFSA considers the terms ‘probiotic’, ‘prebiotic’ and the words ‘live’ or ‘active’ when used in relation to bacteria, to be health claims. Legislation on products purporting to carry health claims are strictly controlled although in recent years countries including Spain, Denmark and the Netherlands have released national guidelines allowing use of the word probiotic under certain conditions. This has renewed appeals to the EU Commission to reconsider the strict regulation. Unfortunately, in the US and Canada the FAO/WHO guidelines are not followed and indeed the use of the term probiotic has not been controlled by legislation. This means that any product can use the word ‘probiotic’ on its packaging thereby making it extremely difficult for consumers to determine which products are genuine probiotics that may actually be beneficial for their health (14).

In order to be considered efficacious, a probiotic must have the capacity to survive in the gastrointestinal (GI) tract, must resist the low pH of the stomach, must lack antibiotic resistance genes and must provide a clear benefit to the host (15). Of all probiotics, Lactobacillus species are the most widely used and studied (16). The main probiotic Lactobacillus species include: L. acidophilus, L. brevis, L. casei, L. delbrueckii subsp. bulgaricus, L. delbrueckii subsp. lactis, L. fermentum, L. gasseri, L. helveticus, L. johnsonii, L. paracasei subsp. paracasei, L. plantarum, L. reuteri and L. rhamnosus. There is much research into the potential health benefits of Lactobacillus species, although evidence indicates that many features of these probiotic bacteria are both species and strain -dependent (17). Despite this it has been observed that a single probiotic species may demonstrate improvement in different patient cohorts eg. L. rhamnosus GG (18) and additionally that a range of different probiotics or probiotic combinations may demonstrate efficacy in the same condition eg. C. difficile infection (19) highlighting the existence of conserved beneficial features. As is the case for many translational therapies, efficacy is not always maintained from in vitro observations through preclinical to clinical studies for a myriad of factors. Unfortunately, for many probiotics, one of these factors being that the mechanisms of action by which beneficial clinical outcomes are achieved have yet to be elucidated (20). The consequences for this mean that we are not utilising these tools to their full potential, opportunities for improving existing treatments may not be realised and we are at risk of probiotic treatments resulting in worse outcomes for particular subsets of patients (21). Additionally, mechanistic data may be required in order to gain approval from regulatory bodies for health claims – a mode of action is defined by the World Health Organisation (WHO) and EFSA as ‘a biologically plausible sequence of key events leading to an observed effect supported by robust experimental observations and mechanistic data’ (22). Kleerebezem and colleagues (23) propose the establishment of a translational pipeline connecting mechanistic insights to probiotic efficacy in order to improve the initial selection of probiotic strains by being able to predict their expected outcomes while supporting the design of the most appropriate clinical trials in well-defined subpopulations. They also suggest that this would be used in the inverse allowing us to predict explanations for observed clinical effects by drawing on existing knowledge of the probiotic modes of action. Determining the precise beneficial features of probiotics would certainly allow us to make better predictions for improved health outcomes.

On this note, further research is exploring ways to increase the efficiency, efficacy, safety and quality of probiotics by isolating probiotic-derived biomolecules. These have been described as postbiotics, paraprobiotics, heat-killed probiotics, Tyndallised probiotics among others: generally referring to metabolic products or secreted products of the bacteria, non-viable microbial cells (intact or broken) or crude cell extracts; specifically this includes enzymes, secreted peptides/proteins, bacteriocins, short chain fatty acids (SCFA), organic acids and cell envelope components of bacteria including peptidoglycans, teichoic acids, cell surface proteins and cell wall polysaccharides (24). The International Scientific Association for Probiotics and Prebiotics (ISAPP) has released a consensus statement on the definition of postbiotics establishing it as a “preparation of inanimate micro-organisms and/or their components that confers a health benefit on the host. Effective postbiotics must contain inactivated microbial cells or cell components, with or without metabolites, that contribute to observed health benefits”. (25). Postbiotics maintain several advantages over probiotics as described by Pique et al. (26): (I) No risk of translocation from the gut lumen to blood among vulnerable subjects, (II) No risk of acquisition and transfer of antibiotic resistance genes, (III) No risk of interference with normal gut colonisation in neonates, (IV) Release of active molecules from the disrupted inactivated cells, pass through the mucus layers and stimulate epithelial cells more directly, (V) Loss of viability by cell lysis can produce further more complex beneficial effects and (VI) Easier to extract, standardize, transport, and store. Accordingly, the use of postbiotics may very well represent a much-improved alternative to live probiotics and would be a likely replacement for them in future. A recent review has nicely summarised the composition and beneficial functions of postbiotics from Lactobacillus species (27). In short, postbiotics derived from Lactobacillus comprise a range of molecules which have various beneficial effects including immunomodulation, epithelial barrier protection, anti-pathogenic effects and anti-tumour effects.

Lactobacilli have demonstrated efficacy in treating various conditions including bacterial vaginosis, atopic dermatitis, and upper respiratory tract infections (28–30). However, as first proposed by Mechnikov over 100 years ago, the majority of Lactobacillus probiotics are consumed with a view to improving GI health. In the century since this hypothesis, interest and knowledge surrounding this subject has grown massively, however the potential for further growth in this area is exponential and much more work will be required before we fully understand and profit from the complexities of the relationships between Lactobacillus and gut health.

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Lactobacillus spp. and Intestinal Barrier Integrity

The GI mucosa is the largest and one of the most critical barrier sites of the body where foreign antigens, microbes and potential pathogens come into close contact with the host’s immune system. It is a semi-permeable barrier which allows for the absorption of nutrients and immune sensing while restricting the influx of potentially harmful antigens or microbes. The GI barrier is composed of four major elements: the commensal microbiota, the mucus layer – which contains secretory IgA molecules (sIgA) and anti-microbial peptides, the intestinal epithelial cell (IEC) monolayer, and the gut associated lymphoid tissue (GALT) – which constitutes various populations of immune cells in compartments along the GI tract. The complexity of regulating this semi-permeable barrier is mitigated by dynamic inter-regulation between these elements which work together to maintain intestinal barrier integrity and homeostasis (31). Loss of intestinal barrier function has been implicated as an early event in the pathogenesis of various GI disorders, such as coeliac disease and inflammatory bowel disease, as well as systemic disorders including type I diabetes, obesity and multiple sclerosis (31).

Intestinal barrier function may be enhanced with the intake of non-pathogenic micro-organisms which augment the physical barrier of the mucus layer, enhance innate defence against pathogens and decrease paracellular permeability of IECs (32). Lactobacillus strains consumed as probiotics are thought to modulate the native intestinal microbiota and improve health via multiple mechanisms of action. As illustrated in Figure 1, probiotics strengthen intestinal barrier function by increasing mucus production, stimulating release of anti-microbial peptides, and production of secretory immunoglobulin A (sIgA) production, increasing tight junction integrity of IECs and providing a competitive resistance against pathogens such as for host colonisation receptors (33, 34).

Figure 1

Probiotic mechanisms of intestinal barrier enhancement.

Mucus Production

Goblet cells (GC) of the GI tract express rod-shaped mucins which either adhere to the epithelium or are released into the GI lumen. These mucins are highly glycosylated and link together via di-sulfide bonds to form a glycoprotein matrix that shields the intestinal epithelium from gut luminal contents (containing digestive enzymes), prevents interaction between pathogenic antigens/bacteria and the epithelial monolayer, and also aids GI motility. The mucus layer is generally between 50-800 µm thick and in healthy individuals the first 30 µm closest to the epithelial surface should be free of microbes. Lactobacillus species are believed to enhance intestinal barrier defence by promoting mucus secretion. In vitro studies have demonstrated that conditioned media from L. casei T21 can up-regulate the mucosal protective MUC2 gene in colonic epithelial cells (Caco2 and HT29) challenged with C. difficile (35). Although it has been proposed that acid may stimulate enteric cells to produce mucins (36) incubating HT29 cells with lactic acid did not replicate these findings indicating that other substances secreted by L. casei T21 are responsible for the increased gene expression. Similar results have also been obtained in the Caco-2 intestinal epithelial cell line using L. casei GG (37). In terms of in vivo studies, L. rhamnosus CNCM I-3690 has recently been shown to protect and/or restore the GC population and protect mucus layer thickness in mice following low-grade colon inflammation (38). Similarly, mice administered one of two strains of L. reuteri (L. reuteri R2LC or 4659) and exposed to DSS colitis displayed reduced colitis severity which the authors attribute at least partly to the increase in mucus thickness seen in mice given the probiotic both in control and inflammatory conditions (39).

The commercially available probiotic VSL#3 contains a combination of eight lactic acid producing bacteria of which four are Lactobacilli (L. plantarum, L. delbrueckii subsp. Bulgaricus, L. casei, L. acidophilus, Bifidobacterium breve, B. longum, B. infantis and Streptococcus salivarius subsp. thermophilus). Although the contribution of each bacterial strain cannot be clarified, both in vitro and in vivo experiments by Caballero-Franco et al. (40) using this probiotic in rats have indicated enhancement of the mucus layer measured by over-expression of mucin genes and increased basal luminal mucin content. Conversely, a similar study in mice failed to show altered mucin expression or mucus layer thickness using this probiotic (41). Further work is required to determine whether the in vitro effects of probiotics on mucus production are maintained in vivo.

Anti-Microbial Peptides/Factors

Host-produced GI anti-microbial peptides are generally categorised into cathelicidins and defensins. Cathelicidins are α-helical cationic peptides constitutively expressed in the GI tract which may also be activated by butyrate. Butyrate is produced by the enteric microbiota however few studies have examined the effect of probiotics on cathelicidin expression. Defensins are small, cationic peptides further classified into β-defensins, produced by epithelial cells throughout the intestine, and α-defensins, expressed in the small intestine. Defensins are constitutively expressed in the GI tract and display anti-microbial activity against many bacteria, fungi and some viruses. L. acidophilus PZ1138 and L. fermentum PZ1162, were shown to induce expression of human β-defensin-2 gene in Caco-2 cells via classic pro-inflammatory mechanisms (42). L. reuteri (FINELACT^®) administered to broiler chicks was associated with anti-microbial peptide modulation in the cecum and ileum in addition to upregulation of pro-inflammatory mediators (43).

In addition to host-derived anti-microbial peptide stimulation, commensal bacteria also produce anti-microbial factors to aid in host barrier defence. These factors include short chain fatty acids (SCFA), hydrogen peroxide and bacteriocins. Lactobacilli alter luminal pH by producing lactic acid. This inhibits the growth of some bacteria and damages the outer cell membrane of Gram-negative bacteria, including E. coli O157:H7, Pseudomonas aeruginosa, and Salmonella enterica serovar Typhimurium making them more vulnerable to other anti-microbial molecules (44). Anti-microbial activity by L. johnsonii NCC533 has been associated with lactic acid and hydrogen peroxide production (45). Bacteriocins are small, ribosomally synthesised, heat-stable peptides produced by many species of bacteria which function to inhibit the growth of (bacteriostatic), or kill (bactericidal), other bacteria (46). Bacteriocins produced by Gram-positive bacteria generally exert their antibiotic effects by destabilisation of membrane function, typically against other Gram-positive bacteria, though some Gram-negative bacteria may also be susceptible (47). Lactobacillus strains produce SCFAs including acetate, propionate and butyrate, which have been shown to shown to increase transepithelial electrical resistance and stimulate the formation of tight junction in Caco-2 intestinal epithelial cells in vitro via inhibition of the NLRP3 inflammasome and autophagy (48). L. plantarum strains produce several bacteriocins which demonstrate anti-microbial activity against food borne pathogens such as Listeria monocytogenes as well as food spoilage bacteria are applied in food production to reduce the use of chemical preservatives (49). Corr et al. (50) demonstrated that Abp118 produced by L. salivarius UCC118 in vivo protects mice against L. monocytogenes infection. Two other bacteriocins analogous to Abp118 have since been identified by comparative genome hybridisation analysis from L. salivarius DPC6488: salivaricin L and T. Both bacteriocins demonstrated inhibitory activity towards L. delbrueckii subsp bulgaricus LMG 6901 with salivaricin L additionally inhibiting L. monocytogenes NCTC 11994 and L. innocua DPC3572 (51).

Secretory IgA

The production of IgA is an important strategy utilised by the GI tract to generate immune protection in a non-inflammatory mode (52). IgA dimers (secreted by intestinal B cells located in Peyer’s patches or lamina propria) interact with the polymeric IG receptor (pIgR) on the basolateral surface of epithelial cells, translocate to the surface of the epithelial cells and are released as sIgA (53). sIgA primarily promotes the maintenance of suitable commensal bacterial communities in the gut by binding dietary antigens and potential pathogens in the mucus and down-regulating the expression of pro-inflammatory bacterial epitopes on commensal bacteria (54). Furthermore, sIgA enhances the intestinal barrier by blocking microbial components involved in epithelial adherence, facilitating intraepithelial defence against pathogens and microbial products and enabling antigen sampling (55). In addition, locally released IgA dimers function to remove micro-organisms that have breached the epithelial barrier by facilitating their removal or promoting their clearance by binding to the CD89 receptor on immune cells such as dendritic cells, neutrophils and other phagocytes (56). Although commensal bacteria are believed to induce sIgA expression in the GI tract the mechanisms are not well understood, although there appear to be differences in the microbes responsible for small intestine and large intestine sIgA induction (57). Various Lactobacillus strains including L. paracasei MCC1849, L. gasseri SBT2055, and L. plantarum AYA are known to increase sIgA levels in the small intestine (58–60). In a clinical trial of children 12 to 24 months old, supplementation with L. plantarum IS-10506 increased sIgA faecal titres and a significant positive correlation was observed between this and TGF-β1/TNF-α ratios (61). The authors propose a probiotic induced immune activation of TGF-β1, which in turn increases the production of sIgA.

Epithelial Cell Barrier

As previously described, IECs form a monolayer of cells which act as a physical barrier between the external environment of the gut lumen and the host’s immune system. The integrity of this barrier is ensured by tight junctions (TJ) which are multi-protein complexes that bind the cells tightly together as well as adherens junctions, gap junctions and desmosomes. TJs are located towards the apical side of the epithelial cells. They consist of transmembrane proteins (claudin, occludin, and junctional adhesion molecules) which interact extra-cellularly with similar proteins of TJs in neighbouring cells and intra-cellularly with the cells own cytoskeleton via zonula occludens (ZO) proteins and filamentous actin (62). Loss of TJ integrity has been observed in chronic inflammatory disease, and mechanisms of disrupting TJ proteins in order to breach the GI barrier have been observed in infection by enteric pathogens such as C. difficile, E. coli, Salmonella Typhimurium, C. rodentium, Vibrio cholera among others (62). It has been demonstrated that L. rhamnosus GG ATCC 53103 up-regulates ZO-1, claudin and occludin expression in Caco-2 cells (63). This probiotic strain has been observed to increase levels of ZO-1 expression and enhance distribution of claudin-1 protein as a protective mechanism against enterohemorrhagic E. coli O157:H7 infection (64). Increased expression of ZO and occludin was also observed using various L. plantarum strains (L. plantarum WCSF1, CGMCC 1258, and MB 452) (65–67). L. plantarum WCSF1 administration into the duodenum of healthy human subjects increased ZO-1 and occludin staining in the vicinity of TJ structures via activation of TLR-2 (65). The addition of a TLR-2 agonist PCSK to Caco2 monolayers in vitro increased staining of occludin in TJ regions and was protective against epithelial barrier disruption. TLR-2 ligand binding leads to PKC activation which has been demonstrated to cause translocation of tight junction components (68) thereby it is likely that barrier integrity is enhanced by alterations to composition of tight junction proteins rather than an increase in these proteins. Lactobacillus species may also stabilise adherens junctions by increasing expression of E-cadherin, as well as by strengthening the E-cadherin/β-catenin complex (which connects adherens junctions to the cytoskeleton) via enhanced phosphorylation of β-catenin (69). In a clinical study of small intestine barrier function, biopsy samples demonstrated that L. plantarum strain TIFN101 and to a lesser extent L. plantarum WCFS1 and CIP104448, modulated an increase in gene expression of TJ and adherens junction proteins (70).

Competitive Resistance

Lactobacilli also aid intestinal barrier resistance to invading pathogens by competing for binding sites on IECs, glycoproteins in the mucus layer or to the plasminogen of extracellular matrix (71). In order to facilitate the necessary interactions with host cells, Lactobacillus species display various different components on their outer surface. These may include cell wall proteins, S-layer proteins, pili proteins, and moonlight proteins (72) (see Figure 2). These surface proteins facilitate adhesion of Lactobacilli to the host, for example LPXTG proteins found in several Lactobacillus strains are cell surface proteins covalently bound to the peptidoglycan layer and can bind to both mucus and epithelial cells (73). Several Lactobacillus strains possess a crystalline, glycoprotein surface layer, also known as the S-layer, non-covalently anchored to the peptidoglycan cell wall (74). The S-layer S-proteins of L. acidophilus ATCC 4356 have demonstrated anti-viral activity against alphavirus and flavivirus infection of 3T3 cells by blocking pathogen adhesion to C-type Leptin receptors (DC-SIGN) an attachment factor which strongly promoted viral infection (75). Further work is required to elucidate the mechanism for this, which may be multi-faceted, though the time-dependant aspect of the anti-viral function may indicate that S-layer proteins are activating downstream anti-viral signalling pathways.

Figure 2

Representation of the Lactobacillus cell surface structure including important effector molecules.

Pili are long protein structures, first observed in a non-pathogenic bacteria in L. rhamnosus GG, which protrude from the bacterial cell playing a major role in adhesion to the epithelium. In L. rhamnosus GG (ATCC 53103) SpaC pili have been demonstrated to out-compete the pathogenic Enterococcus faecium (76).

Moonlighting proteins are multifunctional proteins in which one polypeptide chain performs more than one unrelated biochemical or biophysical function (77). In Lactobacilli, moonlighting proteins may have a primary function as intracellular proteins but are also found on the cell surface where they facilitate adhesion, for example, L. plantarum 299v (78), L. acidophilus (79), L. reuteri ZJ617 (80), display GAPDH on their surface to mediate adhesion and colonisation of the GI tract. So far in the case of L. plantarum 299v it has been demonstrated that this results in competitive exclusion and displacement of pathogenic bacteria (81). The mechanism for the secretion of moonlighting proteins to the cell surface has not yet been elucidated.

L. rhamnosus R0011 and L. acidophilus R0052 adhere to Hep-2 and T84 intestinal cell lines in vitro preventing the binding of enterohemorrhagic E. coli and enteropathogenic E. coli (82). In Caco-2 cells, various strains of L. reuteri (LR5, LR6, LR9, LR11, LR19, LR20, LR26, and LR34) have been shown to adhere and inhibit and displace the binding of E. coli ATCC 25922, S. Typhi NCDC 113, L. monocytogenes ATCC 53135, and E. faecalis NCDC115 (83). It should be noted that competition for binding sites is species and strain -specific; L. rhamnosus ATCC 53103, L. gasseri DSM 20243, L. casei ATCC 393 and L. plantarum ATCC 14917 pre-treatments did not block enterohemorrhagic E. coli binding to human colon epithelial cell line C2BBe1 cells (although the L. rhamnosus strain prevented internalisation of E. coli into the cell line) (84). In a chronic stress model in vivo, pre-treatment with L. helveticus R0052 and L. rhamnosus R0011 reduced commensal adherence and translocation (85). Interestingly, in a hemorrhagic shock model in vivo, L. rhamnosus LMG P-22799 but not L. fermentum NumRes2 reduced bacterial translocation and cytoskeleton rearrangement despite both strains displaying similar pathogen exclusion properties in vitro in Caco2 cells (86). Indeed, L. fermentum NumRes2 increased bacterial translocation, primarily Lactobacillus spp., to the spleen highlighting the need for careful characterisation of the effects of individual.

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Lactobacillus spp. and Gastrointestinal Infection

Understandably, the beneficial impact on gut health is one of the most widely studied topics in probiotic research. As discussed in the previous section, Lactobacilli protect the intestinal barrier from infection by promoting mucus production and barrier-related proteins, secreting anti-microbial substances such as SCFAs, bacteriocins and hydrogen peroxide which inhibit the growth of or kill pathogens, by modulating the host’s immune response to pathogens, and preventing adherence of pathogens and competing for binding sites. Thus, Lactobacilli are capable of preventing intestinal damage caused by certain bacterial infections. Lactobacillus probiotics have been demonstrated to inhibit the development of infection by pathogenic bacteria, such as C. difficile and C. perfringens (87), Campylobacter jejuni (88), S. Enteritidis (89), E. coli (90), Staphylococcus aureus (91), and Yersinia (92), among others. Two major GI disorders resulting from infection, H. pylori infection and antibiotic-associated diarrhoea, have been shown to greatly benefit from Lactobacillus probiotics and are outlined below.

H. pylori Infection and Lactobacilli

H. pylori infection is one of the most common bacterial infections in the world with more than half of the global population infected; though prevalence ranges from 24% in Oceania to 70% in Africa (93). H. pylori infects the epithelial lining of the stomach causing disorders such as peptic ulcer disease, chronic gastritis, and gastric cancer although many infected individuals are asymptomatic (94). Twenty percent of infected patients develop symptomatic gastritis, gastric or duodenal ulcers, gastric adenocarcinoma, or non-Hodgkin’s gastric lymphoma. The current recommended treatment for H. pylori infection involves multiple antibiotic drugs as well as a proton pump inhibitor however the effectiveness of this treatment is decreasing as H. pylori antibiotic resistance rises. The addition of a Lactobacillus probiotic (L. casei DN-114 001 (OAC-LC) and L. casei Shirota separately) and an L. acidophilus LB postbiotic have been shown to improve the efficacy of this therapy in various randomised controlled trials (95–97), however some trials have found no or only slight beneficial effects (98–101). Although the probiotic L. johnsonii NCC533 failed to eradicate H. pylori infection when administered alone, it did decrease inflammatory scores and urea breath test (used for the diagnosis of H. pylori infection) values (102, 103).

Cell-free spent culture supernatants (CFCS) derived from L. casei Shirota exhibited pH-dependant bactericidal activity against H. pylori in vitro (104). The CFCS of L. johnsonii NCC533 and L. acidophilus LB both resulted in the loss of H. pylori viability (105–107). Furthermore, the CFCS from these three Lactobacillus strains resulted in altered morphology of H. pylori bacteria to U-shaped or coccoid forms which are dormant forms of the bacteria with the coccoid form being less capable of colonising and inducing inflammation (108, 109). L. johnsonii NCC 533 and L. casei Shirota are also known to produce bacteriocins which are active against H. pylori (110). H. pylori is a spiral-shaped bacterium with multiple flagella allowing it to swim in the gastric mucus layer and interact with epithelial cells, an ability which is required for colonisation in the stomach (111). L. casei Shirota has been demonstrated to cause H. pylori to lose its flagellar motility due to transformation into dormant forms with no flagella and also by secretion of small anti-microbial compounds which inhibit swimming ability (104). Similarly, L. johnsonii NCC 533 also secretes compounds that inhibit the swimming ability of H. pylori (112). In order to survive in the low pH of the stomach, H. pylori expresses urease as a surface protein to neutralise the surrounding acidic environment. CFCSs from L. acidophilus LB and L. johnsonii La1 have been demonstrated to reduce urease activity of H. pylori (105, 106). In terms of adherence, L. acidophilus CFCS prevented the adhesion of H. pylori onto human HT-29 cells resulting in the death of adhering cells and reducing the urease activity of remaining adherent cells causing their lysis (105).

Antibiotic-Associated Diarrhoea and Lactobacilli

Antibiotic-associated diarrhoea (AAD) results from disruption of the normal microbiota of the gut by antibiotics with symptoms ranging from mild diarrhoea to more serious disease like pseudomembranous colitis (PMC) (113). AAD occurs in 5-30% of patients receiving antibiotics either during antibiotic therapy or up to 2 months after cessation of treatment. One of the major pathogens associated with AAD is C. difficile, responsible for 10-30% of normal AAD cases and 90-100% of severe cases such as PMC (114). Although other microbes including C. perfringens, S. aureus and Klebsiella oxytoca are associated with this disorder, they are not common (113). As the cause for AAD is known to be disruption of the normal intestinal microflora, and also due to the fears surrounding anti-microbial resistance, recent therapeutic research has focused on the use of probiotics or faecal microbiota transplantation to restore microbial equilibrium (115, 116). Though the mechanism of action of probiotics is not explicitly known in this case their efficacy seems to be maintenance of gut flora, out-competing pathogenic bacteria, preservation of intestinal barrier function and potentially immunomodulation. Treatment with several Lactobacillus strains including L. rhamnosus GG (ATCC 53103) and L. gasseri have been shown to be effective as a preventive measure for AAD (117). However, the effects are strain-dependent. A systematic review examined 51 randomised controlled trials and found that L. rhamnosus GG was significantly more effective than other probiotics, however L. casei species were most effective against C. difficile infection (118). Another recent review demonstrated similar results in children concluding that L. rhamnosus GG (ATCC 53103) can be safely given to prevent AAD and additionally to manage symptoms of acute gastroenteritis (119).

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Lactobacillus spp. and Intestinal Inflammation

In humans, the immune system can be divided into the innate immune system and the adaptive immune system. Innate immunity is the first line of immune defence and is a non-specific response which acts as an immediate reaction to pathogens. Phagocytic cells such as natural killer (NK) cells, macrophages, monocytes and neutrophils recognise pathogenic targets and engulf and destroy them. Antigen presenting cells (APC) such as dendritic cells (DC) maybe activated via the innate response and in turn activate the adaptive immune response. The adaptive immune response relies largely on activation and differentiation of B and T cells. B cells recognise antigens via B cell receptors and act by secreting antibodies (humoral immunity). T cells recognise antigens via T cell receptors and differentiate into T helper cells (Th; CD4+) or cytotoxic T cells (CD8+). Th cells recognise antigen via MHC class I complexes and CD8+ cells do this via MHC class II complexes. Th cells differentiate into Th1 or Th2 effector cells which activate and regulate macrophages (Th1) and B cells (Th2) while CD8+ cells convert into cytotoxic T cells. In the GI tract the immune system is made up of the epithelial layer, the lamina propria and the gut associated lymphoid tissue. The GALT is populated by B and T cells as well as plasma cells, macrophages and M cells. APCs in Peyer’s patches take IgA antigen from epithelial cells to activate T cells and also transport it to lymphoid tissue of the lamina propria and mesenteric lymph nodes. M cells present in Peyer’s patches of the small intestine transport antigens, macromolecules, micro-organisms and inert peptides from the gut lumen into the tissue via adsorptive endocytosis. These antigens may then activate the innate and adaptive immune systems.

As alluded to in the previous sections, Lactobacilli play an immunological role within the GI tract of the host, strengthening the intestinal barrier and conferring protection from potential pathogens. Lactobacilli can interact with both the innate and adaptive immune response systems via micro-organism-associated molecular patterns (MAMPs) interacting with pattern recognition receptors such as Toll-like receptors (TLRs), nucleotide-binding oligomerization domain (NOD) receptors and C-type lectins expressed on immune cells or on tissues including intestinal epithelium (120). The Lactobacillus cell envelope comprises several types of molecules which act as MAMPs including the peptidoglycan multi-layer, teichoic acids (lipoteichoic acid (LTA) bound to the cell membrane and wall teichoic acid bound to the peptidoglycan layer), exopolysaccharides (EPS) along with cell surface adhesion molecules previously discussed (see Figure 2). The immunomodulatory effect of Lactobacilli is achieved with the release of cytokines, including interleukins (IL), tumour necrosis factors (TNF), interferons (IFN), transforming growth factor (TGF), and chemokines from immune cells (121). The inflammatory process depends on pro-inflammatory versus anti-inflammatory cytokines and in this way probiotics may act in an immunoregulatory or immunostimulatory manner. Immunoregulatory probiotics decrease inflammatory responses protecting the host against autoimmune diseases, inflammatory bowel disease and allergy and are characterised by IL-10 and regulatory T cell (Treg) production. IL-10 is an anti-inflammatory cytokine produced by monocytes, T cells, B cells, macrophages, NK cells and DCs to inhibit pro-inflammatory cytokines, chemokines and chemokine receptors protecting against intestinal inflammation. Immunostimulatory probiotics defend the host against infection and cancer development activating NK cells and developing Th1 cells via IL-12 production, and also defend the host against allergy by balancing Th1 and Th2 production. Mounting evidence would suggest that probiotic Lactobacilli have the potential to prevent or treat certain inflammatory conditions (122).

The activation of specific immune receptors by MAMPs on Lactobacillus species has been characterized to an extent. Peptidoglycan of L. casei Shirota, L. johnsonii JCM 2012 and L. plantarum ATCC 14917 has been shown to down-regulate IL-12 production via TLR2 (123). Peptidoglycan from L. rhamnosus CRL1505 demonstrated an enhancement of innate and adaptive immune responses ameliorating the Th2 response when administered nasally in mice (124). LTA of L. plantarum has been shown to elicit an anti-inflammatory response in both human and porcine intestinal epithelial cells via inhibition of IL-8 (125, 126). The knockout mutant for the SpaCBA pilus of L. rhamnosus GG demonstrated that not only are these pili essential for adhesion but also the knockout demonstrated an increase in IL-8 likely via LTA TLR2 signalling which suggests an immunomodulatory role for this adhesion molecule (127). The protective exopolysaccharide layer has also demonstrated immunomodulatory capabilities with EPS from L. rhamnosus RW-9595M inducing macrophage production of IL-10 and no induction of TNF-α, IL-6, or IL-12 (128) and L. plantarum 14 EPS decreasing the IL-6 and IL-8 production in response to an enterotoxigenic E. coli challenge in porcine epithelial cells (129). In mice, EPS derived from L. delbrueckii subsp.bulgaricus OLL1073R-1 fermented yogurt had an immunostimulatory effect, activating natural killer (NK) cells and inducing IFN-γ production in the spleen (130).

Some immunomodulatory effects are mediated by the metabolites of Lactobacillus, such as SCFAs, in particular, propionate, acetate, and butyrate. These postbiotics bind to specific receptors on intestinal epithelial cells to inhibit pro-inflammatory activity and Treg suppressive effects of neutrophils and macrophages (131–133). Indeed butyrate enemas have demonstrated efficacy and become an accepted treatment for diversion colitis though this is believed to be due to a relaxation effect on smooth muscle (134).Lactobacilli are also capable of producing antioxidants like glutathione (GSH) and can induce reductions in oxidative stress. Two strains of L. bulgaricus (L. delbrueckii subsp. bulgaricus B3 and A13) have been demonstrated to reduce lipid peroxidation, increase measurements of antioxidant enzymes, and reduce oxidative stress in a rat model of colitis (135). In a mouse model of gastric damage L. fermentum Suo significantly reduced malondialdehyde (MDA; a measure of oxidative damage) concentrations and serum concentrations of IL-6, IL-12, TNF-α, and IFN-γ (136). L. casei 114001 administered to rats increased the antioxidant capacity of plasma, liver and intestines and decreased MDA plasma concentration (137). In healthy human subjects, L. casei capsules administered with prebiotic inulin significantly decreased MDA and glutathione disulphide (GSSG; another measure of oxidation) concentrations and increased concentrations of antioxidant indicators: GSH, total GSH (GSHt) and free sulfhydryl group (-SH) in the plasma (138). Pre-treatment with L. acidophilus NCDC15 with inulin and L. rhamnosus GG MTCC 1408 with inulin in a model of colon cancer in mice lead to a reduction in MDA and an increase in antioxidants GSH-reductase, GSH-peroxidase and superoxide dismutase as well as fewer dysplastic changes (139).

Lactobacilli may also modulate the immune system by secretion of proteinaceous compounds. Proteins p40 and p75 released from L. rhamnosus GG ATCC 53103 both activated the Akt signalling pathway, inhibiting TNF-a –induced apoptosis in human and murine colonic epithelial cells and murine colon explants (140). Pre-treatment with L. rhamnosus GG milk prior to induction of dextran sulphate sodium –induced colitis in mice significantly reduced colonic inflammation and injury, suppressing cytokine-induced apoptosis and reducing H₂O₂-induced disruption of TJs. Depletion of two soluble proteins found in L. rhamnosus milk, p40 and p75, abolished these anti-inflammatory effects (141). L. rhamnosus GG ATCC 53103 increased production of the heat-shock proteins HSP25 and HSP72 in murine colon cells via secretion of soluble peptides which function via activation of MAPK signal transduction pathway (142).

There have been many reports of Lactobacilli influencing the immune system while also enhancing the intestinal barrier. In vitro, L. acidophilus PZ1138, L. fermentum PZ1162, and L. paracasei LMG P-17806 induced expression of human β-defensin-2 gene in Caco-2 cells via modulation of nuclear factor kB (NF-kB) and the activator protein 1 (AP-1) resulting in IL-8 expression (42). L. salivarius Ls33 peptidoglycan induced anti-inflammatory IL-10 production, and stimulated Treg responses via NOD2 rescuing symptoms in a tri-nitrobenzene sulfonic acid (TNBS) -induced colitis murine model (143). Enteral administration of L. rhamnosus GG decreased inflammation in the developing mouse colon, attenuating pro-inflammatory MIP-2 and TNF-α concentrations in an IL-10 receptor-dependent manner (144). In Caco-2 cells L. plantarum WCSF1 has been shown to enhance ZO-1 trafficking to TJ regions in a toll-like receptor (TLR)-2-dependent manner (65). In a porcine intestinal cell line, L. rhamnosus GG ATCC 7469 pre-treatment increased ZO-1 and occludin protein expression in a TLR-2-dependent mechanism and also attenuated enterotoxigenic E. coli –induced increases in TNF-α via a partly TLR-2-mediated mechanism (145).

Lactobacilli may interact with enterocytes, DCs, Th1, Th2 and Treg cells in their immunomodulatory capacity in the intestine. Studies in vitro and in vivo demonstrated that L. paracasei and L. acidophilus strains induced early innate and adaptive immune responses in developing mice and rats in terms of phagocytosis, polymorphonuclear cell recruitment and TNF-α, IL-6, IL-10, IFN-γ production in a TLR-dependent mechanism (146). Homogenates prepared from several probiotics including L. rhamnosus GG ATCC53103, L. rhamnosus LC-705, L. acidophilus NCFB-Lb1748, and L. bulgaricus ATCC 11842 have demonstrated the ability to suppress peripheral blood mononuclear cell proliferation and L. acidophilus homogenates also down-regulated expression of IL-2 and IL-4 (147). In a mouse model of colitis where IL-10-deficient mice were infected with H. hepaticus, the combination of L. paracasei 1602 and L. reuteri 6798 reduced mucosal inflammatory cytokines TNF-α and IL-12 and also reduced intestinal inflammation (148). In an in vitro model, L. sakei LTH681 induced the inflammatory cytokines IL-1β, IL-8 and TNF-α in Caco-2 cells while L. johnsonii La1 failed to induce pro-inflammatory cytokines and instead induced production of anti-inflammatory TGF-β (149). Co-culture of ileal explants from patients with Crohn’s disease with L. casei DN-114001 and L. bulgaricus LB10 resulted in decreased TNF-α expression as well as decreased numbers of CD4+ T cells within the inflamed mucosa (150). CFCS from L. acidophilus ATCC 4356, L. casei ATCC 334, L. lactis ATCC 11454 and L. reuteri ATCC 55148 down-regulated IL-8 expression in human HT-29 cells and had differing strain-dependent efficacies in decreasing pro-inflammatory cytokines (IL-1β, IL-6, TNF-α) and in increasing anti-inflammatory IL-10 production in LPS-stimulated monocyte-derived macrophages (151).

Inflammatory bowel disease (IBD) is an example of an intestinal inflammatory disease which may be modulated by Lactobacilli probiotics. IBD is a chronic, relapsing and remitting disorder characterised by inflammation of the GI tract with two main classifications: Crohn’s disease and ulcerative colitis. Although the cause of IBD is unclear, dysbiosis of the GI microbiota is a feature of the disorder and it is believed probiotics may have a therapeutic benefit by restoring microbial balance and also by immunomodulation (152). Data from both in vitro and in vivo studies in animal models of colitis are extremely promising in terms of reducing inflammatory markers and decreasing colitis severity (153–155), however the same cannot be said for clinical trials of probiotics in IBD. Although it would appear that probiotics have beneficial effects in inducing remission and increasing remission times in UC (156) this has not yet been demonstrated for CD (157). A meta-analysis recently showed that L. rhamnosus GG displayed no beneficial effects in IBD patients, though VSL#3 (a combination of eight lactic acid bacteria strains – of which four are Lactobacilli) was better than placebo in terms of a higher remission rate and lower relapse rate (158). Similarly, another recent meta-analysis and systematic review concluded that a combination of Lactobacillus probiotics and prebiotics were effective in UC, although probiotics in general were not effective in CD (159). Further randomised, placebo controlled, clinical trials will be required to clarify the role of Lactobacilli in IBD and to elucidate the most beneficial strain, dose, and mode of administration.

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Conclusion and Future Perspectives

There is increasing evidence to suggest that commercial and clinical use of probiotics is outpacing proven science. A recent study in healthy human subjects given probiotic supplements indicated that the colonisation of the GI tract featured person, region and strain -specific differences. In some individuals colonisation did not occur with the GI tract demonstrating colonisation resistance to the probiotics. The authors conclude that considering the transient, individualised effect of probiotics, the development of new personalised probiotic approaches is merited (160).

Despite the ever-increasing prevalence of probiotic use, there are also many limitations and unknowns (161–163). Data from research trials on efficacy of probiotics in the treatment and prevention of disease can often have conflicting results with similar studies pointing to opposing conclusions. These confusing data are somewhat to be expected and may be accounted for given the extremely complex nature of host – probiotic – microbiota interactions. One must allow for the unique individual differences in human microbiota composition, due to age, health, diet etc., which may affect the response to the intervention and may even account for adverse effects. Risks associated with probiotic use are generally concerned with the safety of vulnerable patient cohort such as the elderly or the immunocompromised. Thorough elucidation of mechanistic properties and host interactions will required in order to determine the probiotic strains and required intake levels required to achieve the desired health outcomes. It is also of note particularly for probiotic use in healthy individuals, and indeed for mechanisms requiring microbe-host interaction, that evidence indicates that probiotics are unlikely to be capable of maintaining colonisation in the host with any differences in microbiota composition being transient and dependent on continued probiotic intake. In terms of study design, it is often the case that mechanistic observations are founded in in vitro cell populations which cannot give the full picture of host and microbiota interactions. These are not always supported by in vivo observations in animal models which themselves may be flawed given incompatibilities or inconsistencies between human and animal microbiomes. On top of this the variety of available and potential new probiotics is vast and, as we have seen, beneficial effects can be species or strain specific and may require combination with other probiotics or prebiotics to be effective. Additionally, it is often the case that probiotic trials are initiated and funded by components of the probiotic industry who have commercial interests and may have a motive to downplay adverse effects. Although systematic reviews and meta-analyses of existing studies go some way in trying to overcome biased or underpowered research and allow for observation of overall trends, they are not themselves immune from the introduction of bias. Large, long-term, multicentre randomised controlled trials of probiotics chosen based on mechanistic information with specific beneficial outcomes for specific human cohorts in mind and involving collaborations with non-affiliated groups should be the aim to truly separate the good from the ineffective or bad.

It is clear that we have a long way to go in understanding all of the complexities of the microbiota and the effects of probiotic bacteria for health. Far more in-depth clinical testing will be required in order to substantiate the health claims of commercially available probiotic health supplements. Further elucidation of the modes of action of beneficial probiotics in clearly defined subsets of populations will hopefully allow us to make better predictions about efficacy, improve clinical trial design and enable improvement in development of probiotic health strategies. Expansion in the field of bacterial-derived products i.e. postbiotics signals a more precise, effective and safer future for the probiotic health market. In the interim, those looking to improve their overall health by enhancing their GI microbial complexity might find it more advantageous to focus on consuming a healthy varied diet of grains, fruit, vegetables and fermented foods such as miso, nattō, kimchi and sauerkraut.

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Author Contributions

Writing—original draft preparation, ED; writing—review and editing, ED and SC; Conceptualization, ED and SC; Funding acquisition, SC. All authors have read and agreed to the published version of the manuscript.

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Funding

Funding for the Corr Lab is provided by Science Foundation Ireland [grant 19/FFP/6499].

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Conflict of Interest

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

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Publisher’s Note

All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article, or claim that may be made by its manufacturer, is not guaranteed or endorsed by the publisher.

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The Functional Roles of Lactobacillus acidophilus in Different Physiological and Pathological Processes

Abstract

Probiotics are live microorganisms that can be consumed by humans in amounts sufficient to offer health-promoting effects. Owing to their various biological functions, probiotics are widely used in biological engineering, industry and agriculture, food safety, and the life and health fields. Lactobacillus acidophilus (L. acidophilus), an important human intestinal probiotic, was originally isolated from the human gastrointestinal tract and its functions have been widely studied ever since it was named in 1900. L. acidophilus has been found to play important roles in many aspects of human health. Due to its good resistance against acid and bile salts, it has broad application prospects in functional, edible probiotic preparations. In this review, we explore the basic characteristics and biological functions of L. acidophilus based on the research progress made thus far worldwide. Various problems to be solved regarding the applications of probiotic products and their future development are also discussed.

Keywords: Probiotics, Lactobacillus acidophilus, intestinal flora, cholesterol, immunity

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Introduction

The Food and Agriculture Association (FAO) and World Health Organization (WHO) have highlighted that probiotics are live strains of microorganisms that have been carefully selected. When administered in sufficient amounts, probiotics can bring health benefits to the host [1]. There are a large number of probiotic bacteria that colonize the human intestine, which can also interact and co-evolve with the human body. They help the host to digest and absorb nutrients in food, metabolize toxic waste products, and produce amino acids and short-chain fatty acids necessary for normal human activities. They can provide definite health effects such as improving the host microecological balance while exerting other beneficial effects on the intestinal tract [2].

Since the early 1990s, a plethora of “probiotic” health products have swept throughout the global market. In the meantime, “probiotics” have become a hot international research topic. Probiotics have been extensively studied in a variety of diseases and have been demonstrated to produce a range of potential health effects. The most studied species include lactobacilli, bifidobacteria, and yeasts [3]. Among them, L. acidophilus, an important intestinal probiotic in the lactic acid bacteria (LAB) family, has had a great deal of focus placed upon it in terms of research and development, especially as it is so closely linked to human health. As such, L. acidophilus is widely considered to have probiotic effects and is one of the most commonly recommended microorganisms for dietary use [4]. Compared with many other probiotics, L. acidophilus has better resistance to both acid and bile salt. These characteristics facilitate the survival and proliferation of L. acidophilus in the harsh environment of the gastrointestinal tract. Its ability to survive under these conditions provides further opportunities for its products to successfully function in the human body. When the total amount of L. acidophilus reaches a certain threshold value, health promotion can be achieved. L. acidophilus has multiple effects on the human body, including nutritional effects, regulation of intestinal flora balance, enhancement of immunity, age-delaying and anti-cancer effects, and support of cholesterol reduction [5, 6].

In this review, the basic characteristics of L. acidophilus are summarized, its biological functions in various diseases are discussed, and future research directions and applications in the form of probiotic products are explored. We hope to unveil the relationships between L. acidophilus and various life activities and disease development so as to provide a theoretical basis for later research and application direction.

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Basic Features and Functional Mechanisms of L. acidophilus

L. acidophilus was initially isolated from infant feces in 1900 and was officially named Lactobacillus acidophilus. Subsequently, a series of biological characteristics and functions have been studied. L. acidophilus is subdivided into many strain types, including L. acidophilus LA-1, LA-5, NCFM, and ATCC4356, DDS-1 [7]. Different strains also confer differing probiotic properties and functions. Since a strain may have multiple names, it is easy to confuse the strains during the process of understanding them and when undertaking research. Fortunately, most of the work on L. acidophilus, especially the work relating to its probiotic effects, has been done on particular strains.

Basic Features of L. acidophilus

L. acidophilus, within the genus Lactobacillus in the family Lactobacillaceae, is a gram-positive bacillus that does not form spores. They present as slender rods with a circular end, measuring 2-10 μm long. Most L. acidophilus strains are microaerobic bacteria, which grow better in anaerobic environments, or in 5~10% CO₂, rather than in aerobic environments. Their optimum culture temperature is generally 35~38°C, and they basically do not grow in temperatures below 20°C. L. acidophilus has poor heat resistance and its optimum pH is 5.5~6.0. The growth characteristics of different strains are also slightly different from each other. L. acidophilus is eosinophilic and has good resistance toward acids and bile [8, 9]. It can grow and reproduce in environments where other LAB cannot grow. It can also use glucose, fructose, lactose and sucrose to carry out homotype fermentation and can produce DL-lactic acid via fermentation [10].

L. acidophilus is a species of beneficial microbial flora and has been proven to have many good probiotic characteristics that can be roughly divided into two categories. The first category covers the essential probiotic properties of L. acidophilus which have been demonstrated in vitro and include tolerance to low pH, bile resistance, adhesion to human colon cells in cell culture, antibiotic production, lactase activity, and product stability [11–17]. The second category includes the overall probiotic effects that have been observed in animal-level feeding studies, such as regulation of host immune responses, reduction of host serum cholesterol, improvement of host lactose metabolism, and prevention or treatment of infection [18–20]. Here, we summarize the basic probiotic properties and main biological functions of L. acidophilus (Fig. 1).

Fig. 1

Probiotic properties and biological functions of Lactobacillus acidophilus.L. acidophilus is a species of beneficial microbial flora and has been proven to play an important role in many pathological and physiological processes. It has been shown to improve CVD and lactose intolerance, prevent and treat cancer, regulate immunity, and improve gastrointestinal diseases.

Functional Mechanisms of L. acidophilus

According to current studies, L. acidophilus participates in the host intestinal tract mainly through the production of metabolites and regulation of intestinal microbiota [21, 22].

First, L. acidophilus can regulate the balance of intestinal flora by reducing the intestinal pH and producing metabolites [21, 23]. The optimal pH of many intestinal pathogenic bacteria is neutral or slightly alkaline. Lactic acid produced by L. acidophilus metabolism can reduce pH, thus inhibiting the growth and reproduction of pathogenic bacteria [23]. In addition, some pathogenic microorganisms produce enzymes that can catalyze the conversion of carcinogenic precursors to carcinogens, such as azo reductase, nitro reductase, and β-glucosidase [24, 25]. L. acidophilus can not only inhibit the growth of these pathogenic microorganisms and reduce the production of these enzymes, but can also inhibit enzyme activity [25, 26]. Second, competition for adhesion sites with pathogenic bacteria is an important mechanism for L. acidophilus to inhibit the function of pathogenic bacteria, thereby interfering with their invasion into cells [27]. Surface the S-layer protein, extracellular polysaccharide and lipoteichoic acid of many strains can compete for adhesion with pathogenic bacteria [21, 28]. Third, the role of L. acidophilus in many diseases also depends on its ability to reduce serum cholesterol level [29, 30]. L. acidophilus can absorb and assimilate cholesterol [31, 32].

Although some mechanisms have been found, neither these mechanisms nor the influencing factors of L. acidophilus in the host have been fully studied and efforts should be made to explore them further.

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Biological Functions of L. acidophilus

Risk Reduction of Cardiovascular Disease

Cardiovascular disease (CVD) is the leading cause of morbidity and mortality worldwide, accounting for about one third of global deaths [33]. The occurrence of CVD is related to many factors [34–36]. Increasing blood cholesterol is one risk factor that directly impacts CVD. In the 1970s, Mann and Shaper found that populations of particular African tribes generally possessed lower incidences of high serum cholesterol [37]. After investigation, they found that the residents of these tribes regularly drank yogurt fermented by L. acidophilus, suggesting that this bacteria might regulate blood lipids [37]. Since then, more researchers have paid attention to the uses of L. acidophilus and other probiotics relevant to cholesterol reduction and the cholesterol-lowering effects of L. acidophilus have been confirmed. In addition, studies have investigated the effects of L. acidophilus intervention on cholesterol reduction and atherosclerosis development in animal models.

Harrison and Peat reported that the addition of L. acidophilus to baby feed reduced infant serum cholesterol from 147 mg/100 ml on the 5th day down to 119 mg/100 ml by the 8th day of intervention [38]. This decrease in serum cholesterol levels was accompanied by a significant increase in the number of LAB. The number of Escherichia coli present in fecal samples also decreased [38]. Stepankova et al. found that supplementation of L. acidophilus ATCC 4356 also promoted the proliferation of bifidobacteria [39]. Gilliland and Walker showed that L. acidophilus NCFM was able to remove cholesterol from laboratory growth media [40, 41]. NCFM has been reported to ingest cholesterol in the presence of bile and in the absence of oxygen, both of which occur in the gut. The researchers tested these effects on young pigs and the results showed that feeding L. acidophilus to pigs significantly inhibited the increased serum cholesterol levels that are usually observed in individuals fed a high-cholesterol diet. Park and colleagues have reported that adding L. acidophilus 43121 to a high-cholesterol diet given to rats resulted in reduced serum cholesterol [42, 43]. Song et al. showed that L. acidophilus NS1 can reduce plasma LDL-C by increasing the expression of LDLR and SREBP2 in the liver [44].

Huang et al. found that L. acidophilus ATCC 4356 had a significant cholesterol-lowering effect on rats fed with a high-cholesterol diet by inhibiting the expression of NPC1L1 in the small intestine [31, 45]. Chen and colleagues found that L. acidophilus ATCC 4356 alleviated atherosclerotic lesions in ApoE^−/− mice[46]. L. acidophilus ATCC 4356 inhibited oxidative stress by regulating the production of MDA, oxLDL and SOD, suppressed inflammation via regulations of TNF-α and IL-10 levels, and improved intestinal flora, resulting in blocked progression of atherosclerosis. However, it did not significantly reduce cholesterol levels. In different experimental models, many studies have produced different results due to inconsistent experimental methods. Therefore, the role and functional mechanism of L. acidophilus in reducing cholesterol and alleviating atherosclerosis require further detailed exploration.

Improvement of Gastrointestinal Disease Outcomes

Studies have shown that probiotics can regulate intestinal flora, play a beneficial role in inflammatory diseases such as ulcerative colitis (UC), and have been used effectively to treat and suppress human intestinal infections. Lightfoot and colleagues described the role of L. acidophilus NCFM surface layer protein A as a key effector in the prevention of colitis in mice [47] . Chandhni et al. also showed that the surface proteins in NCFM strains could reverse histopathological damage caused by colitis [48], thus providing a potentially safer option for the treatment of inflammatory bowel disease.

In the normal intestinal flora in humans, L. acidophilus plays a key role in inhibiting the growth of pathogens such as Salmonella enteritidis, Staphylococcus aureus, and Shigella dysenteriae. Therefore, studies have shown that L. acidophilus exhibited strong anti-inflammatory activities [49]. Moshiri et al. reported that L. acidophilus PTCC 1643 could affect the expression of TLR2 and TLR4 in HT29 intestinal epithelial cells under the action of Salmonella enterica serovar Enteritidis (SesE), and inhibit the inflammatory response caused by SesE infection [50]. Small intestinal bacterial overgrowth (SIBO) refers to the changes in the number or types of flora in the small intestine. It is considered to be a condition that can exist for many years without causing obvious symptoms although it is related to chronic digestive problems. Studies by Simenhoff and colleagues have shown that NCFM can inhibit the overgrowth of small intestinal bacteria, reduce the levels of toxic metabolites such as dimethylamine and nitrosodimethylamine in the blood, and positively affect intestinal colonization [51, 52], thus improving the nutritional status of patients. These observations support the use of L. acidophilus for the prevention and treatment of intestinal diseases. Further in vivo and in vitro studies are needed to elucidate the detailed mechanisms of these anti-inflammatory effects.

Improvement of Lactose Intolerance

Lactose intolerance, also known as lactose indigestion or lactose malabsorption, refers to the state in which the human body does not produce the enzyme lactase. After consuming milk or dairy products, some people might have diarrhea and other symptoms of intestinal discomfort due to the osmotic effect of the undecomposed lactose.

Previously, many studies have proved that LAB have the ability to be a source of lactase in the small intestine, which helps people with lactase deficiency to digest lactose. Related fermented dairy products may also enhance lactose tolerance [53].

Some probiotic studies have shown that L. acidophilus can improve lactose digestion or symptoms in lactose-intolerant patients [54, 55]. Among these studies, in vitro evaluation of the lactase levels of various probiotics has shown that the lactase levels of L. acidophilus NCFM were high when compared to all of the probiotics tested. Multiple studies have also shown that NCFM can improve lactose digestion and relieve symptoms of lactose intolerance such as bloating and diarrhea [56, 57]. A study speculated that the bacteria might metabolize lactose during digestion and transport it through the gastrointestinal tract. The study by Pakdaman et al. found that L. acidophilus DDS-1, a unique and edible strain, can improve lactose intolerance symptoms such as diarrhea, cramps, and vomiting [58]. However, a number of studies have shown the opposite effects. For example, Newcomer et al. demonstrated that dairy products containing L. acidophilus NCFM did not significantly improve human lactose intolerance [59–61]. The reason for these contradictory results has been associated with the levels of NCFM of L. acidophilus. Therefore, in order to better apply the functional properties of L. acidophilus and to improve lactose intolerance, it is essential to explore and adjust the probiotics levels and the formula with each product.

Prevention and Treatment of Cancer

Probiotics are considered a safe and cost-effective way to prevent or treat a variety of cancers, including colon and liver cancer. Several studies have suggested that consumption of cultured dairy products may reduce colon cancer risk, since the effects of diet are mediated by metabolic effects of intestinal organisms. The activities of β-glucuronase, nitroreductase, azoreductase and other microbial enzymes have been used to monitor colon cancer changes. Goldin and Gorbach observed that adding live L. acidophilus into the diet of carnivorous rats significantly reduced azoreductase, nitroreductase and glucuronidase activity [24, 25]. The incidence of colon cancer in rats with L. acidophilus NCFM was also lower. Their later study found that NCFM alongside antibiotics inhibited the growth of colon tumors in rats. In human, daily consumption of milk containing NCFM reduced the activity of these three fecal enzymes by a factor of two- to four-fold and reduced the incidence of colon cancer [24, 25]. In addition, they found that nitroreductase activity continued to decrease even three weeks after fermented milk intake was stopped, thus indicating a long-term change in colonic flora [24, 25].

Studies have shown that the extracellular polysaccharides (EPSs) synthesized by L. acidophilus have exerted health benefits by stimulating the immune response and fighting tumor cells [62]. The anticancer and immunomodulatory activities of EPSs synthesized by L. acidophilus have been proven to combat colon cancer and inflammatory liver cancer. Khedr and colleagues used male rats as a model and confirmed that L. acidophilus ATCC 4356 EPSs had immunomodulatory effects on liver cancer induced by diethylnitrosamine (DEN) and gamma radiation (IR) [63]. They proposed that L. acidophilus ATCC 4356 EPSs might be used as a safe and effective probiotic to prevent and treat liver cancer.

Regulation of Immune Capacity

The immune function of L. acidophilus is mainly conducted via regulating the body’s immune system, limiting pathogen colonization within the body, and controlling metabolic disorders and enteritis. Probiotics are used clinically to treat diseases caused by immune system disorders. This can significantly reduce infection time and respiratory tract infection frequency and also improve the therapeutic effects for allergic asthma.

The role of L. acidophilus in regulating the body’s ability to respond to immune responses has been demonstrated in previous studies. Wagner et al. confirmed that NCFM induced antibody- and cell-mediated responses to Candida albicans in immunodeficient mice [64]. The serum levels of IgG, IgA, and IgM were higher in euthymic immunocompromised mice and were thought to reduce the severity of candidiasis. Yoghurt prepared with yoghurt cultures containing NCFM, Streptococcus thermophilus, Lactobacillus bulgaricus and Bifidobacterium were tested for their effects on mucosal and systemic IgA and IgG responses in mice immunized orally with cholera toxin. The results showed that IgA against the cholera toxin was higher in the intestine and serum of the mice fed the formulated yogurt than that observed in the mice fed skim milk [65]. These results suggest that coculture including NCFM may increase immune responses to oral antigens.

Other Functions

We summarized the biological functions, processes, and effects of L. acidophilus– related strains in pathological and physiological processes (Table 1). However, the biological functions of L. acidophilus are far more extensive than what we have mentioned. The role of L. acidophilus in many other diseases is constantly being explored and new discoveries are being made. Studies have shown that kidney tissue damage can be alleviated by reducing oxidative stress, inflammation, and cell death [66]. Zhang et al. first explored the relationship between ATCC 4356 and renal ischemia-reperfusion injury (IRI) [67]. They found that L. acidophilus ATCC 4356 alleviated renal IRI through antioxidant stress and anti-inflammatory responses and improved intestinal microbial distribution in renal IRI mice. In the following treatment with ATCC 4356, the levels of anti-inflammatory factors (IL-4 and IL10) were upregulated, whereas the levels of pro-inflammatory factors (IL-1β, IL-8, TNF-α and IFN-γ) were downregulated. In addition, renal tissue apoptosis in IRI mice was reduced [67].

Table 1

The main biological effects of related strains of L. acidophilus.

Type of strain	Function	Major biological processes and their effects	Reference
L. acidophilus ATCC 4356	Inhibit CVD progression	Inhibit oxidative stress by modulating the productions of MDA, oxLDL and SOD; suppress inflammatory status by regulating TNF-α and IL-10 levels; inhibit NPC1L1 expression in the small intestine; improve intestinal microflora; inhibit the development of atherosclerosis.	[31, 40, 45, 46]
L. acidophilus NCFM		Assimilate cholesterol and control cholesterol levels.	[40, 41]
L. acidophilus 43121		Affect cholesterol metabolism and reduce blood cholesterol levels.	[40, 42, 43]
L. acidophilus NS1		Reduce plasma LDL-C by increasing hepatic LDLR and SREBP2 expression.	[44]
L. acidophilus NCFM	Improve gastrointestinal diseases	Strain surface layer proteins play an important role; alleviate Tcell-induced colitis by significantly reducing the proinflammatory response; preserve microbiome composition and intestinal barrier function; reverse histopathological damage caused by colitis; reduce the level of toxic metabolites.	[47, 48, 51, 52]
L. acidophilus PTCC 1643		Modulate the expression of TLR2 and TLR4 in HT29 intestinal epithelial cells challenged with SesE; enhance anti-inflammatory effects.	[50]
L. acidophilus NCFM	Improve lactose intolerance	Strain has a higher level of lactase, which metabolizes lactose during digestion and transits through the gastrointestinal tract, thereby improving lactose digestion.	[56, 57]
L. acidophilus DDS-1		Assist in breaking down lactose; improve lactose intolerance symptoms such as diarrhea, cramps and vomiting.	[58]
L. acidophilus ATCC 4356	Prevent and treat colon cancer, liver cancer and other cancers	The exopolysaccharides of the strain have immunomodulatory and antitumor activities; regulate the TLR2/STAT-3/P38-MAPK pathway associated with inflammation against HCC.	[63]
L. acidophilus NCFM		Stimulate the immune response; reduce the activities of β-glucuronase, nitroreductase, azoreductase and other microbial enzymes; produce compounds that inhibit tumor proliferation; reduce the incidence of colon cancer and inhibit the growth of colon tumors.	[24, 25]
L. acidophilus NCFM	Regulate immune capacity	Reduce levels of pro-inflammatory cytokines significantly and mobilize a systemic immune response; limit pathogen colonization in the body, control metabolic disorders.	[47, 64, 65]
L. acidophilus ATCC314	Manage inflammatory disorders	Regulate the secretion of inflammatory cytokines; reduce oxidative stress.	[70]

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Studies have shown that oral L. acidophilus can improve heart function in mice with myocardial infarction. Sadeghzadeh and co-researchers found that L. acidophilus was able to improve the hemodynamic and histopathological indicators of the ISO-induced myocardial injury rat model [68], providing obvious myocardial protection. In the future, probiotic supplements may become a new option for patients with ischemic heart disease.

L. acidophilus has been shown to have potential applications in the prevention and control of genitourinary and vaginal infections. Reid et al. precultured L. acidophilus NCFM with urinary and vaginal epithelial cells from healthy women and subsequently exposed them to different urinary tract pathogens. Results showed that NCFM competitively excluded these pathogens and effectively prevented and suppressed urinary tract and vaginal infections [69].

Rheumatoid arthritis (RA) is a common inflammatory joint disease. It has been reported that the ingestion of L. acidophilus ATCC 314 exerted anti-inflammatory and potent antioxidant properties in a collagen-induced arthritis (CIA) rat model [70, 71]. This suggests that L. acidophilus is a promising treatment that should be tested further in RA patient preclinical trials.

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Applications and Future Prospects of L. acidophilus

As people pay more and more attention to health issues, it is of great importance that different kinds of probiotics within food are able to play a healthy role. Of these probiotics, L. acidophilus is one of the most commonly used microorganisms, as it is thought to have various beneficial effects on human health. These advantageous effects include lowering blood cholesterol, improving gastrointestinal diseases, and reducing the risk of lactose intolerance and carcinogenicity [72, 73]. Research and development into L. acidophilus has received widespread attention. It is referred to as the third-generation yogurt starter strain. L. acidophilus has good acid and bile salt resistance and produces a variety of antibacterial substances during metabolism. Due to these attributes, L. acidophilus strains have broad application prospects as functional, edible bacteria.

Despite these favorable characteristics, through our analysis of studies on L. acidophilus which highlighted our present understanding of the current application status, we found that there are also many problems and limitations in the research and application of L. acidophilus. First, due to different naming methods, the same strain may have multiple names. This may lead to confusion during literature searches and research. Important findings could be missed, resulting in incomplete information collection. Second, due to the different research methods used to investigate probiotics, results from different research groups may deviate from each other. Different concentrations and ratios of probiotics have been shown to have different effects, therefore the health benefits of certain disease symptoms remain to be proven. Further research on the optimal strains, doses and dosing algorithms are of key importance for future research. In addition, different species of L. acidophilus can exhibit similar probiotic effects in vitro, but their properties differ significantly when evaluated in vivo.

Currently, probiotic regulation of intestinal flora is recognized as an interesting way to prevent certain diseases. Recent studies have proposed many mechanisms by which probiotics function, but the effectiveness of many probiotics has not been proven in different conditions, which has presently limited the promotion and application of probiotics. There are probably several main reasons why these research limitations occur, including too many low-quality studies, variability within the microbiome, and great diversity between the probiotic strains used. However, some studies have reported reasonable and encouraging results that support further research into probiotics. With this in mind, we should put more effort into overcoming the difficulties. First, because most studies have, so far, focused on animal studies or small human research groups, it is difficult to assess the possible health effects of these probiotics in the general population. Therefore, we need to conduct more extensive epidemiological evaluations which take into account the variability between patients. Due to the high cost of such interventions, it is necessary to characterize strains well to select the strains that are most effective for a particular application. Second, we should identify bacterial markers of the microbiome in related diseases in order to gain sufficient clinical trial capacity. Furthermore, new methods for analyzing the microbiome and its function will greatly facilitate the research when studying large numbers of samples. Probiotics could serve as a low-cost, low-risk alternative to antibiotic treatment in order to prevent infection. We believe that the development of probiotics will open up another impressive field of research. Further research in this area may provide exciting avenues for healthcare strategies, as well as creating more economic and social benefits.

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Acknowledgments

This work was supported by the National Natural Science Foundation of China (Grant No. 91849209) and Shandong Provincial Natural Science Foundation, China (Grant No. ZR2020QH016).

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Footnotes

Conflict of Interest

The authors have no financial conflicts of interest to declare.

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How to incorporate chia seeds into your diet

The Truth News — Thu, 30 May 2024 14:11:40 +0000

How to incorporate chia seeds into your diet

It’s very easy to incorporate chia seeds into your diet. You can simply sprinkle a tablespoon or two on foods such as yogurt, cereal, or salads. You can add chia seeds to smoothies or soups, or mix them into pancake batter or another breakfast food. Chia seeds have a mild flavor, so they are not likely to affect the taste of your food.

Another popular way to get chia seeds into your diet is to make a simple chia pudding. When mixed with liquid, chia seeds develop a gelatinous coating, expanding in size and creating a pudding-like consistency,

Grocery stores stock a variety of chia seeds. Products that contain chia seeds include chia pudding, chia kombucha and granola with chia seeds.

Chia seeds have a mild flavor and can easily be added to many foods you already enjoy. Try adding whole or ground chia seeds to smoothies, juices, milk, yogurt, oatmeal, pancakes or a granola bar recipe. Try them sprinkled on salads or cereal, baked into muffins or breads, or made into chia pudding using the recipe below.

These recipes provide about one-third of your recommended daily amount of fiber:

Overnight chocolate chia seed pudding

Serves 4

1½ cups almond milk
⅓ cup chia seeds
¼ cup unsweetened cocoa powder
4 tablespoons maple syrup
½ teaspoon ground cinnamon (optional)
½ teaspoon vanilla extract

Add all ingredients except chia seeds to a mixing bowl and whisk vigorously to combine. Mix in chia seeds until well-combined. Let rest covered in the refrigerator overnight. The pudding can be stored covered in the refrigerator for 2–3 days. Serve chilled with desired toppings, such as fruit or a dollop of whipped topping.

Nutrition information per serving: 165 calories, 8 grams fat, 1 gram saturated fat, 75 milligrams sodium, 25 grams carbohydrates, 9 grams fiber, 4 grams protein

Carrot cake overnight oats

Serves 1

This oatmeal is loaded with calcium, protein, fiber and vitamin A. The amount of carrot in this recipe provides 100% of your vitamin A for the day, which is good for your eyes and immune system.

½ cup rolled oats
⅔ cup skim milk
⅓ cup plain, nonfat Greek yogurt
¼ cup finely grated carrot
1½ teaspoons chia seeds
2 teaspoons maple syrup
½ teaspoon cinnamon
½ teaspoon vanilla extract
1 tablespoon pecans, chopped
1 tablespoon shredded coconut, unsweetened

Mix all ingredients, except for the pecans and coconut, in a bowl or Mason jar. Top with pecans and coconuts, and cover with lid. Refrigerate overnight and eat chilled.

Chia pudding recipe

Add 2 tablespoons of chia seeds into 1/2 cup of milk (almond, soy, and dairy all work). Use a mason jar or other container with a lid.
Close the lid tightly and shake well. Wait 10 minutes, then shake again, making sure there aren’t any clumps.
Refrigerate for at least 15 minutes, though overnight or for least four hours will allow the pudding to thicken better.
Add berries, nuts, cinnamon, and a touch of sweetener.

Chia seed pudding is one of those meals or snacks that not only tastes good, but is very good for you. Whether you’re looking to change up your breakfast game, or are searching for a healthier alternative to that nightly bowl of ice cream, chia seed pudding will get the job done, all while helping to keep your body in tip-top shape.

That’s because chia seeds—the titular ingredient in chia seed pudding—are tiny nutritional powerhouses. These edible seeds, which were a staple in ancient diets, are excellent sources of satiating fiber and calcium, which helps keep bones healthy and strong. Chia seeds also pack a solid amount of protein and omega-3 fatty acids in a small package, which may help reduce the risk of heart disease. Per a 2014 study, there is a link between chia seeds and reduced blood pressure in people with hypertension. Additionally, antioxidant-rich chia seeds have been scientifically proven to promote heart and liver health, and boast anti-cancer properties. If that’s not reason enough to add chia seeds to your diet, then we don’t know what is!

That’s where chia seed pudding comes in. The popular dish is one of the easiest ways to enjoy chia seeds in a meaningful quantity, which means you can really reap all of the nutritional benefits. And while it might seem difficult to make this trendy food yourself, whipping up a batch of chia seed pudding isn’t nearly as tricky as you might think.

How to Make a general Chia Seed Pudding

There are three main ingredients in chia seed pudding—chia seeds, milk of your choice, and a sweetener of your choice. However, you can also add some of your favorite spices and/or fresh fruit to kick things up a notch.

In a bowl, combine ¼ cup chia seeds with 1 cup of your favorite milk and stir. Make sure all of the chia seeds are completely coated in milk in order to ensure proper absorption.
Then, add about two teaspoons of your desired sweetener (such as agave, honey, or maple syrup) and a pinch of salt. Stir to combine. (Note: If you like vanilla, feel free to add half a teaspoon of vanilla extract to the mixture. You can also toss in a dash of cinnamon, nutmeg, or other go-to spices before stirring.)
Cover the mixture and place it in the refrigerator until it thickens. This should take about two hours, but you can also leave the mixture in the fridge overnight.
To serve, garnish the pudding with fresh fruit.

3-Ingredient Chia Seed Pudding, with a Compote

The classic chia seed pudding only requires three ingredients. On top of this pudding, you can add any kind of fruit, or this strawberry rhubarb compote.

INGREDIENTS

Chia Pudding Mixture:

3 cups coconut milk (full fat/canned)
¾ cup chia seeds
1½ teaspoons vanilla extract

Compote Mixture (Optional):

5–6 rhubarb stalks, chopped
1½ cups strawberries
2 tablespoons maple syrup
⅓ cup water
top with shredded coconut flakes/cacao nibs

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INSTRUCTIONS

Mix well the first 3 ingredients in a bowl and place in the refrigerator.
For the optional compote, chop up the fruit and add it to a small pot. Cook over medium heat or until rhubarb is tender, about 8 minutes.
Add mixture, maple syrup and water into a blender and blend until well combined.
Distribute chia seed pudding evenly into four glasses and top with the compote, once it has cooled. Place in refrigerator and allow to chill for up to 1 hour.
Serve topped with shredded coconut flakes and/or cacao nibs.

Chia seeds are a serious superfood. They’re full of fiber, so adding them to foods helps you feel full for longer. They’re great for digestion and can even boost your energy. While you can sneak them into smoothies or juices, chia seeds are also really tasty — not to mention fun — when you use them to make chia seed pudding.

See, when you add chia seeds to a liquid and let them soak in it, the chia seeds absorb the liquid and puff up in size, transforming from a seed-like texture to a gel consistency that’s reminiscent of pudding.

Best of all, this chia seed pudding can be eaten as breakfast, snack or dessert. You have to try it!

3-Ingredient Chia Seed Pudding

This is the classic chia seed pudding, with just three ingredients: a nondairy milk, chia seeds and vanilla extract. Each serving is roughly two tablespoons of chia seeds, a half-cup of nondairy milk (coconut or unsweetened almond milk work best) and a quarter teaspoon of vanilla.

Because of the fiber in chia seeds, this classic version also doubles as a keto chia seed pudding, with only 4 net carbs per serving. It’s also friendly to nearly any kind of diet, including vegan and Paleo.

Beyond the benefits of chia seeds, coconut milk adds great creamy texture, electrolytes and healthy fats. As an alternative, almond milk contains far fewer calories and contains half a day’s recommended intake of vitamin E, a significant amount of vitamin D and a hearty dose of calcium.

Optional Toppings

If you want to dress up this pudding, consider making a strawberry rhubarb compote.

Rhubarb does more than give the pudding a gorgeous color. The vegetable lowers inflammation and eases digestion while adding a tart taste to this chia seed pudding.

Add the rhubarb mixture plus maple syrup and water to a blender, and blend until all the ingredients are well combined.

Remove the chia seed pudding from the refrigerator and separate into four glasses, topping with the strawberry rhubarb compote once it has cooled.

Place the glasses in the fridge for about an hour to let them chill and set. Top them with coconut flakes, cacao nibs or both and serve! (This pudding will also last in the fridge for a week.)

This strawberry rhubarb chia seed pudding is easy to take on the go to work — just put in a portable container. It also doubles as a super healthy dessert that the entire family will enjoy.

Start by mixing the first three ingredients — coconut milk, chia seeds and vanilla — in a bowl and place in the refrigerator.

Next, chop up the rhubarb and strawberries, then add to a small pot over medium heat. Cook until the rhubarb is tender.

If you want to reduce the calories, use reduced fat coconut milk or unsweetened almond milk.
Rather than a compote, you can also simply add some fresh fruit: blueberries, strawberries, pineapples, cherries, etc.
Coconut flakes, raw sliced almonds, hemp seeds and cacao nibs all offer good toppings, with or without fruit.

NUTRITION

Serving Size: 1 serving (135g) of pudding only
Calories: 327
Sugar: 0.1g
Sodium: 18mg
Fat: 30.5g
Saturated Fat: 22.1g
Unsaturated Fat: 6.7g
Trans Fat: 0g
Carbohydrates: 12.1g
Fiber: 7.1g
Protein: 5.7g
Cholesterol: 0mg

Keto Smoothie Recipe with Avocado, Chia Seeds & Cacao

INGREDIENTS

1–1¼ cups full-fat coconut milk
½ frozen avocado
1 tablespoon nut butter of choice
1 tablespoon chia seeds, soaked in 3 tablespoons of water for 10 minutes
2 teaspoons cacao nibs, cacao powder or cocoa powder OR 1 scoop of chocolate protein powder made from bone broth
1 tablespoon coconut oil
ice (optional*)
for topping: cacao nibs and cinnamon
¼ cup water, if needed

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INSTRUCTIONS

Add contents into a high-powered blender, blending until well-combined.
Top with cacao nibs and cinnamon.

Have you heard about the keto diet? It’s possibly the best diet for weight loss, and it can even reverse insulin resistance and reduce cardiovascular risk factors, according to recent research. No wonder more and more people are starting to go “keto.”

This keto smoothie is an easy way to get started. It’s a perfect keto drink that includes protein foods and healthy fats, while being very low in carbohydrates. All of the ingredients in this smoothie are nutritious, heart healthy and keto-friendly — plus, they’re delicious!

What Does “Going Keto” Mean?

“Going keto” means putting your body into a state of ketosis, which is a metabolic state that occurs when most of the body’s energy comes from ketone bodies in the blood, rather than from glucose (or sugar).

On the keto diet, you are tricking your body into thinking it’s fasting by eliminating glucose that is found in carbohydrate foods. Your body begins burning fat for energy rather than carbohydrates, so after going keto, most people lose excess body fat rapidly, even when consuming lots of fats and adequate calories through their diet.

The ketogenic diet, like any other low-carb diet, works through the elimination of glucose. Our bodies normally run on glucose for energy, but once glucose is no longer available from food sources, we begin to burn stored fat for energy instead. This process will not only help you to shed those extra pounds, but it also helps to control the release of hormones like insulin, which plays a role in the development of diabetes and other health problems.

Nutrition Facts

One serving of this keto smoothie recipe using cacao powder and without toppings contains the following, including only 6.1 net carbs (total carb grams minus fiber grams):

394.5 calories
40.1 grams fat
11.64 grams carbohydrates
5.5 grams fiber
3.68 grams protein
2.52 grams sugar
22 milligrams sodium
189.5 milligrams magnesium (45.1 percent DV)
6.85 milligrams iron (38.1 percent DV)
328.5 milligrams phosphorus (26.3 percent DV)
2.45 milligrams vitamin E (16.3 percent DV)
2.49 milligrams niacin (15.5 percent DV)
0.17 milligrams thiamin (14.2 percent DV)
0.16 milligrams riboflavin (12.3 percent DV)
36 micrograms folate (9 percent DV)
96 milligrams calcium (7.4 percent DV)
0.73 milligrams zinc (6.6 percent DV)
229 milligrams potassium (4.9 percent DV)
0.073 milligrams vitamin B6 (4.3 percent DV)
2.5 milligrams vitamin C (2.8 percent DV)

How to Make A Keto Smoothie

A keto smoothie is made up of healthy fats and protein, all foods that are naturally low in carbohydrates. Using a high-powered blender, add in these heart-healthy, keto diet–friendly foods.

My keto smoothie recipe starts with 1 to 1¼ cups of full-fat coconut milk as the base. Coconut milk contains a beneficial fat called lauric acid, a medium-chain fatty acid that’s easily absorbed and used by the body for energy. It serves as a great keto diet food.

Next add in 1 tablespoon of chia seeds (soaked in 3 tablespoons of water for 10 minutes), which contain essential fatty acids, plus vitamins A, B, E and D and minerals including iron, magnesium, niacin and thiamine. And then add 1 tablespoons of your favorite nut butter to the mix, whether it’s almond butter or even sunflower seed butter. (I recommend that you avoid peanut butter.)For the next ingredient for this keto smoothie, you have a choice of either 2 teaspoons of cacao nibs, cacao powder or cocoa powder, or 1 scoop of chocolate protein powder. Protein powder made from bone broth is packed with protein, low in carbs and low in sugar. You can get the benefits of bone broth easily by adding it to your keto smoothie.

Cacao nibs or powder is also healthful and packed with nutrients that fuel the body.

The last two ingredients for my keto smoothie are ½ frozen avocado and 1 tablespoon of coconut oil. Adding avocado to this smoothie will give it a delicious creamy texture and its an excellent source of healthy fats, which is especially important when you’re going keto.

Now all you have to do is blend the ingredients until they are well-combined, adding water if necessary, and you’re done! If you want to add some bulk to the texture of your keto smoothie, or if you don’t have a frozen avocado on hand, add in some ice, too.

Top your keto smoothie with cacao nibs and cinnamon, and enjoy!

My keto smoothie is an easy way to get started on the keto diet, or just as a great breakfast. It includes protein foods and healthy fats, while being very low in carbohydrates. All of the ingredients in this smoothie are nutritious, heart healthy and keto-friendly — plus, they’re delicious!

NUTRITION

Serving Size: 1 glass
Calories: 394
Sugar: 2.5g
Sodium: 22mg
Fat: 40.1g
Carbohydrates: 11.6g
Fiber: 5.5g
Protein: 3.7g

Berry Chia Seed Smoothie Bowl

Chia Seed Smoothie Bowl

No need to buy an overpriced smoothie bowl at a hip cafe. Instead, just get these lovely ingredients and whip up your own.

INGREDIENTS

2 bananas, sliced
4 dates, pitted and halved
2 cups coconut milk yogurt (or Greek yogurt)
¼ cup coconut water
1 cup blueberries
¼ cup chia seeds
optional toppings: hemp seeds, blackberries, raspberries, sliced strawberries

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INSTRUCTIONS

Place the first 6 ingredients in a food processor and blend until smooth.
Place in an airtight container and allow to chill for 20 minutes prior to serving.
Add to bowls and top with hemp seeds, sliced strawberries, blackberries and raspberries.

NUTRITION

Serving Size: 1 bowl (253g)
Calories: 239
Sugar: 20.3g
Sodium: 76mg (5% DV)
Fat: 8.7g
Saturated Fat: 3.1g
Unsaturated Fat: 5.1g
Trans Fat: 0g
Carbohydrates: 35.9g
Fiber: 8.7g
Protein: 7.5g
Cholesterol: 16mg

It’s the time of year when smoothie bowls become popular again. You know those breakfast bowls: They’re colorful, full of fruits and look like something you need to hit up a trendy cafe to enjoy.

Smoothie bowls — like the popular acai bowl recipes — are super easy to make right at home. This coconut yogurt chia seed smoothie bowl is the perfect way to kickstart your mornings, made in the comfort of your own cozy kitchen in just 5 minutes.

By using coconut yogurt in this recipe, I’ve kept it dairy free, but still packed with flavor and creamy texture.

Key Smoothie Bowl Ingredients

Yogurt is a must for a good smoothie bowl, as it adds creamy texture as well as fats. I prefer coconut milk in order to avoid dairy. It also contains natural fatty acids that provide extra energy. If you prefer dairy, go with Greek yogurt, which has the added advantage of being high in protein for a yogurt.

Coconut water is also included in this smoothie bowl, for it’s a great way to start the day. Why? Coconut water contains multiple vitamins, minerals and phytochemicals plus plenty of potassium, making it a high electrolyte beverage.

I’ve added chia seeds, one of my favorite sneaky superfoods, for extra nutrients plus crunch texture. Chia is rich in protein (amino acids), omega-3 fats, fiber, manganese, phosphorus and calcium.

Bananas are a great addition because they blend so well with the yogurt and add natural sweetness, plus they’re loaded with fiber.

Speaking of sweetness, rather than resorting to sugar or even honey or maple syrup, go with dates. They’re rich in fiber, vitamins and minerals.

I’ve used blueberries to add some color and a heap of antioxidants, but you can use your favorite berries. Let’s make this photo-worthy breakfast!

How to Make a Smoothie Bowl

Start by adding the first six ingredients to a blender or food processor and blending until nice and smooth. Those benefit-rich blueberries give this coconut yogurt smoothie bowl that lovely hue.

Place the blended mix in an airtight container and let it chill in the refrigerator for about 20 minutes. Then add the smoothie mix to a bowl and go wild with the toppings.

I love adding berries, coconut flakes and hemp seeds for a dose of healthy fats. Don’t forget to take a photo of your awesome coconut yogurt chia seed smoothie bowl before serving and enjoying!

Grain-Free Oatmeal Recipe

Are you a fan of hot oatmeal? The dish is a wonderful, fiber-full breakfast — unless you’re not so hot on gluten. Fortunately, this Gluten-Free Oatmeal is for you! Honestly, whether you love oatmeal or are just getting used to the hot cereal, this gluten-free oatmeal recipe is for you. It’s so hearty that you won’t miss the grains in it one bit — all while providing oatmeal nutrition benefits.

We’ll kick things off by combining all the ingredients in a large bowl and mixing ’em together. This is a great point to personalize your “oatmeal,” by the way. Move the mix into a wide-mouth quart jar and store in the refrigerator.

Next, prepare a serving of oatmeal. Place 1/2 cup of the dry mix in the bowl and then 1 to 1–1/2 cups of almost-boiling water to the mix. Let the ingredients soak and sit for the next 3–5 minutes.

Next, add the 1 serving of oatmeal, 1/2 cup of dry mix and 1–1 1/2 cups of almost-boiling water. Mix it all up and allow it all to sit for 3–5 minutes.

Then take the gluten-free oatmeal and add in fresh fruits, chocolate, coconut milk or honey — whatever your tastebuds want to make the flavor pop! This “faux-meal” is super easy to customize to your family’s preferences, and you’ll love that there’s no gluten or grains in it.

INGREDIENTS:

2 cups shredded coconut
½ –1 cup hemp seeds (less if you choose to add dried fruit to your base mix)
½ cup chia seeds
½ cup whole or coarsely ground flaxseeds
¼ teaspoon sea salt
OPTIONAL
½ cup chopped dried fruit
¼–½ teaspoon various spices. My favorite flavor combos are (1) cinnamon, cardamom, ginger; (2) cinnamon, cumin, cardamom, black pepper, coriander; (3) cloves, allspice, nutmeg, ginger, cinnamon; (4) rosemary, garlic, sage, cayenne

DIRECTIONS:

Combine all ingredients in a bowl and stir together thoroughly.
Include any optional ingredients you like.
Transfer to a wide-mouth quart jar to store in the refrigerator.
To prepare 1 serving of oatmeal, place 1/2 cup of dry mix in a bowl and add 1–1½ cups very hot water (just shy of boiling).
Stir well and allow to sit for 3–5 minutes.
Add fresh fruits, nuts, unsweetened chocolate, bacon crumbles, chicken or turkey sausage, coconut or almond milk, honey, coconut oil, or grass-fed butter to make it exciting.

Chia seed benefits: What you need to know (click here)

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Chia seed benefits: What you need to know

The Truth News — Wed, 29 May 2024 18:11:26 +0000

Chia seed benefits: What you need to know

Packed with fiber, protein, omega-3 fatty acids, and antioxidants, tiny chia seeds pack a nutritional punch. From adding them to prepared dishes or as a topping on oatmeal, cereals, or smoothies, you can easily incorporate chia seeds into many foods to give them a nutritious boost.

Chia seeds are frequently featured as the star ingredient in many healthy eating recipes, ranging from baked goods to protein bars to smoothies and beyond.

Why are chia seeds good for you? Apart from offering a pop of flavor and texture to your favorite foods, they also provide health perks, such as helping balance blood sugar and support heart health.

Keep reading for a complete list of chia seeds benefits and potential side effects, as well as preparation instructions and simple ways to add them to your diet with some clever chia seed recipes.

What Are Chia Seeds?

Chia seeds (Salvia hispanica) are tiny superfoods that are grow on a species of flowering plant that’s in the mint family. They are native to areas of Mexico and Guatemala but are commonly cultivated in many areas in North and South America.

Chia is typically easy t digest when prepared properly and can be a very versatile ingredient that works well in a variety of recipes. Plus, the seeds offer a long list of important nutrients, including:

Chia seeds are tiny black or white seeds derived from the Salvia hispanica plant, a member of the mint family native to Central America. These small seeds have been a part of human diets for over 5,000 years. Chia seeds were a staple food for the Aztecs and Mayans.

Where Do Chia Seeds Come From?

Originally grown in Mexico, chia has long been highly valued for its medicinal properties and nutritional value. In fact, it was even used as currency at one point.

Chia means “strength” in the Mayan language, and chia seeds were known as “runners’ food” because runners and warriors would use them as fuel while running long distances or during battle. Aztec warriors ate them to give them energy and endurance, claiming that just one spoonful could sustain them for 24 hours.

Salvia hispanica has also been used for its potent healing properties in many branches of traditional medicine for centuries. According to Ayurveda, chia seeds can help nourish the blood and promote digestive regularity thanks to their ability to absorb water in the gastrointestinal tract, forming a gel-like substance.

They can also reduce inflammation, promote kidney health and support proper hydration.

Health benefits of chia seeds

Chia seeds are packed with nutrients that may support numerous health benefits. Among them:

reducing blood pressure
lowering cholesterol levels
supporting digestive health
aiding in weight management
reducing inflammation
helping to control diabetes
protecting against chronic disease
improving anxiety and depression.

When chia seeds are ingested, they form a gel-like substance in the stomach that can increase your feeling of fullness and decrease your appetite and calorie intake.

Nutrition Facts

Chia is rich in protein (amino acids), fiber, manganese, phosphorus and calcium. Plus, as mentioned above, it’s a good source of omega-3s (polyunsaturated fatty acids), such as α-linolenic and linoleic acids.

Additionally, it’s rich in polyphenols and antioxidants, such as caffeic acid, rosmarinic acid, myricetin, quercetin and others. It’s also considered a low-carb food because the net carbs (total carbohydrate grams minus fiber grams) are relatively low.

Chia seeds: Nutritional heavyweights

fiber
protein
manganese
calcium
antioxidants
omega-3 fatty acids

Chia seeds contain a variety of nutrients including fiber, protein, omega-3 fatty acids, antioxidants, and various vitamins and minerals like calcium, magnesium, and phosphorus that are beneficial to your health.

Omega-3 fatty acids

Chia seeds are a powerhouse of omega-3 fatty acids. This type of fatty acid is primarily found in fatty fish, nuts, and seeds.

Omega-3 fatty acids play an important role in brain function, heart health, and reducing inflammation in the body. Incorporating omega-3s into the diet promotes overall well-being, benefiting cardiovascular and cognitive functions.

Chia seeds are rich in a type of omega-3 fatty acid known as alpha-linolenic acid (ALA). The body cannot produce ALA its own, so it must be obtained through food. Consuming ALA has been linked to a decreased heart disease risk.

Fiber

Incorporating chia seeds into your diet is also an excellent way to increase your intake of fiber. Just one ounce of chia seeds (two to three tablespoons) provides approximately 9.8 grams of dietary fiber.

Research has shown that adequate fiber intake is associated with a decreased risk of:

coronary heart disease
type 2 diabetes
several types of cancer
inflammation
digestive disorders.

On the heart health front, fiber helps lower LDL (“bad”) cholesterol and triglyceride levels, and helps increase levels of heart-protective HDL cholesterol.

The fiber in chia seeds can also aid healthy digestion by softening the stool and providing bulk to it. This allows the stool to pass more quickly through the intestines and can help alleviate constipation.

Antioxidants

Chia seeds are packed with antioxidants including tocopherols, phytosterols, carotenoids, and polyphenolic compounds. Antioxidants play a crucial role in protecting the body from damage caused by free radicals, which can build up in the body and lead to cell damage and disease.

Thanks in part to their antioxidant content, chia seeds may help protect against:

inflammation
diabetes
cancer
heart disease
Alzheimer’s disease.

Protein

Chia seeds are also a valuable source of protein. Chia seeds contain all nine essential amino acids. The protein in chia seeds can help stabilize blood sugar levels and provide a steady source of energy.

Chia seeds pack nutritional punch

Chia seeds are small round seeds, and can be black, brown and white in color. They are harvested from a flowering plant in the mint family known as Salvia hispanica. It’s native to parts of Mexico and Guatemala. Edible chia seeds are closely related to the chia plants made popular by Chia Pets, but they are not the same seed.

A gel forms around the chia seed when mixed with liquid, which gives chia beverages their distinctive texture. Chia seeds can absorb up to 12 times their weight in liquid, which makes them useful in keeping baked goods moist.

Chia Seeds Benefits: The Omega-3, Protein-Packed Superfood

Chia seeds have many nutritional benefits. They are high in omega-3 fatty acids and fiber. Chia provides a similar amount of omega-3 fatty acids as ground flaxseed in the form of alpha linolenic acid, or ALA. They can help with weight loss.

Chia seeds are an excellent source of fiber, which can improve heart health, reduce cholesterol levels and promote intestinal health. Fiber takes longer to digest and makes you feel satisfied longer, which is how it can help with weight loss and decrease your risk of developing diabetes or heart disease. Eating a diet rich in fiber also is shown to protect against colorectal cancer.

One serving of dried chia seeds is about 2.5 tablespoons. This has 140 calories, 5 grams of protein, 10 grams of fiber, 12 grams of carbohydrate and 9 grams of fat, of which 8 grams are heart-healthy fats.

A one-ounce serving of dried chia seeds (about 28.4 grams) contains approximately:

Calories: 137
Total Carbohydrates: 11.9 g
Fiber: 9.8 g
Total Fat: 8.7 g
Saturated Fat: 0.9 g
Polyunsaturated Fat: 6.7 g
Monounsaturated Fat: 0.7 g
Trans Fat: 0.04 g
Protein: 4.7 g
Sodium: 4.5 mg (0.2% DV)
Manganese: 0.8 mg (35% DV)
Copper: 0.3 mg (33% DV)
Phosphorus: 244 mg (20% DV)
Calcium: 179 mg (14% DV)
Zinc: 1.3 mg (12% DV)
Potassium: 115 mg (2% DV)

*Daily Value: Percentages are based on a diet of 2,000 calories a day.

In addition to the nutrients listed above, chia contains some vitamin A, vitamin B, vitamin E and vitamin D, plus minerals such as iron, iodine, magnesium, copper, niacin and thiamine.

Benefits

What are the benefits of eating chia seeds? Here are nine reasons to add more of them to your diet, including because they can decrease risk for several common diseases:

1. Support Healthy Skin

Chia is jam-packed with antioxidants, which are compounds that fight free radical damage and prevent oxidative stress while also promoting tissue repair and protecting against skin damage.

Interestingly enough, researchers from Mexico recently uncovered that they have a total antioxidant concentration nearly two times higher than previously reported. In fact, the antioxidant activity of Salvia hispanica seeds was shown to stop up to 70 percent of free radical activity.

As one of the most high-antioxidant foods on the planet, adding some to your diet may help fight premature aging and protect the skin cells from things like ultraviolet and environmental damage.

2. Promote Digestive Health

Chia is loaded with fiber, squeezing nearly 11 grams of fiber into a single ounce. This means that adding just one ounce to your daily meals my can supply a whopping 44 percent of your fiber needs for the entire day.

Because of their rich fiber content, chia seeds benefit digestive health by promoting regularity and increasing stool frequency to prevent constipation. The fiber also acts as a prebiotic to provide fuel for the beneficial bacteria in the gut, which plays a central role in many aspects of health and disease.

Fiber also absorbs a good amount of water and expands in the stomach, helping keep you feeling fuller for longer.

3. Improve Heart Health

Thanks to their high content of antioxidants, fiber and heart-healthy fats, chia seeds have been shown to help prevent cardiovascular disease in several ways.

One of the most powerful effects is it ability to reduce inflammation and decrease several risk factors of heart disease, such as high cholesterol and blood pressure. Inflammation can put extra strain on blood vessels and is thought to contribute to heart disease along with a slew of other chronic conditions.

Chia is high in omega-3 fatty acids, boasting even more omega-3s per gram than salmon. Omega-3s work to protect the heart by lowering blood pressure, cholesterol levels and inflammation. Meanwhile, the fiber found in chia seeds can help manage cholesterol levels and keep the arteries clear to minimize the risk of coronary heart disease.

A 2021 study also found that chia can help reduce high blood pressure/hypertension. In this study, adults with hypertension experienced significantly reduced blood pressure levels compared to a control group when they consumed 40 grams per day of chia seeds (about 1.5 ounces) for 12 weeks.

4. Balance Blood Sugar

Rich in both alpha-linolenic acid and fiber, evidence from several studies suggests that chia can help maintain normal blood sugar levels and fight development of type 2 diabetes and insulin resistance.

Animal and human studies have found that adding them to a high-sugar diet helps prevent changes in blood sugar and lipid levels. What’s more, human studies have also found that adding these seeds to white bread reduces the glycemic response and can help prevent spikes and crashes in blood sugar levels.

5. Boost Energy and Exercise Performance

Chia is often used by athletes for carb loading, a strategy that helps maximize the storage of glycogen in the muscles and liver to optimize endurance and boost exercise performance.

In fact, a study published in the Journal of Strength and Conditioning concluded that consuming chia seeds enhanced exercise performance for workouts that lasted 90 minutes the same way a sugar-laden sports drink would but without all the unhealthy sugar. In the study, half of the athletes drank 100 percent Gatorade, while the others consumed half Gatorade and half chia drink.

In the end, the runners’ times were matched, but the chia group consumed far less sugar.

Plus, studies show the protein content of these seeds is among the highest of all seeds and grains, giving it the ability to help build muscle mass and increase strength. Research shows that consuming protein as a post-workout meal can aid in the repair of muscle tissues and can also build new muscle to speed up recovery time between workouts.

6. Build Stronger Bones

Chia can help strengthen bone health and preserve bone density while reducing the risk of serious conditions like osteoporosis. This is because the seeds are loaded with calcium and manganese, two minerals that are needed to maintain bone health.

With about 99 percent of the calcium in your body stored in your bones, calcium serves an important role in maintaining bone strength and density. Manganese is also involved in bone metabolism, with studies showing that a deficiency in this key nutrient can impair bone resorption and decrease bone formation.

Impressively enough, a single ounce of chia seeds contains 18 percent of the calcium you need in a day while also meeting 30 percent of your daily manganese requirements.

7. Aid in Weight Loss

Chia seeds rank among the top plant-based protein foods, which is why they are great to consume for those trying to put on lean muscle, burn fat, and manage hunger and appetite.

How can chia seeds help you lose weight? Studies show that increasing your intake of protein can help promote weight loss by curbing cravings and cutting caloric intake.

One study published in the American Journal of Clinical Nutrition, for example, showed that increasing protein intake by just 15 percent of daily calories led to significant decreases in energy intake and appetite. Other research shows that chia may help reduce levels of ghrelin, the hormone responsible for stimulating hunger.

8. Fight Cancer Growth

Chia is rich in alpha-linolenic acid (ALA), a type of omega-3 fatty acid that gives it the potential to act as a cancer-fighting food.

One in-vitro study published in the Journal of Molecular Biochemistry found that ALA helped limit the growth of both breast and cervical cancer cells. Researchers also found that it caused cell death of the cancer cells without harming the normal healthy cells in the body.

While more research still needs to be done to find out the deeper implications of ALA on other types of cancer, this is a great discovery for women struggling with these increasingly common types of cancer.

9. Enhance Oral Health

Because chia is full of calcium, phosphorus, vitamin A and zinc, it helps promote dental and oral health.

Calcium is the building block of your teeth and necessary for maintaining oral health. Meanwhile, zinc prevents tartar by keeping plaque from mineralizing onto your teeth and has an antibacterial effect that keeps bad breath germs away.

Vitamin A and phosphorus are also important for strong teeth and a healthy mouth.

Risks and Side Effects

There are very few side effects associated with chia seeds when they’re eaten in moderation.

Occasionally, some people may experience stomach discomfort when consuming high amounts, mostly due to the high fiber content. As with any food, increase your intake slowly, and drink plenty of water.

If you have any concerns or experience any persistent side effects, consider decreasing your intake, and be sure to discuss with your doctor.

Can chia seeds make you gain weight? They shouldn’t, as long as you don’t eat too many. Stick to about two to three tablespoons daily.

Conclusion

The chia seed is a type of seed that comes from a flowering species in the mint family of plants and is native to Mexico and Guatemala.
The chia nutrition profile boasts a good amount of protein, fiber, omega-3 fatty acids, and important minerals like manganese, calcium and phosphorus — thus explaining why chia seeds benefits are so plentiful.
So what are chia seeds good for? Chia seeds benefits include increased weight loss, better blood sugar levels, improved heart health, enhanced regularity, increased weight loss and more.
From chia seed pudding to protein bars and baked goods, there are plenty of chia seeds recipe options that you can try to fit this nutrient-rich seed into your diet and get chia seeds benefits.
Soak, grind or enjoy whole for a nutritious and delicious way to boost the benefits of your diet and take advantage of the multitude of chia seeds benefits.

How to incorporate chia seeds into your diet (click here)

source source source

Here’s What Happens When You Stop Drinking

The Truth News — Fri, 10 May 2024 17:19:30 +0000

Here’s What Happens When You Stop Drinking

What happens when you stop drinking alcohol? Pretty much everything you’d expect—and also plenty that you might not.

Like, better sleep, less anxiety, and a clearer head, for one. And, glowier skin, hotter sex, and maybe even more connected relationships as well. But that’s not all: Recent studies show that the list of social, psychological, and physical benefits of teetotaling is ever-growing. It includes everything from more balanced hormones to a stronger immune system to reduced risks of heart disease, liver disease, and cancer. Plus, the potential of increased self-awareness, self-confidence, and higher self-esteem, too. As one doctor I recently interviewed put it, when you quit alcohol, “your entire body and soul improves.”

But swapping our evening glass of red wine for non-alcoholic spritzes and mocktails isn’t always super easy to do—even if you don’t officially struggle with an alcohol use disorder. That’s because alcohol is literally everywhere; its consumption is ingrained in our culture and societal norms. “Alcohol is the only socially-accepted mind-altering beverage in the world,” says Dr. Rafaat Girgis, a triple-board certified psychologist and the medical director at Moment of Clarity, a mental health treatment center in Orange County, California. “It’s served at parties, during meals, and on holidays; for most people, it’s just a part of daily life.” Which is why taking even just a short break for Dry January or Sober October—not to mention, quitting long-term—can often feel like it requires heroic levels of discipline.

One way to make it all a little easier: having a firm understanding of when you can expect to experience all the benefits. Anticipating everything that can occur after one day, one week, one month, and beyond can help you stay connected with the positive changes as they unfold— and remind you to give yourself some grace when temptations emerge. “Getting your body back to normal functioning depends on many factors, including your gender, current health, and your willingness,” explains Dr. Girgis. “Accept it, learn, and gain insight as you go.” After all, the body and the soul don’t improve overnight.

To that end, it’s also important to stay patient—and persistent. Good advice for any challenging situation, really, and especially when it comes to cutting back on or quitting alcohol. Tanya Mezher, a certified dietary nutritionist and the founding practitioner at functional medicine platform Malla agrees. “Recovery takes time, and setbacks may occur,” she warns. “Stay committed to your goals. The timeline varies from person to person, but noticeable improvements in physical and mental health can often be seen within a few weeks to months.”

With that in mind, here’s an overview of what you can expect in the short term and the long term when you stop drinking. Plus, a few more tips to help you succeed at every juncture in the journey. And remember: if you’re feeling hopeless or out-of-control because of heavy drinking, it’s important to seek professional medical support. You don’t have to go it alone and quitting cold turkey is not advisable. Call the Substance Abuse and Mental Health Services Administration hotline, which operates 24/7, 365 days a year, at 1-800-662-HELP (4357) for more information.

@clarkkegleyPowerful Lessons From Quitting Alcohol

♬ original sound – Clark Kegley

What happens you stop drinking after one day

For many, experiencing the intense flu-like symptoms of a hangover—nausea, headache, chills, sweating, restlessness, anxiety, bowel upset, and inflammation—can be a powerful impetus for deciding to quit or, at the very least, cut back. Therefore, depending on how much alcohol you typically consume, the first day off can be a little, ahem, rough. But the good news is, the first 12 to 24 hours of sobriety is when the healing also begins. Notably, you’ll experience increased hydration as your reduced blood alcohol levels reduce. “This could be the most critical part of stopping without a medical intervention,” Dr. Girgis says.

After three days

It’s not uncommon to experience alcohol withdrawal symptoms and cravings within the first few days of quitting; fitful sleep and low-level depression are also common. “This is the time where you are most vulnerable physically,” Dr. Girgis says, noting that this is often the point when many hopeful quitters succumb to the temptation to quell discomfort with a little “hair of the dog.” If you’re able to resist, the results will be worthwhile: you should start to experience better sleep, increased energy, and improved digestion by the 72-hour mark—and also noticeable skin clarity and increased levels of energy thanks to improved hydration. The liver, which is responsible for metabolizing alcohol, will also begin to reset and repair.

After one to two weeks

By now, you should be feeling a marked difference—and any improvements you’ve recently seen in your skin, energy, and sleep quality will only increase. Your immune system should be firing more effectively now, too, which can mean less chance of sickness, inflammation, and infection. Withdrawal symptoms should also have noticeably subsided at this point, freeing you to relish in the improvement in mental clarity and sharpness.

After one month

Like a downhill skier picking up speed, the momentum—and benefits—really start to build after a month. Liver enzyme levels and blood pressure have normalized, reducing the risk of cirrhosis and heart disease. Cardiovascular levels are also improved, which may also contribute to weight loss and visible changes in your physique.

After three months

You may suddenly notice you’re seeing the world through a rosier lens: At three months, emotions and mental health have stabilized leading to a more positive outlook and much cheerier moods. You may be feeling more creative and motivated, too, as any alcohol-induced brain damage or shrinking should begin to repair. Sleep patterns should be completely regulated by now, which means you could be jumping out of bed faster than you ever have before.

After six months to a year—and beyond

This is when most people really start to feel like a whole new version of themselves in all ways. Everything from anxiety to depression to sexual function should be majorly improved by now—and will only continue to benefit as the body repairs. The risk of developing certain cancers, as well as liver and heart disease are also more markedly reduced. And, many people also report more fulfillment in their relationships and work as their self-esteem and confidence increase. “My feelings is that it truly takes one year for your body to return to normal,” Dr. Girgis says. This is also when you may decide to never look back again; when you realize that quitting alcohol might just be, as he puts it, “the best choice you will ever make.”

Staying committed long-term

When it comes to staying on the wagon, both Dr. Grigis and Mezer say that it’s helpful to continue to set clear goals and seek support—whether that’s through a professional therapist, a medical advisor, family and friends, or organized groups. “Share your intentions with friends and family who can provide encouragement,” Mezer advises. And, don’t neglect the self-care basics. “Nutrition and hydration are your friends,” says Dr. Grigis. “Choose healthy foods and beverages, and remember to be physically active—even if it’s just walking around the neighborhood.” They both say these things can really help you stay focused and avoid potential triggers, both important factors in long-term success. “Know this,” Dr. Grigis says. “The decision to stop drinking is yours, and though it’s a daily commitment, it is possible—and wonderful.” source

I Quit Alcohol for 365 Days (why I’m NEVER going back)

HOW QUITTING ALCOHOL CHANGES YOUR BODY

“Life is so precious! Live with love, joy, happiness, and abundance.” I believe that the greatest gift you can give your family and your loved ones is a healthy you. I am sure that everyone has heard about alcohol abuse and addiction.

Alcoholism is one of the most common addiction forms. Alcoholism is a bad habit that affects all aspects of your life. Drinking problem can have a negative impact on our health, relationships, finances and many more.

Before you get to the point how quitting can change our lives, you should know about the consequence and effects of drinking alcohol:

INTERPERSONAL PROBLEM

People with Alcoholism suffer the interpersonal problem. They begin to draw out from family, relatives, and friends. They become argumentative and strained at home, at work, and with friends. Some people won’t even realize how badly they are affecting their family.

>HEALTH PROBLEM

Drinking is done for a short period of time but its effects are long term. It affects our complete body. Heavy drinking puts you at a risk of developing serious health problems.Such as heart disease, liver disease, certain forms of cancer and pancreatitis.

>LIVER DISEASE

Long-term heavy drinking develops alcoholic hepatitis or inflammation of the liver. It causes fever, jaundice and abdominal pain and can cause death.

>HEART DISEASE

Drinking alcohol causes the greatest risk of heart attack, increase blood pressure and heart disease.

>PANCREATITIS

The Pancreas help to regulate the body’s blood sugar. The Pancreas also digest food when we eat. Drinking cause inflammation of the pancreas which causes abdominal pain and weight loss.

OTHER ISSUES

There are many other problems related to drinking. As soon as you recognize it, you will know that you have a problem or the beginnings of a problem. Problems include thinking often about drinking, trying to stop drinking but unable to do, feeling guilty and embarrassed.

After reading these effects of alcoholism you sure want to quit alcohol. Quitting alcohol can be a life-altering decision and when you quit alcohol you will see how your life will improve. Here are the changes in your body when you quit alcohol.

After 1 hour

>Body kicks into full-blown detox mode to clear the alcohol from your body.

>Liver starts working overtime.

>Pancreas starts producing extra insulin which causes intense carb craving.

After 12–24 hours

> Blood sugar normalizes.

> Because of the diuretic effect booze has on bodies, you are going to be Dehydration.

After 48 hours

> Your body finishes its biggest detox hurdle.

> Cause headaches and tiredness.

After 72 hours

> Hangover side effects now out from your body you will start sleeping more deeply.

>Energy will restore.

>Quicker immune response in your body.

After 1 week

>Skin begins to look dewier and more youthful.

>Hydration restores.

>Reversal of alcohol-related liver damage.

After 1 month

>15% increasing its ability to filter toxins out of the body.

>Metabolism will restore leading to fat loss

>Reduce risk of cancer and decreased stress level.

After 1 year

> Risk of mouth, liver and breast cancers reduces.

> Blood pressure and pulse drop.

> Your liver fat will start decreasing.

After quitting alcohol you will feel that your life will improve. These are some reasons to quit alcohol. Though it’s not easy to quit but not impossible. There are many hospitals which provide Alcohol De-addiction services. source

These 7 Body Benefits Will Spur You to Quit Drinking

Stopping Drinking Safely: Understanding the Detox Process

If you decide to stop drinking, it is important to remember that it will take some time for your body to physically wean itself away from alcohol. This is because over time, the central nervous system adjusts to the depressive effects of alcohol, which causes the brain to ramp up its response in order for the body to stay functional. In the absence of alcohol, this altered state causes a range of physical responses that make up what we know as withdrawal.

How Long Does it Take to Detox from Alcohol?

For people who have a moderate dependency on alcohol, the first 24 hours of sobriety may be uncomfortable as their bodies detoxify, but after three days generally people begin to feel better. Most people will have completely recovered from the physical symptoms of withdrawal after a month, and are beginning to notice their health returning at this time.

For heavier drinkers, symptoms of withdrawal may be more severe and require medically-supervised detox. Like for moderate drinkers, these symptoms will begin within 24 hours of stopping alcohol use, but generally continue for a longer period of time.

Symptoms of Alcohol Withdrawal

Symptoms of withdrawal can differ based on the severity of the body’s dependency on alcohol, as well as what stage of withdrawal you are in. Generally, symptoms can occur as follows:

6 hours after your last drink: Symptoms during this period can feel a lot like a hangover, and may include things like a headache, nausea, sweating, vomiting, shaky hands, anxiety, and insomnia.
12-48 hours after your last drink: During this time, more serious problems can develop, including seizures and hallucinations.
48-72 hours after your last drink: A small percentage of people will experience deliriums tremens, or DTs, a severe symptom of withdrawal marked by delusions and lifelike hallucinations. This can be accompanied by heavy sweating, fever, elevated blood pressure, confusion, and a racing heartbeat.

If you are unsure of how your body will react to quitting drinking, consider reaching out to an addiction specialist to talk through different detox options and get a sense of what the first phase of recovery may involve. source

Long-term effects of alcohol

Alcohol use can also lead to more lasting concerns that extend beyond your own mood and health.

Some long-term effects of frequently drinking alcohol can include:

persistent changes in mood, including anxiety and irritability
insomnia and other sleep concerns
a weakened immune system, meaning you might get sick more often
changes in libido and sexual function
changes in appetite and weight
problems with memory and concentration
difficulty focusing on tasks
increased tension and conflict in romantic and family relationships

Alcohol’s physical effects on the body

Here’s a breakdown of alcohol’s effects on your internal organs and body processes.

Digestive and endocrine glands

Drinking too much alcohol over time may cause inflammation of the pancreas, resulting in pancreatitis. Pancreatitis can activate the release of pancreatic digestive enzymes and cause abdominal pain.

Pancreatitis can become a long-term condition and cause serious complications.

Inflammatory damage

Your liver helps break down and remove toxins and harmful substances (including alcohol) from your body.

Long-term alcohol use interferes with this process. It also increases your risk for alcohol-related liver disease and chronic liver inflammation:

Alcohol-related liver disease is a potentially life threatening condition that leads to toxins and waste buildup in your body.
Chronic liver inflammation can cause scarring, or cirrhosis. When scar tissue forms, it may permanently damage your liver.

Sugar levels

The pancreas helps regulate how your body uses insulin and responds to glucose. If your pancreas and liver don’t function properly due to pancreatitis or liver disease, you could experience low blood sugar, or hypoglycemia.

A damaged pancreas can also prevent your body from producing enough insulin to use sugar. This can lead to hyperglycemia, or too much sugar in the blood.

If your body can’t manage and balance your blood sugar levels, you may experience greater complications and side effects related to diabetes.

Experts recommend avoiding excessive amounts of alcohol if you have diabetes or hypoglycemia.

Central nervous system

One major way to recognize alcohol’s impact on your body? Understanding how it affects your central nervous system.

Slurred speech, a key sign of intoxication, happens because alcohol reduces communication between your brain and body. This makes speech and coordination — think reaction time and balance — more difficult. That’s one major reason why you should never drive after drinking.

Over time, alcohol can cause damage to your central nervous system. You might notice numbness and tingling in your feet and hands.

Drinking can also affect your ability to:

create long-term memories
think clearly
make rational choices
regulate your emotions

Over time, drinking can also damage your frontal lobe, the part of the brain responsible for executive functions, like abstract reasoning, decision making, social behavior, and performance.

Chronic heavy drinking can also cause permanent brain damage, including Wernicke-Korsakoff syndrome, a brain disorder that affects memory.

Digestive system

The connection between alcohol consumption and your digestive system might not seem immediately clear. The side effects often only appear after the damage has happened. Continuing to drink can worsen these symptoms.

Drinking can damage the tissues in your digestive tract, preventing your intestines from digesting food and absorbing nutrients and vitamins properly. In time, this damage can cause malnutrition.

Heavy drinking can also lead to:

gas
bloating
feeling of fullness in your abdomen
diarrhea or painful stools
ulcers or hemorrhoids (due to dehydration and constipation)

Ulcers can cause dangerous internal bleeding, which can sometimes be fatal without prompt diagnosis and treatment.

Circulatory system

Chronic drinking can affect your heart and lungs, raising your risk of developing heart-related health issues.

Circulatory system complications include:

high blood pressure
irregular heartbeat
difficulty pumping blood through the body
stroke
heart attack
heart disease
heart failure

Difficulty absorbing vitamins and minerals from food can cause fatigue and anemia, a condition where you have a low red blood cell count.

Sexual and reproductive health

Drinking alcohol can lower your inhibitions, so you might assume alcohol can ramp up your fun in the bedroom.

In reality, though, heavy drinking can:

prevent sex hormone production
lower your libido
keep you from getting or maintaining an erection
make it difficult to achieve orgasm

Excessive drinking may affect your menstrual cycle and potentially increase your risk for infertility.

Alcohol use during pregnancy

No amountTrusted Source of alcohol is considered safe for pregnant people.

That’s because drinking during pregnancy doesn’t just affect your health. It can lead to miscarriage, stillbirth, or premature delivery.

Children exposed to alcohol in the womb may experience a range of complications after birth, including:

learning difficulties
long-term health issues
increased emotional problems
developmental concerns

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Skeletal and muscle systems

Long-term alcohol use can affect bone density, leading to thinner bones and increasing your risk of fractures if you fall. Weakened bones may also heal slower.

Drinking alcohol can also lead to muscle weakness, cramping, and eventually atrophy.

Immune system

Drinking heavily reduces your body’s natural immune system. A weakened immune system has a harder time protecting you from germs and viruses.

People who drink heavily over a long period of time are also more likely to develop pneumonia or tuberculosis than the general population. The World Health Organization (WHO) links about 8.1 percentTrusted Source of all tuberculosis cases worldwide to alcohol consumption.

Drinking alcohol can also factor intoTrusted Source your cancer risk:

Frequent drinking can increase your risk of developing mouth, throat, breast, esophagus, colon, or liver cancer.
Drinking and using tobacco together can further increase your riskTrusted Source of developing mouth or throat cancer.

Psychological effects

Long-term alcohol use can lead to changes in your brain that can affect your:

memory and concentration
impulse control
emotions, mood, and personality

Regular drinking can also affect overall mental health and well-being, in part because alcohol may worsen symptoms of certain mental health conditions, including anxiety, depression, and bipolar disorder.

You might also notice feelings of anxiety with a hangover.

Alcohol-induced mental health conditions

Alcohol use can factor into mental health symptoms that closely resemble those of other mental health conditions.

The latest edition of The Diagnostic and Statistical Manual of Mental Disorders (DSM-5), which mental health professionals use to diagnose mental health conditions, includes diagnostic criteria for:

alcohol-induced bipolar disorder
alcohol-induced psychotic disorder
alcohol-induced sleep disorder
alcohol-induced depressive disorder
alcohol-induced anxiety disorder

With these conditions, you’ll only notice symptoms during alcohol intoxication or withdrawal. These symptoms typically improve quickly when alcohol use stops.

Dependence

Some people who drink eventually develop a tolerance to alcohol. As a result, they eventually need to drink more to notice the same effects they once did.

Drinking alcohol on a regular basis can also lead to dependence, which means your body and brain have grown used to alcohol’s effects.

When you stop drinking, you might notice a range of physical, emotional, or mental health symptoms that ease as soon as you have a drink.

Tolerance and dependence can both happen as symptoms of alcohol use disorder, a mental health condition previously referred to as alcoholism, that happens when your body becomes dependent on alcohol. This condition can be mild, moderate, or severe, depending on the number of symptoms you have.

Key symptoms may include:

cravings
withdrawal
drinking more over time
having difficulty stopping after one drink
inability to stop drinking when you try
continuing to drink alcohol even when it has a negative impact on your health or daily life
spending a lot of time on activities related to alcohol use

Learn more about the signs of alcohol use disorder.

Alcohol withdrawal

Alcohol withdrawal can be difficult and, in some cases, life threatening. Depending on how often you drink and how much, you may need support from a healthcare professional if you want to stop drinking.

It’s always best to connect with your doctor before quitting alcohol. The “cold turkey” approach might not always be safe.

Symptoms of alcohol withdrawal include:

anxiety
nervousness
nausea
tremors
high blood pressure
irregular heartbeat
heavy sweating

Seizures, hallucinations, and delirium may occur in severe cases of withdrawal.

Medical detoxification can help you stop drinking safely. Your doctor may recommend treatment at a clinic or at home, depending on your risk for withdrawal symptoms.

Risk factors for alcohol use disorder

Certain factors may increase your chances of experiencing alcohol use disorder.

Some of these include:

heavy drinking
binge drinking
ongoing stress
having peers or family members who drink a lot of alcohol
having genes that affect your sensitivity to alcohol
having anxiety, depression, schizophrenia, or another mental health condition
having a close relative, especially a parent, with the condition

source

3 Ways Your Appearance Changes When You Quit Drinking

Alcoholism can ravage all aspects of your life, altering your behavior, damaging your relationships, wrecking your health, and destroying your self-esteem. Over time, the toll of alcoholism can leave you feeling and looking different from the person you want to be. You will see many beneficial appearance changes after you quit drinking, including in the mirror.

Negative Effects of Alcohol

Alcohol can have many negative effects on your health, including:

Physical health

Alcohol can cause chronic diseases like heart disease, stroke, liver disease, and digestive problems. It can also damage your heart, causing problems like cardiomyopathy, arrhythmias, and high blood pressure. Heavy drinking can lead to liver inflammations, including fatty liver, alcoholic hepatitis, fibrosis, and cirrhosis.
Mental health

Alcohol can cause depression, anxiety, and other mental health problems. It can also weaken your immune system, making you more vulnerable to serious infections.
Cognitive health

Alcohol can cause learning and memory problems, including dementia and poor school performance. It can also damage the brain, which can lead to problems with thinking and memory.
Other health problems

Alcohol can cause cancer of the breast, mouth, throat, esophagus, voice box, liver, colon, and rectum. It can also cause diabetes, nutrition-related conditions, and overweight and obesity.

Short-Term Health Risks

Excessive alcohol use has immediate effects that increase the risk of many harmful health conditions. These are most often the result of binge drinking and include the following:

Injuries, such as motor vehicle crashes, falls, drownings, and burns.^6,7
Violence, including homicide, suicide, sexual assault, and intimate partner violence.^6-10
Alcohol poisoning, a medical emergency that results from high blood alcohol levels.¹¹
Risky sexual behaviors, including unprotected sex or sex with multiple partners. These behaviors can result in unintended pregnancy or sexually transmitted diseases, including HIV.^12,13
Miscarriage and stillbirth or fetal alcohol spectrum disorders (FASDs) among pregnant women.^6,12,14,15

Long-Term Health Risks

Over time, excessive alcohol use can lead to the development of chronic diseases and other serious problems including:

High blood pressure, heart disease, stroke, liver disease, and digestive problems.^6,16
Cancer of the breast, mouth, throat, esophagus, voice box, liver, colon, and rectum.^6,17
Weakening of the immune system, increasing the chances of getting sick.^6,16
Learning and memory problems, including dementia and poor school performance.^6,18
Mental health problems, including depression and anxiety.^6,19
Social problems, including family problems, job-related problems, and unemployment.^6,20,21
Alcohol use disorders, or alcohol dependence.⁵

By quitting drinking, you can reduce the risk of these short- and long-term health risks. source

Below are three ways quitting alcohol can help you look (and feel) your best.

1. You Will Lose Weight

While Drinking: Consuming alcohol in excess can significantly impact someone’s body shape. For starters, alcohol is very high in calories. There are seven calories in every gram of alcohol; for context, protein holds four calories per gram and fat has nine calories per gram. In addition, drinking alcohol activates the brain cells in the hypothalamus that make people feel hungry. This is the reason why after a night of drinking people tend to have the munchies. Lots of drinks plus extra eating equals a lot more calories than your body needs.

Alcohol also makes it more difficult for your body to burn any foods you eat. The body flags alcohol as a toxin, and the liver focuses on breaking down alcohol before any fat, carbohydrate, or protein. When the liver is constantly working to process alcohol rather than food, you start to gain weight. In the case of heavy drinkers, alcohol can cause so much damage to the liver that it stops functioning properly, which can lead to deadly conditions such as fatty liver disease or cirrhosis.

After Quitting: Weight loss happens during sobriety when someone replaces their old habits with new ones: sticking to healthier meals, no longer binge eating extra food while drinking, and, of course, no longer drinking all those empty calories. After quitting alcohol, your body can once again focus on metabolizing nutrients.

2. Your Skin Will Glow

While Drinking: When you are struggling with alcoholism, your skin is probably the least of your concerns. But the effects of drinking may be more serious than you think. Alcohol is a diuretic, which means that it causes more water to be processed through the kidneys. This leaves you dehydrated and causes dry patches, dull skin, fine lines, and dark under-eye circles. Your skin may become sensitive to the touch and feel uncomfortable, even itchy.

Chronic alcohol consumption also elevates the level of the stress hormone cortisol in the body, triggering alcohol-related premature aging. This stress can break down the skin’s collagen and cause inflammation, leading to wrinkles. Cortisol can also aggravate other skin conditions like rosacea or acne, causing flareups and breakouts.

After Quitting: By replacing alcoholic drinks with plenty of water, you are allowing your skin to rehydrate and flush out toxins through urine and sweat. Your skin will regain its natural, healthy glow as you replenish the necessary vitamins and minerals lost from active addiction.

3. Your Hair Will Grow

While Drinking: When alcohol dehydrates your body, it also dehydrates your hair. The lack of moisture causes thinning, hair loss, and dandruff on the scalp. Hair shedding is compounded by alcohol triggering increased production of cortisol and the hormone estrogen.

Alcohol also inhibits nutrient absorption by harming the lining of your digestive system over time, damaging your intestines until they can’t transfer nutrients to the blood. Without proper protein, the production of keratin slows; this protective agent bonds hair cells together and your hair becomes prone to split ends and breakage. Similarly, zinc and folic acid, which are essential for hair growth, aren’t soaked up by your follicles.

After Quitting: Your hair will regain its former strength as your body begins to repair itself from the effects of alcohol. The rate your hair grows will increase, and you’ll notice the change from hair loss to fuller, shinier locks.

Leaving alcohol behind and pursuing sobriety brings favorable changes to your appearance that you might not have anticipated. As you start to look good, you’ll feel good about yourself, and when you look in the mirror, you’ll see the old you again. source

‘I Gave Up Alcohol a Year Ago—I Feel 10 Years Younger’

I come from a family of drinkers so I grew up around alcohol. Whether we were celebrating or commiserating, alcohol was always involved. My paternal grandfather was actually born in a pub and named after it.

From about the age of 15, I started experimenting with drinking alcohol at local parks with friends. The first time I drank when I was out was at a local youth disco. We probably didn’t even drink that much and it wasn’t a late night, but we got very drunk and an on-site ambulance service had to tend to us. But you only remember the fun parts, so it went on from there.

I’m 45 now, so my generation grew up in the ’80s and ’90s, during the rave scene in the U.K. All the people I hung out with drank. We’d go to bars and clubs and we had some really good times but it was just a given that you drank. I never really questioned it.

I got into a cycle of drinking every weekend and recovering at the start of the week. Then mid week would arrive and I would start having a few drinks in the evenings, waiting for the weekend to come. That went on for years. source

‘I Quit Alcohol Four Years Ago—My Life Changed Completely’

By the time I was 34 years old, I was getting up every day and drinking alcohol. I knew where I could buy the cheapest hard liquor with the highest percentage of alcohol and no matter where I went, I usually had a mini bottle or two of liquor in my pocket.

The same year—2016—I was driving home from a date with my wife one night when she asked for my coat to use as a blanket. When I realized I had mini bottles of liquor in the pockets, I selfishly told her I wanted my coat back for myself, just so I could hide the alcohol from her and so she wouldn’t realize I was driving while likely over the limit. At that time, I also always drank the moment I got home from work. Sometimes I couldn’t wait and I drank on the way home and I would be drunk when I arrived. My life was an absolute train wreck.

Growing up in Vancouver, alcohol was always a fixture in my home. But though my parents both drank, they weren’t alcoholics and I only started drinking during senior year in high school as a way to socialize. In college, and throughout my 20s, I only ever consumed two or three drinks at a time; I could take it or leave it. I didn’t consider my drinking to be problematic, although I suspect a doctor may tell you differently.

I had also been an obese child and then struggled with my weight my whole life. In 2012, at 30 years old and nearly 350lbs, I had gastric bypass surgery. In less than a year I lost 190lbs. The surgery meant that alcohol was digested differently, it was sort of like drinking on an empty stomach. Soon, I began to notice that my relationship with alcohol had changed. I regularly needed to quench an absolutely uncontrollable thirst for alcohol; I wanted to drink until I was sick or blacked out.

I wasn’t drinking to escape any real emotional trauma, despite having been through a lot. My relationship with alcohol just got seriously out of control. It was like a switch had been flipped.

I would tell my wife that something wasn’t right and stop drinking for a month or two. I even had one stretch of sobriety that lasted 14 months; I felt I’d taken care of the problem. But when I drank after that, even though I would swear to myself that I would only have one or two, I would end up having 12 to 24 alcoholic drinks a night in secret.

Sometimes I would buy wine in a box, decant it into a litre sized water bottle in the garage or bathroom and slug that down quickly. My behaviour became erratic and I wasn’t able to meet my commitments at work. When I was drunk, I would look in the mirror and say, “How did I get like this?” and then the next might I would be drunk again.

I was also an emotional wreck. I had trouble relating to my family and I would get angry very easily. I was irritable, restless and I didn’t sleep well. I got to a point where I knew that if I didn’t reach out for help, I would be a dead man.

On November 2, 2016, I had a week of vacation starting and I bought myself a case of 24 beers. I was going to ration them out and have three or four beers a night. I put my son to bed at 8pm and cracked open my first beer. By 11pm I had finished 19 of them. Something inside of me said: “Kenny, your life is no longer manageable.” It was true.

I reached out to a friend of mine who I knew was in recovery from alcoholism, something I had never done before. The next morning she took me to a meeting for addicts. I knew I was home amongst those people because each of them told a story that could have been mine. I finally realized then: I’m an alcoholic.

In the 12 Step program I learned that stopping on my own is not something that I have the physical or emotional capability of doing. That program worked for me, but if something else works for other people, that’s great. There are many ways to get sober and 12 Step is just one of them. However, it was foolish of me to stop drinking on my own without consulting a doctor.

In that first week I had to call a complete stranger, someone who had been through the program, and ask them to be my sponsor. That was hell. But that guy told me to call him and go to a meeting every day. When I said that was too much, I remember he replied, “well, you drank every day.” I had no rebuttal.

For the first 30 days I was on what is called the “pink cloud.” I was very happy; it was like coming out of a bad relationship. The “pink cloud” ended when my sponsor said that I had to clean up the mess I had made of my life and all the people that I had harmed. That was when it got difficult and I started having doubts about recovery. You have to address what led you down the path to wanting to alter your state in the first place. I just wanted my life back, but instead I was encouraged to fix the old one.

It took me about 10 months to get through all 12 Steps and eventually I chose to put my trust in a higher power, something I was taught by the program, though it doesn’t have to be God.

I realized that I had been angry about many things in my life, all the way from childhood. Part of the program is recognizing that and letting it go. Then you have to make a list of all the people that you’ve harmed and make amends to them. It’s not just apologizing, you actually have to mend the situation.

When I was drinking I would go onto social media every night and lash out at people. I was angry, spiteful and resentful to my friends and peers, and sometimes strangers. I had a lot of situations that I needed to make right.

I had also stolen from people and I had to pay them back. That was hard. I’m a family man so it was difficult for me to accept that I had stolen whilst under the influence of alcohol, or in order to become under the influence of alcohol.

So, life as a sober person was very difficult at the beginning. Although my wife doesn’t drink, I couldn’t go to places where alcohol was served and I became a bit of an introvert. At our family Christmas in 2016, I noticed there was no alcohol and a few hours in I asked my father why they weren’t drinking. He told me not to worry. I realized my family had collectively decided to abstain from alcohol for my sake. It was very emotional and it absolutely meant the world to me. Now, I don’t have an issue being around alcohol, but it was hard for a while. source

Healthy Eating Habits – How They Affect Our Kids

The Truth News — Thu, 25 Apr 2024 19:51:46 +0000

From the first day, we worry about our kids getting enough to eat. Find out how parent-child interaction during feeding may influence kids’ weight and relationship with food.

How healthy eating habits have positive effect on our kids.

Doctor’s Tip: What our children eat affects their current and future health

We keep reading that childhood obesity is on the rise in the U.S., and — as we export our lifestyle worldwide — in the rest of the world as well. Experts tell us that this is the first generation of kids in history that won’t live longer lives than their parents. We can no longer call type 2 diabetes adult-onset diabetes, because so many overweight kids have it.

The food industry does its best to get Americans — starting at an early age– addicted (literally) to salt, sugar and fat (the latter often in the form of added oil). Let’s look at Amy’s Organic Mac and Cheese for example. Parents think that if it’s organic it must be healthy, so they buy it. One serving has 400 calories, with 16 grams of total fat including 10 grams of unhealthy saturated fat. It also has 640 grams of salt (the maximum safe amount for an adult is 1500 grams, much less for a child). It contains 6 grams of sugar — 4 grams is a teaspoon.

Good nutrition starts in the womb. We know that alcohol during pregnancy causes fetal alcohol syndrome. Eating fish raises levels of PCBs and of heavy metals such as mercury, in the mother and fetus. Eating green leafy veggies increases folate levels in mother and fetus, which is linked to a lower rate of neural tube defects. source

A Lifetime of Health Starts in Childhood

A lifetime of health begins in childhood. The food choices given to children impacts the relationship they have with food as adults.

“Early childhood is the formative, developmental period where children can be set on a lifetime path of good health,” said Dipti Dev, associate professor and child health behavior Extension specialist in the Department of Child, Youth, and Family Studies at the University of Nebraska–Lincoln. “It is during this critical time that children develop eating behaviors that transition into adolescence and adulthood.”

Through Nebraska Extension, Dev works directly with families, teachers, and childcare providers teaching them healthy eating strategies. Specifically, she offers a series of on-demand, online modules with short videos to demonstrate science-based strategies for establishing healthy eating patterns with children, hoping to prevent health issues later in life.

“Healthy eating is important because it is the key modifiable risk factor for preventing obesity and chronic diseases,” Dev said.

Best Practice #1: Promote Healthy Eating Habits Young

Early childhood is the time period where children discover what they like and dislike, according to Dev. Adults can use this to their advantage and lead children to healthy foods to help children make healthy food choices that lower the potential of having health issues later in life.

“Obesity and associated chronic diseases, such as diabetes, cancer, and cardiovascular diseases, can all be modified by improving healthy eating,” Dev said. “If these habits are developed at a young age, it can create a lifetime of good health.”

Unfortunately, the majority of children in the United States fail to meet dietary recommendations, according to Dev. Therefore, she suggests children should be encouraged to eat more fruits, vegetables, whole grains, and lean meats, and less of foods high in sugar and saturated fats.

From birth to five years of age, children are able to self-regulate their caloric intake or eat when they hungry and stop eating when they are full. Adults can support children to actually listen to their internal cues of hunger and fullness. Dev calls this mindful eating. Promoting mindful eating cues carry into a child’s adult life and help them respond appropriate to their hunger and fullness signals.

When children learn to eat healthy options when they are young, they are more likely to continue doing so into adulthood. Dev said promoting healthy eating habits at a young age is critical to overall adult health.

Best Practice #2: Responsive Feeding

The best way to teach children healthy eating is to practice responsive feeding.

Dev said responsive feeding means being active and attentive to the hunger cues of a child. For instance, if the child acts full, ask them if they are “full”, rather than if they are “done.” Doing so sparks a response from the child where they determine if they need more food.

Responsive feeding also pays attention to how the food is being presented to the child.

“Responsive feeding can be as simple as changing the way people present the food to the children,” Dev said.

For example, if children are taught that dessert is a “reward” only after they eat fruits and vegetables, it causes a dislike and resentment for fruits and vegetables. Instead, treating the foods equally changes the way children view those types of food. Doing so can also take the struggle out of mealtime.

Dev warned that forcing or bribing children to eat specific foods is not usually successful.

“Avoid coercing or pressuring a child to eat and avoid giving them bribes or treats,” Dev said. “These are actually counterproductive to encouraging good eating habits.”

Instead, following a child’s hunger cues and presenting food equally can make mealtime much more enjoyable.

Best Practice #3: Role Modeling and Food Exposure

Being a role model for children and exposing them to various foods also promotes healthy eating habits, according to Dev.

“Children are influenced by adults, especially at a young age, so childcare providers, parents, grandparents, and teachers can all serve as role models for healthy eating,” Dev said.

For example, the adult caregiver should try to eat healthy food themselves and have a variety of healthy foods available. They can also use descriptive words such as “crunchy” or “juicy” to create interest in the food for children.

The child may take more interest in food they are exposed to if the adult is also interested, Dev said. The child is also more likely to like these healthy foods and continue to like them into adulthood.

Further, creating exposure can be fun and there is little pressure when children are given different choices.

“Children are naturally curious, and they want to explore,” Dev said. “Allowing them to explore new, healthy foods will expose them to different options and find what they like.”

Dev said offering healthy food options does not need to be expensive and offers suggestions for budget conscious families.

“Families might consider attending farmers markets or creating a garden in the backyard and growing vegetables,” Dev said. “Children will watch and learn these modeled behaviors.”

Frozen fruits and vegetables are an inexpensive way to provide healthy foods for children, Dev said. Families can also purchase bags of lentils or beans for soups, burgers, etc. that last quite a long time or purchase only seasonal fruits to keep down costs.

In the future, Dev hopes to improve healthy eating by creating a Community Learning Healthcare System, seamlessly integrating technology and best practices into one system, while considering all stakeholders within the system. She plans for this to be scalable, transferable, and sustainable for use in hospitals, schools, and nursing homes.

For more information about Dev’s research of promoting healthy eating among young children or the EAT Family Style Programming, visit https://cehs.unl.edu/cyaf/dev-research-and-extension-group/.

source

Encourage Healthy Eating Habits

Healthy eating is essential to a child’s well-being. Children who are overweight are at risk for chronic health problems. The Weight-control Information Network (WIN), a service of the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK), offers guidance to parents and caregivers on how to encourage healthy eating habits in children.

Tips for Families to Help Children Eat Healthy

Eat breakfast every day. Skipping breakfast can leave your child hungry, tired, and looking for less healthy foods later in the day.
Plan healthy meals and eat together as a family. Eating together at meal times helps children learn to enjoy a variety of foods.
Buy and serve more fruits and vegetables (fresh, frozen, or canned). Let your child choose them at the store.
Buy fewer soft drinks and high fat/high calorie snack foods like chips, cookies, and candy. These snacks are OK once in a while, but keep healthy snack foods on hand too and offer them to your child more often.
Start with small servings and let your child ask for more if he or she is still hungry. It is up to you to provide your child with healthy meals and snacks, but your child should be allowed to choose how much food he or she will eat. One tablespoon per year of age for each component of the meal is a great place to start when considering serving sizes for young children.
Offer your child water or low-fat milk more often than fruit juice. Fruit juice is a healthy choice but is high in calories.
Eat fast food less often. When you visit a fast food restaurant, try the healthful options offered.
Do not get discouraged if your child will not eat a new food the first time it is served. Some kids will need to have a new food served to them 10 times or more before they will eat it.
Try not to use food as a reward when encouraging kids to eat. Promising dessert to a child for eating vegetables, for example, sends the message that vegetables are less valuable than dessert.
Make healthy choices easy by putting nutritious foods where they are easy to see and keep high-calorie foods out of sight.

Healthy Snack Ideas

Fresh or frozen fruit, or fruit canned in juice or light syrup
Small amounts of dried fruits such as raisins, apple rings, or apricots
Fresh vegetables such as baby carrots, cucumber, squash, zucchini, or tomatoes
Reduced fat cheese or a small amount of peanut butter on whole-wheat crackers
Low-fat yogurt with fruit
Graham crackers, animal crackers, baked pretzels, or low-fat vanilla wafers

The 5-2-1-0 Message Provides Suggestions for Building Healthy, Active Lives

Eat at least 5 fruits and vegetables a day.
Keep screen time (like TV, video games, computer) down to 2 hours or less per day.
Get 1 hour or more of physical activity every day.
Drink 0 sugar-sweetened drinks. Replace soda pop, sports drinks, and even 100 percent fruit juice with milk or water.

Be Supportive

Throughout any process or program that you undertake to address your child’s eating habits, be supportive. Help your child set specific goals and track his or her progress. Reward successes with praise and hugs. Be positive.

Tell your child that he or she is loved, special, and important. Children’s feelings about themselves are often based on how they think their parents and other caregivers feel about them. Children need compassion, understanding, and encouragement from caring adults.

Note: Foods that are small, round, sticky, or hard to chew, such as raisins, whole grapes, hard vegetables, hard chunks of cheese, nuts, seeds, and popcorn can cause choking in children under age 4. You can still prepare some of these foods for young children, for example, by cutting grapes into small pieces and cooking and cutting up vegetables. Children should always be supervised during meals and snacks. source

The challenge of feeding kids

https://goodshepherdmedia.net/wp-content/uploads/2024/04/How-we-Feed-our-Kids-Determines-Their-Life-Made-with-Clipchamp.mp4

Feeding kids healthy is easy…said no parent ever! As a parent, I know feeding kids is challenging. It can require a significant investment of our time and financial resources. I wanted to share with you why I think it is worth it, some ideas on how to approach it, and ways your family might consider making changes.

Teaching our kids the importance of healthy food is a skill worth cultivating.

Showing our children how to prioritize healthy food and moving their bodies can be valuable tools that can help them build health that lasts a lifetime. Like many of the important tools we strive to equip our children with, it is not something that just happens for most parents. I know first hand it can require hard work, preparation, and often perseverance. It is not the path of least resistance, some days it can feel nearly impossible, but in the end it can be a worthy investment of our time and money as parents.

The first five years is an essential time for growth, health, and development for young children.

90% of the physical brain develops in the first five years of life, and nutrition plays a critical role in that brain development. Emerging evidence now places nutrition at the forefront as a tool for mental health prevention for children. Early food experiences and feeding strategies for young children will lay the groundwork for a lifetime of food preferences, behaviors and health. This doesn’t mean that it’s too late to make changes. It just reminds us that the sooner we start, the easier it will be for our children to make these changes sustainable.

When possible, try to model a healthy food relationship for your child.

Help them understand what these foods do for their bodies, teach them to understand their hunger cues, and expose them to as many whole, nutritionally dense foods as possible.Why does this matter? The percentage of children with obesity in the US has more than tripled since the 1970s. Today, 1 in 5 are considered obese (CDC, 2017). Estimates show 25% of children have a chronic health condition (asthma, allergies, eczema, obesity, physical condition, behavior / learning challenges) (CDC, 2017). Trends show that 1 in 3 children born today will have diabetes by 2050 (CDC, 2010). Much, but not all of this is preventable. We as parents of this generation have the ability to change the course of our children’s lives.What we feed our children and physical activity are two of the most powerful choices we can make for your children’s future health outcomes. While your genes play a role in the risk of developing these chronic diseases, we now know that 70%-90% of the outcomes are determined by behavioral and environmental factors (diet, inactivity, and smoking) that we can influence.

We can’t control our children’s genetics, but we can help them make choices that determine how our children’s genetics come to life.

So how do we do this as parents?

We as parents decide what, when and where children eat (this especially rings true for younger children). Our children decide how much and if they will eat at all. This approach, often referred to as the division of responsibility, a term coined by feeding expert Ellyn Satter. I encourage parents to focus on providing regularly scheduled meal times, a distraction free space for eating, and access to a variety of healthy foods throughout the day (vegetables, fruit, whole grains, legumes, seeds, nuts, healthy fat, and lean protein) with as little distractions as possible. When you prepare a meal, build a meal that offers at least one thing you believe each child will enjoy and hope for the best. This doesn’t mean there are not days your children are incredibly disappointed with your choices. You will not get it right all the time. Children are unpredictable beings, so we just enjoy the ride! Celebrate the good days and remember there is always tomorrow.

Give your child(ten) room to decide if they will eat and how much they will eat. This can empower children to navigate their relationship with food and help reduce your power struggles around food. It is normal for children’s appetite to fluctuate. Try not to place to much energy and attention on the meals that your child barely touches from time to time. With this division of responsibility, children can have space to explore their hunger cues, learn how to eat appropriate portions to fuel their body and cultivate the language to articulate when they are full and when they are hungry. In most cases, children are incredibly capable of knowing how much to eat to fuel their bodies when given a range of good choices.

Try not to offer a 2nd meal on the days your kids feel less inclined to participate. If your child persists with hunger post dinner time, offer a healthy alternative when necessary. For us this might include a handful of nuts, olives, banana with almond butter, applesauce, or carrots.

What we feed children, influences what they will like.

Research validates that it takes children 10-20 experiences before they will enjoy and accept a new food. It is normal for children to be cautious around new foods and new flavors. The experiences we are creating for our children in utero and beyond are developing their taste buds. From an early age, try to offer a range of food experiences and flavor profiles. Introduce your children to the foods and flavors your family enjoys. Consistent exposure of new foods will help your children flex their muscles at being willing to explore a larger variety of foods. If children experience the same meals over and over again, this can lead to children a narrow list of foods they are willing to eat.

One of my favorite ways to increase variety in a child’s food preferences is to start by offering their favorite foods in a range of preparations. Once they find more flexibility in how they are willing to eat some of their favorite foods, you can expand from there.

Can you find the time to sit down to a meal with your family?

Sometimes siting down to family meals can feel impossible, especially with full time working parents and long commutes. I make this request as someone who understands that time is not always on our side and so many of our family schedules feel as if they are conspiring against us. Yet, I also know some families with these circumstances who found ways to prioritize this and have seen great shifts in their children’s relationships with food. Sitting down for a family meal helps children understand healthy food is a priority for your family and it gives children an opportunity to slow down and appreciate their food. Family meals can be a chance to connect with your family and create good eating habits. Even if it’s only on Sundays or the weekends, try to make space for sitting down together when you can.

If you are hoping to make changes or shifts to your family eating routine, making a plan and including your children in the process can be helpful.

Remember, changes can feel hard to everyone. Try setting realistic goals for your family and share your goals with the children. Weekly meal planning can often set families up for success. Consider creating a grocery list and budget to ensure you have what your family needs to stay fueled throughout the days ahead. Make a list of dinners for the week and ask your children to each come up with one dinner idea for the week. Creating this list allows your family to consider your busiest days and upcoming kids activities.Talking to your kids about changes you plan to make in order to get their buy in. If age appropriate, include your children in coming up with ideas or alternatives food ideas that fit into your new goals. Consider other ways you can invite them to be a part of the plan. Can they help clean out the pantry, grocery shop, explore the vegetables in the produce aisle, chop vegetables, cook, pack their lunches, and read labels? For younger children, you could explore ways to eat your way through the rainbow in fruits and vegetables, make it fun! Small changes and conversations can send big signals to children about what is important.

A great place to start when trying to make changes is by reducing the presence of distracting foods in your home and finding alternatives for these foods.

Clean out the foods that you feel are the biggest distractions towards your family goals. Often these foods get in the way of being able to make better choices. Start by not restocking the foods you no longer want in your home. Find a place to start; the snack foods, the breakfast options. There is a time and place for sometimes foods, but reducing their abundance in your home will make your job a lot easier. Be sure to offer alternative ideas for your children to replace these foods and consider their input. Go at a pace that is sustainable for your family and allows you to make lifelong lifestyle changes.

When possible and your budget allows, look for whole, minimally processed foods. Experts agree, eating whole foods is best choice your health. Whole food is defined as food that is been minimally processed and refined and does not include additives. This means that the foods are as close to the original source as possible. Rely heavily on whole, unprocessed foods to fuel your growing family. Eating a diet rich in vegetables, fruits, legumes, nuts, seeds, eggs, and whole grains will be valuable for growing bodies. Eating the rainbow of vegetables and fruits will allow your children to access so many important nutrients they need.

Thank you for allowing me to be a part of your parenting adventure. The internet is filled with a vast amount of resources, ideas and support groups to help family learn more and find ways to overcome the challenges that their individual family’s experience. Remember, there is not one “right way” to eat for every individual. Everyone is making compromises in some way as we navigate the complex food system. Try to find balance between foods that serve your family’s health, the convenience foods that get you through a busy week, and sometimes foods your family enjoys for special occasions. Some days will be better than others. We are all a work in progress! source

The Fake Meat Scam – Plant Meat Chemistry! Is Plant Based Meat Safe?

The Truth News — Thu, 09 Mar 2023 07:49:51 +0000

The Fake Meat Scam – Plant Meat Chemistry! Is Plant Based Meat Safe?

Using strategies to position it as a healthy alternative for natural meat, the industry’s fake meat is just another name for ultra-processed food, full of GE and pesticide-laden ingredients designed to look as much like meat as possible.

If you understand biology, chemistry, chemical engineering, genetics and economics you too can create fake meat to help speed up your death!

Just a little Leghemoglobin (meat flavor) will do ya…… in eventually! some makers of fake meat are well aware along with the FDA that they chemicals do not meat GRAS (generally regarded as safe)! Tests not only show glyphosate present but 46 unknown proteins not yet tested for safety in humans! Leghemoglobin made with GM soybeans

Story at a glance:

Ultra-processed foods typically have five or more ingredients, many of which are not commonly used in home kitchens. This aptly describes the Impossible Burger and Beyond Burger, including fake blood processed from genetically engineered yeast to mimic the taste and texture of real beef.
Although the soy-like hemoglobin used in the Impossible Burger is classified as generally recognized as safe, no tests have been done by independent labs on the product’s safety. However, tests on lab rats altered the animals’ blood chemistry; the company did not follow up on the results.
The parent companies for Impossible Burger and Beyond Burger commissioned studies to assess the environmental impact of production against typical concentrated animal feeding operation (CAFO) beef production. Not surprisingly, they found their product had a lower impact. But it’s not nearly as low as the beef production at White Oaks Pastures, which uses regenerative farming practices to produce natural beef products.
If a plant-based, genetically engineered (GE) meat alternative is not enough of a science fiction adventure, consider the “meat” scientists are growing from stem cell cultures in the lab. Some see these alternatives as the lesser of two evils, but when holistic herd management improves the environment, your best choice is to seek food from natural sources.

The junk food industry has a new product they are offering in exchange for your health and finances.

Using strategies to position it as a healthy alternative for natural meat, the industry’s fake meat is just another name for ultra-processed food, full of GE and pesticide-laden ingredients designed to look as much like meat as possible.

In an effort to get you hooked on it, it’s marketed as healthier and better for the environment — which may lead you to believe you’re eating good food while protecting your local air and water supplies.

The manufacturers are so intent on mimicking foods found in nature that they’ve even genetically engineered “blood” for their fake meat products.

Food critics are divided on the taste, with some finding the texture pleasing, but not tasting like a burger. Others say that only when the burger is piled high with caramelized onions, vegan mayo and mashed avocado does the flavor likely approximate meat.

When it comes to organic offerings, food manufacturers would like you to believe they can improve on nature but, historically, this has been nearly impossible to achieve.

Ultra-processed foods have contributed to the obesity epidemic, rising rates of cardiovascular disease and an increased risk of all-cause mortality.

If you think ultra-processed foods are only found in the junk food aisle, though, it may surprise you to learn that, according to Current Developments in Nutrition, many foods you eat most likely include fake meat ingredients:

“Besides salt, sugar, oils, and fats, ingredients of ultra-processed foods include food substances not commonly used in culinary preparations, such as hydrolyzed protein, modified starches, and hydrogenated or interesterified oils.

“Additives whose purpose is to imitate sensorial qualities of unprocessed or minimally processed foods and their culinary preparations or to disguise undesirable qualities of the final product, such as colorants, flavorings, nonsugar sweeteners, emulsifiers, humectants, sequestrants, and firming, bulking, de-foaming, anticaking, and glazing agents.”

Lets face it with 7,888,000,000 or approx 8 billion people on earth feeding us is taking its toll and is unsustainable if consistent growth continues, making cheap slop for you too eat saves space, makes more money, and adds toxic chemicals to your diet, thanks soy Glyphosate which is sprayed on GM Soybeans and lingers in your plant based burgers!

Health is not driving a meat makeover

The Heart and Stroke Foundation of Canada warns you should not be swayed by deceptive marketing tactics using words such as “healthy” and “natural” when you make food choices.

Unfortunately, it appears that some consumers believe the advertising promises.

While called a plant-based meat alternative, Beyond Burgers and Impossible Burgers are an ultra-processed conglomeration of chemicals, concocted by pulling protein from soy and a few other processed concentrates.

Amy Keating, registered dietitian and Consumer Reports nutritionist commented:

“… while its starting materials may be plants, the main ingredients are all highly processed concentrates, oils, and flavors. If you want the health benefits of plants, eat them as whole foods with their nutrients and fiber naturally present.”

Adding to the discussion, both Impossible Burger and Beyond Burger have nearly the same amount of total fat and calories as real beef burgers. In addition, both also have much more processed sodium added.

As a reporter at NBC News so succinctly pointed out:

“If eating more realistic fake meat was about health, the offerings would be far lower in salt content, contain fewer calories and have a bit less dietary fat. None of them do, because the point was never to live up to the marketing of healthier eating. It was to simply act as a smooth replacement for the meat we worried about eating in our day-to-day lives.”

The fake meat industry is riding the coattails of the real risk that CAFOs pose to the environment and to human health.

However, fake meat manufacturers have turned to the laboratory to boost profits and drive sales rather than support sustainable and environmentally-friendly real food production.

Chemical-packed fake meat contains GE blood

After they mimicked the look and texture of meat, manufacturers gave consumers the taste and color of blood using a compound produced by genetically engineered yeast cells.

The compound is called soy leghemoglobin, coming from the roots of the soybean plant.

On a chemical level, it’s similar to the heme iron molecule found in mammal blood and it adds some of the texture and bloody look of an all-beef patty.

But manufacturing it to scale is impossible with just soybeans — it takes one full acre of soybeans to produce 1 kilo of leghemoglobin.

Plus, it requires genetic work in the lab to insert the soy leghemoglobin into engineered yeast cells. During the fermentation process, the GE yeast produces large quantities, in addition to dozens of other proteins.

Impossible Burger’s scientists fed the leghemoglobin to rats for 28 days to determine the risk of allergic reaction or toxicity.

Dana Perls, from Friends of the Earth, pointed out that the rats exhibited alterations in blood chemistry, which the company did not follow up on.

Unfortunately, the U.S. Food and Drug Administration (FDA) only requires research by the manufacturer to determine food safety and has not conducted any independent tests.

Michael Hansen, Ph.D., Consumer Reports senior scientist, notes there is no long-term data demonstrating the effect of soy-like hemoglobin in humans.

The process of manufacturing the compound yields at least another 45 by-product proteins, also consumed with the leghemoglobin.

The FDA has classified the Impossible Burger as generally recognized as safe using data provided by the University of Nebraska and the University of Wisconsin.15 Other experts are not convinced.

According to the Center for Food Safety, 94% of the soybean crops grown in the U.S. are genetically altered.

And, Hansen warns there are not enough data to determine human safety when consuming chemical compounds, as these compounds are produced from genetically altered yeast harvested from genetically altered soybeans.

Marketing tactics used to convince consumers

As I’ve written before, junk food is based on junk science, or information aimed at driving profits at the expense of your health.

The fake meat industry has taken a page from other corporate interests such as the sugar and tobacco industries.

You may have noticed a cycle some producers have used, beginning with hype and marketing and often ending up in a revelation, sometimes years later, that the products are not as healthy as you were told.

The cycle is lucrative and makes more money for companies than subsequent lawsuits drain.

Vaping products, opioids, sugar-based products, traditional cigars and cigarettes and junk foods are just a few examples of items that haven’t lived up to the hype and marketing strategies.

Meanwhile, millions — if not billions — flow into manufacturers’ pockets.

One of the claims from the fake meat industry, as an example, is that their products are sustainable and leave a smaller carbon footprint than that of traditional beef productions.

When compared to CAFO facilities, where animals are often treated inhumanely, the waste damages to air and water supplies and the administration of antibiotics that contribute to widespread antibiotic resistance, they may have something to complain about.

However, moving from one broken system to another is never the answer.

Regenerative farms produce clean, healthy environments

To help them “prove” they have a better carbon footprint than live animal farms, Impossible Burger enlisted the help of Quantis, a group of scientists and strategists who help their clients take actions based on scientific evidence.

Beyond Meat commissioned the University of Michigan to conduct an assessment and compare the environmental impact of their production to that of typical beef production in the U.S.

The results were similar for both companies. According to the executive summary published on the Impossible Foods website, their product reduced environmental impact between 87% and 96% in the categories studied, including global warming potential, land occupation and water consumption.

In response, White Oak Pastures in Bluffton, Georgia, commissioned the same analysis by Quantis and published a 33-page study showing comparisons of White Oaks Pastures emissions against conventional beef production.

While the manufactured fake meat reduced its carbon footprint up to 96% in some categories, White Oaks had a net total emission in the negative numbers as compared to CAFO-produced meat.

Yes, negative.

Also of note, emissions for producing beef at White Oaks Pastures was much lower than the average production of soybeans, the base for plant-based burgers and leghemoglobin.

Quantis also found that White Oaks Pastures beef falls within and even below the range of production of other types of protein sources, including beef, pork, chicken and soybeans.

Additionally, emissions by White Oaks Pastures included a large negative soil carbon sequestration, which I’ve explained in many articles is essential to protecting against air pollution and climate change.

Speaking to Consumer Reports, Friends of the Earth’s Perls added that the hype and advertising around alternatives to natural meat will distract from finding better solutions to environmental problems, and noted the true cost of producing fake meat cannot be known until it’s being produced on a large scale.

These costs include damage to your health as well as to the environment. “Rather than creating new products that require more energy, more money, and more processed chemicals, why not invest in a truly sustainable system …” Perls said.

‘Plant-based’ not enough — others ‘growing’ meat in labs

If eating plant-based, GE grown meat alternatives laced with heme molecules to mimic the presence of blood is not enough of a science fiction adventure, consider the fact that scientists in Tel Aviv are “growing” meat in the lab from stem cell cultures.

A CBS News crew traveled to Tel Aviv to report on the story and had to sign a waiver to be able to taste the “meat.”

CEO of Aleph Farms, Didier Toubia, told the crew he believes they can produce meat efficiently, more sustainably and in a healthier fashion than what has been traditionally offered.

When the CBS reporter commented on the “delicate portion” of meat served to him, appearing in the video to be no more than a thinly-sliced, 1-inch square, the scientist cooking the “meat” said:

“Well, just to get this portion is a lot of work.”

To get their product, the researchers have to extract stem cells from chicken and change the mix of protein. Then, they have to direct the cell growth, and it’s all a slow, involved process.

Several other companies are jumping on the bandwagon, though, including Memphis Meats and Mosa Meats for beef and chicken, and Finless Foods and Wild-Type for fish.

Memphis Meats’ leadership believes their controlled production environment may reduce the risk of bacterial contamination.

But Hansen, a senior scientist at Consumer Reports, points out that “bacterial contamination can occur” in laboratory environments and that “antibiotics are often needed to curb bacterial growth in cultured cell products form drug companies.”

At this point, lab-produced meat is not available for sale. Kate Krueger, Ph.D., a New York-based research director focused on cellular agriculture, says it may be “four to six years before ‘ground’ meats are available and a decade or more before we see cuts like steaks,” in the grocery store.

Choose grass fed, not genetically altered food

Although many see lab-created meat substitutes as the lesser of two evils when compared to the CAFO meat that’s currently dominating the market, altering the natural order of the lifecycle is not the answer.

Analyses on regenerative agriculture have demonstrated holistic herd management as having a positive impact on the environment and producing healthy meat and dairy products.

Ultimately, fake food contributes to the rising number of people who suffer from health conditions related to the foods they eat, such as diabetes, heart disease and obesity.

For health reasons, ecological reasons and your future, I recommend skipping meat alternatives and opting for real beef raised using regenerative farming practices.

When you do shop for meat, look for a local organic farmer or Demeter (biodynamic) and American Grassfed Association certifications on the meat.

These accreditations designate foods produced under high-quality, sustainable and environmentally sound practices. source

What crap is in your fake meat?

Dies
Artificial Flavors
Bulking Agents
Leghemoglobin
Hexane
caramel coloring proven to cause cancer in mice
tertiary butylhydroquinone (TBHQ) causees liver enlargement and acute neurotoxic effects in animals exposed to it
Ferric Phosphate (Slug Pesticide/ promoted as iron supplement cheap worst kind at that)
seed oil – Vegetable oils are unsafe – they are linked to heart disease liver damage and cancer

When Tested some extra unexpected finings other than the cheap crap they intentionally threw in your slop burger!

46 unknown proteins
glyphosate

WARNING: Plant-Based Meat Can Have This Carcinogen

Today we’re publishing a new ad in our national campaign about synthetic meats. The ad has run The Wall Street Journal, The Los Angeles Times, and The New York Times and questions whether plant-based meats need a cancer warning label.

Shocked?

You certainly might be if, like many unknowing consumers, you think synthetic meat is healthier because it’s called “plant-based.” After all, plants like fruits and veggies are healthy, no?

Fruits and veggies may be healthy, but fake meats are ultra-processed foods. They don’t grow on vines. Their ingredients are mixed together and heated without precedent. They’re not any better for you than real meat, say nutritionists. And some say there is no assurance about their future impact on health.

And now we have lab tests showing that six fake meat products, when cooked, tested positive for a carcinogen, acrylamide. Acrylamide can be formed when plant-based foods are cooked at high heat–for example, cooking a fake meat burger.

So where does the warning label fit in?

Californians passed a ballot measure in 1986 called Proposition 65, which requires a warning when a company exposes people to chemicals known to the state of California to cause cancer or reproductive harm. And California considers acrylamide a carcinogen and reproductive toxicant.

Under Prop 65, companies that potentially expose consumers to chemicals have to post a warning notice of the exposure. California often has a “safe harbor” limit for these chemicals, below which companies don’t have to warn. But the lab results from six fake meat products show that just one serving could expose consumers to levels of acrylamide that exceed this limit.

View the lab results here.

Full disclosure: We’ve been critical of Prop 65 in the past. But the law is the law, it’s still on the books in California, and we believe everyone should play by the same rules. source

How to Test Eggs for Freshness? Testing Eggs for Freshness

The Truth News — Wed, 08 Mar 2023 00:17:26 +0000

How to Test Eggs for Freshness? Testing Eggs for Freshness

Four Simple Tricks to Decide Whether to Keep or Toss

Although there is a date stamped on the side of an egg carton, that isn’t always a good indication of whether the eggs inside are fresh. Some dates are when they were packed (and often written in code) while others are best-buy dates. The American Egg Board recommends eggs be used four to five weeks after they were packed, but we may not always know when that was.1 In addition, if you remove the eggs from the carton when you return from the store, or purchase fresh eggs from a farm, you may be uncertain how old they are.

Luckily, there are three easy ways to determine if your eggs are still safe to eat, and all you need are your senses, a bowl, and some cold water. Keep in mind that if one egg tests bad it doesn’t mean the rest of the eggs should be tossed.

1. The Sink or Float Test

The egg float test has been around for a very long time.

It is a useful and fast way to check if eggs are fresh and safe to eat.

The interesting thing is nobody really knows how it came to be and where this test came from.

Is this test accurate or just a myth?

In this article we will explain everything you need to know about the egg float test including how to perform the test, if it is accurate and much more…

Like a fun science experiment you may have done in school, this freshness test is not only simple but also can tell you the approximate age of the egg. All you need is the egg, a bowl, and cold water. Fill the bowl with enough cold water to completely cover the egg, then gently drop the egg into the bowl of water.

Your egg can do one of three things and each will determine its freshness. If it sinks to the bottom, turns on its side, and stays there, it is very fresh. If the egg sinks but floats at an angle or stands on end, the egg is a bit older (a week to two weeks old) but still okay to eat. If the egg floats, it’s too old and should be discarded. (If you are looking for more of a cut-and-dry test, dissolve 2 tablespoons of salt in 2 cups of cold water. Put the egg in the water—if it sinks, it’s good; if it floats, it’s too old.)

The science behind this is that as eggs age, the shell becomes more porous, allowing air to flow through. The more air entering through the shell, the larger the air cell becomes (the pocket of air between the membrane and shell in the larger end of the egg). The air sac, when large enough, makes the egg float.

How To Do The Egg Float Test

The float test is a quick and simple way to check the freshness of an egg. It will take you about ten minutes to check a carton.

You will need a bowl that is large enough to put an egg in the bottom and be able to cover it with two inches of water.

Now before you start the egg float test you need to check your egg for cracks. There should be no cracks in the shell so discard any cracked eggs before testing.

Step 1: Fill your bowl with 2 inches of cold water.

Step 2: Gently put an egg into the water making sure that you do not drop it in.

Now you need to watch the egg to see how fresh it is.

Egg stays at the bottom of the bowl and is lying on its side: Very fresh.
Egg touching the bottom of the bowl but one end is slightly raised: Egg is still fresh.
Egg stands upright but remains underwater: It is a bit older but still fresh enough to eat.
Egg floats to the top: The egg is very old and could be rotten – you should throw away this egg.

There you have it – could it be any easier to do?

Is The Egg Float Test Real

Put simply, yes.

The egg float test works and is surprisingly accurate.

People who do this test a lot can tell you with great accuracy how many days old an egg is.

However for our purposes all we need to know is the basics, can we use the eggs or should we toss them? And the egg float test answers this questions with a simple but accurate guide to freshness.

Some folks will tell you that they can sex an egg by floating the egg however this is a myth that is right up there with the shape of the egg and the needle and thread method!

How Does It Work

While the test sounds like magic there are some simple physics and breakdown of organic matter at play.

When an egg is very fresh most of the space inside the shell is taken up with solid matter (yolk and albumin). A fresh egg only has a relatively small air sac at this time. Because of this when the egg is placed in water it will stay submerged because the egg is heavier than the water.

However because eggshells are porous, the older an egg gets the more air will enter the egg.

If you want to learn more about chicken eggs then read how do chickens make eggs? egg laying explained.

Over time the solid matter inside the egg will shrink, this leaves more room inside the egg for air. An egg that is very old will have little content since it will have dried, but it will have lots of air inside the shell.

Once enough air fills the inside of the shell the air will give the egg enough buoyancy to float.

When you place an old egg in the water it will float because it is full of air.

2. The Egg White Test

The second easy method is the plate test.

Simply crack an egg onto a plate and watch how it settles.

This test is a good choice if you plan on cracking the egg before cooking it or adding to a baked good recipe. Crack the egg onto a plate or other flat surface and look closely at the consistency of the egg white—it should be slightly opaque, not spread out too much, and appear thick and somewhat sticky. If it is watery, clear, and runny, the egg has lost its freshness. This is due to the fact that as eggs age, the white turns liquidy and breaks down. You will also notice the yolk will be slightly flat on top instead of rounded.

3. The Sniff Test

Often when there is a sulfur odor—whether it has to do with eggs or not—it is described as “rotten eggs.” That is because eggs that have gone bad emit a strong sulfur smell. If the egg is really past its prime, you may smell it through the shell; but if not and you’re concerned about freshness, take a whiff after you crack it.

Whether to Toss or Use

Obviously, if your egg fails any of these tests, you should get rid of it. But if the egg is showing signs of age but not ready for the trash, you can still use it. Older eggs are ideal for hard boiling—since the air cell is larger, there is more space between the shell and the egg, making it easier to peel.

Proper Egg Storage

Eggs should be stored in the refrigerator in the carton they came in.1 The packaging helps keep out odors and flavors from other foods in the fridge and protects the eggs from breakage. Also, you can use the date stamped on the carton as a guide. Make sure to keep the eggs upright, so the larger end is facing up; the yolk is more prone to spoiliage than the white, and this position keeps the air cell at the top, reducing the chances of harmful bacteria from making its way into the yolk. You can also freeze eggs for longer storage.

Egg Cooking Safety

Because salmonella and other pathogenic bacteria are present in most eggs, it is recommended that you should always cook your eggs to well done.2 The bacteria can be inside the shell, so even if you wash the egg or soft-cook it, you could get sick if it’s undercooked. Always cook fried eggs to well done, cook scrambled eggs until they are 165 F, and cook hard-cooked eggs until they are completely firm. And always refrigerate cooked eggs.3 While it’s true that most eggs are not contaminated, if one is, you can get very sick.

If someone in your home has a compromised immune system, is pregnant, or is young or elderly, consider buying pasteurized eggs. (Pasteurized eggs are also good to use in recipes calling for raw eggs, like hollandaise sauce.) These are eggs that have been quickly heated to a temperature high enough to kill bacteria but low enough so the egg remains uncooked. Follow expiration dates to the letter with this product.

source source