Anti-Aging Effects Of L -Arginine

On This Page

1. Nitric Oxide and NOS
2. Blood Flow and Pressure
3. Arginine Health Benefits Dosage, Side Effects

L-arginine is one of the most metabolically versatile amino acids. In addition to its role in the synthesis of nitric oxide, l-arginine serves as a precursor for the synthesis of polyamines, proline, glutamate, creatine, agmatine, and urea. Several human and experimental animal studies have indicated that exogenous l-arginine intake has multiple beneficial pharmacological effects when taken in doses larger than normal dietary consumption.

4.1 Nitric Oxide and NOS

L-arginine (2-amino-5-guanidino-pentanoic acid) is a conditionally essential, proteinogenic amino acid that is a natural constituent of dietary proteins ( 1 ). Besides its role in protein metabolism, l-arginine is involved in various metabolic pathways, such as the synthesis of creatine, l-ornithine, l-glutamate, and polyamines ( 2 ). Decarboxylation of l-arginine can produce agmatine, a biogenic amine metabolite. L-arginine is also involved in protein degradation by the ubiquitin-proteasome pathway ( 2 ).

L-arginine is a semi-essential amino acid that is particularly rich in certain foods such as meats and nuts. L-arginine is the substrate for the enzyme nitric oxide synthase (nos), which is responsible for the production of nitric oxide. Nitric oxide produced in the vascular endothelium by endothelial nos is responsible for smooth muscle cell relaxation and essential for reducing blood pressure.

4.3 Blood Flow and Pressure

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Being anti-inflammatory in nature, l-arginine helps reduce the level of inflammation in the blood vessels. Individuals suffering from coronary heart diseases are directed to consume l-arginine supplements as it helps improve cardiovascular health and function. L-arginine helps reduce high blood pressure and improves blood flow by unblocking the clogged arteries.

By improving blood flow in the body, some proponents claim that l-arginine may help heart conditions, such as chest pain (angina), high blood pressure, leg cramping, and weakness due to obstructed arteries (a condition known as intermittent claudication), and erectile dysfunction (ed). Some people use l-arginine to boost the immune system, improve athletic performance, shorten recovery time after surgery, and promote weight loss.

The two main functions of l-arginine in the human body are to make nitric oxide and to create proteins to build muscle and other tissues. For both of these paths, there are many health benefits that can be seen. Lowered blood pressure
when nitric oxide is in the blood, it helps to dilate, which means to open up, the blood vessels.

6 L-Arginine Health Benefits Dosage, Side Effects

L-arginine is a conditionally essential amino acid that plays a role in building the proteins in our body. Although arginine is synthesized in the body, it is not made in sufficient quantities to meet the metabolic requirements during certain health conditions. In such cases, l-arginine supplements may help. This nutritionally essential amino acid has many health benefits and has been used to treat several ailments.

This nutritionally essential amino acid has many health benefits and has been used to treat several ailments. It may treat heart disease, reduce high blood pressure, ease inflammation in the digestive tract, aid diabetes treatment, heal wounds, and boost immune health. This article discusses the potential health benefits, dosage, risks, and side effects of l-arginine. Read on to know more.

 

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Best Anti Aging Supplements For Men

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1. Zinc At The Top Of The List
2. Zinc And Sexual Health
3. Zinc And Prostate Cancer
4. Food Sources For Zinc
5. Have You Heard of Fisetin
6. Reduces Inflammation
7. Fisetin And The Heart
8. Collagen for Connective Tissue
9. Vegetable Nitrates
10. Garlic and Health
11. Garlic Can Reduce Blood Pressure
12. More Garlic Benefits

When it comes to health there are no better supplements than the ones found in your diet. I believe that a healthy body comes from a healthy lifestyle. That being said, sometimes supplements can help. Especially when you consider the mass production of our foods today. If you are a male in your 30s or beyond here are some supplements that you may want to consider.

Zinc At The Top Of The List

When it comes to men’s health, for me, zinc is at the top of the list. Zinc has many different roles within the body. It is involved in your immune health, cell division, wound healing and much more. Another important role for zinc within the body of men is testosterone levels. Zinc deficiency has been linked to low testosterone. Research has shown that zinc can help increase testosterone levels and boost sexual competency. Zinc is an important trace mineral for a man’s prostate and protecting against tumor development.

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Some of the side effects of zinc deficiency include slow growth in children weight loss lack of appetite if not addressed, a zinc deficiency can result in hair loss, eye and skin lesions, and delayed wound healing, among other things. Low zinc is a known culprit in cases of hypogonadism and impotence. Showed a very clear relationship between zinc and testosterone levels. Young men were fed a diet including very little zinc so that they developed a zinc deficiency.

Zinc And Sexual Health

Several clinical trials and studies have looked at the link between zinc and sexual health in men. It has been found previously that zinc seems to play a role in sperm production. Additionally, zinc also assists in the stimulation of hormone production. First, it should be noted that zinc may not have a direct impact on erectile function. This, however, does not mean a deficiency will not affect male sexual health and performance.

Zinc And Prostate Cancer

Zinc also plays an important role in the cell. Since zinc is an antioxidant, it helps protect your cells from oxidative stress. These harmful free radicals, aka “oxidative stress,” can cause disease, aging, and cancer. This antioxidant property also makes zinc a great boost for immune health.

In some studies, amounts of zinc more than 40 mg per day have been administered under medical supervision to treat specific conditions. Should you get tempted to take more than 40 mg per day of zinc, check with your doctor first. Side effects of taking too much zinc can make you feel as miserable as when you have a deficiency.

Mild zinc deficiency is relatively common. If you cannot get an adequate amount of zinc from your diet or if you have a medical condition, you may need to take a zinc supplement. Some reasons that you may be at risk for low levels of zinc in your body could be the result of a restricted diet: vegetarians may need up to 50 percent more than the RDA for zinc due to the low bioavailability of zinc from plant-based.

Food Sources For Zinc

Some food sources high in zinc that you may want to add to your diet include wheat germ, oatmeal, cottonseed flour, pumpkin seeds, wheat bran, and ground ginger. Some herbs that are high in zinc include burdock, cayenne, chamomile, dandelion root, hawthorne, licorice, and spirulina. Other foods to consider high in zinc, egg yolks, legumes, lima beans, mushrooms, soybeans, and seafood.

Have You Heard of Fisetin

Fisetin is a yellow plant pigment and chemical that’s found naturally in foods, especially fruits and vegetables. It is a flavonol, a yellow plant pigment that belongs to the flavonoid group of polyphenols. It gives color to many different fruits and vegetables.
Compared to now-famous plant antioxidants like resveratrol and quercetin, fisetin was unfairly ignored for far too long. It wasn’t until recent years that researchers became increasingly interested in its medicinal potential. Science teams are currently exploring its ability to slow the aging process and extend lifespan.

Research shows that fisetin has the ability to scavenge free radicals that have significant biological effects. These oxygen radicals can damage lipids, amino acids, carbohydrates, and nucleic acids. When we don’t consume enough antioxidant foods, there’s an imbalance of oxygen species that can inhibit the body’s ability to defend itself.

Data suggest that fisetin possesses antiproliferative properties against several cancers, which means that it may inhibit tumor cell growth. Researchers believe that it has potential value in cancer prevention and treatment, as it may reduce the growth of new blood vessels) and suppress tumor growth.

Reduces Inflammation

If you’re looking to increase your consumption of anti-inflammatory foods, start reaching for those strawberries. Strawberries are high in fisetin.

Fisetin and the heart

A number of studies have also found that fisetin is good for the heart. It can help protect the heart’s health in a number of ways. It may protect against oxidative stress and may also help reduce cholesterol and blood pressure.

One animal study found that fisetin helped improve heart function and health in rats that had an abnormal thickening of the heart’s walls. Another study found that fisetin protected the heart tissue and improved function following damage caused by a heart attack.

Whether you decide to supplement with Fisetin or not this is one supplement to keep an eye on with regard to healthy aging!

Foods high in fisetin include strawberries, apples, mangoes, and grapes. Vegetables high in fisetin include tomatoes, onions, and cucumbers.

Collagen for Connective Tissue

Collagen is a connective tissue protein that works like “scaffolding”, holding the body’s cells together to provide them with strength, structure, and flexibility. Collagen is the most important building block of cartilage, tendons, bones, muscle, and blood vessels, and is the main structural component (75%) of the skin.

Why do i need to supplement with collagen? As we age and get older, the production of collagen begins to slow down, as with most processes in the body. When this happens, our skin becomes less elastic and more fragile. You may also notice that your hair begins to lose its color and your joints aren’t as flexible. One way to prevent this decline is by supplementing your diet.

Pain, inflammation, loss of bone density, cartilage degeneration, loss of elasticity in the skin, and slower recovery from physical activity are all signals for the body to urgently send collagen, the body’s most effective “repair material” to those cells.

While everyone starts out losing collagen in adulthood at the same rate, it increases drastically for women during menopause, and eventually slows down to a loss of 2% per year — but that initial rate of 1% per year remains constant for men. Still, no matter your gender, taking collagen supplements can be beneficial to your health.

There are no foods that have a meaningful or effective amount of collagen (except for bone broth ), so that means that you need to take it as a supplement, like perfect keto grass-fed keto collagen, for it to be bioavailable and effective in getting the benefits listed above.

Vegetable Nitrates

Actually, this is not a supplement at all. It is nitrates that are found in vegetables. Considering that nitrates in meat have been linked to cancer you want to avoid those nitrates.

As we age (starting around age 40), the body naturally begins to produce less nitric oxide. The nitric oxide you produced in your twenties could be reduced by half or more in your 50, 60s, and beyond. If you can’t produce adequate NO, you might have an increased threat of major health conditions, such as heart issues, diabetes, and erectile dysfunction.3

The best nitric oxide foods are the most plentiful in dietary nitrates. These are nutrients that are discovered in a variety of foods and supplements. Your body uses them in the production of nitric oxide.

Plant nitrates are quite beneficial and help the body produce an important molecule called nitric oxide (N.O.). Over 160,000 scientific articles have been released about different elements of nitric oxide. The studies have shown that nitric oxide supplies a wide range of health benefits, including delivering oxygen and other nutrients to your muscles and tissues Research studies recommend that increasing N.O. levels might have similar benefits to high blood pressure medications.

Foods high in dietary nitrateS consist of leafy greens, dark chocolate, beets, citrus fruits, watermelon, and pomegranates. Supplements like Cardio Cocktail can also support nitric oxide production. These supplements provide the body with the right combination of amino acids and vitamins to allow for nitric oxide production.

Garlic and Health

Garlic nutrition contains countless vital nutrients — flavonoids, oligosaccharides, amino acids, allicin and high levels of sulfur Eating this spice regularly has been proven to provide unbelievable health benefits.

Garlic Can Reduce Blood Pressure

Modern research has focused on garlic’s potential to reduce the risk of heart disease and cholesterol levels. Several studies suggest that garlic makes platelets (the cells involved in blood clotting) less likely to clump together and stick to artery walls, therefore acting as an anticoagulant and reducing the risk of heart attacks.

More Garlic Benefits

High doses of garlic may prevent organ damage caused by heavy metals. The sulfur compounds in this herb can drastically reduce lead levels in the blood. They may also prevent the signs of toxicity, such as headaches and blood pressure, and also can aid in better absorption of iron and zinc in the blood.

A 2012 report published in basic and clinical pharmacology and toxicology reveals that garlic can be effective in reducing blood and tissue lead concentrations among human beings and animals alike.

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Increasing Nitric Oxide to Lower Blood Pressure

Why is nitric oxide important in the body? Nitric oxide is a nutrient we constantly produce. But certain deficiencies are said to be associated with low levels of nitric oxide. Accumulated research suggests that the supplementing of nitric oxide in the body may diminish pain and boost the immune system, which can lead to improved healing. What is more, research suggests that giving post-surgical patients this type of drug may be able to shorten the hospital stay. Researchers are also looking at how nitric oxide cuts down on damage to body cells during surgery.

According to an October 2015 study published in the Journal of Pharmacological Sciences, nitric oxide affects a variety of cellular processes. It is a free radical that is a potent vasodilator. The Mayo Clinic says vasodilators are medications that open (dilate) the blood vessels by affecting the muscles in vein and artery walls. Nitric oxide in the body ensures blood can flow more easily through your vessels, keeping the heart from working too hard and bringing down the blood pressure.

Nitric oxide is produced by nearly every type of cell in the human body and one of the most important molecules for blood vessel health. It’s a vasodilator, meaning it relaxes the inner muscles of your blood vessels, causing the vessels to widen. Nitric oxide increases blood flow and lowers blood pressure.

Supplements that increase nitric oxide in the body make up one of the most popular supplement categories today. These supplements don’t contain nitric oxide itself. However, they contain compounds that your body can use to make nitric oxide and have been shown to provide many benefits for health and performance.

The body produces nitric oxide to help regulate blood pressure and to ease muscular and joint pain, but when your body produces too little, it can cause problems. The less blood flow through the vessels and the fewer impediments to blood flow are common reasons for the low production of nitric oxide. Here are some suggestions for boosting your supply of nitric oxide, either by dietary means or supplement formulations.

Foods that can Boost Nitric Oxide

There are a wide variety of nitric oxide foods that can be included as part of a healthy and balanced diet that ensures you get enough nitrates in your body to produce nitric oxide.

Beets are a great source of dietary nitrates, which the body converts to nitric oxide. A December 2015 study published in the International Journal of Food Sciences and Nutrition showed that the amount of nitric oxide in the body increased after drinking 100 milliliters (3.4 ounces) of beet juice.

The study showed that just a cup of beet juice a day for 4 weeks led to a significant 8 point drop in blood pressure due to an increase in NO. Since NO relaxes blood vessels, healthier blood pressure is one of the most common benefits of the regular intake of beet nitrates.

Dark chocolate is a rich source of flavonoids, which the body can convert to nitric oxide. An April 2018 study in Sports Medicine showed that supplementing with cocoa flavanols may improve vascular function, alter fat and carbohydrate burning during exercise and reduce exercise-induced oxidative stress without affecting exercise performance.

Citrus Fruits can help! When it comes to oranges, grapefruit, lemons, and limes, the first thing most of us think about is the vitamin C content. Also known as ascorbate, vitamin C boosts nitric oxide production by enhancing levels of nitric oxide synthase, an enzyme the body needs to make it, as shown in a May 2012 study in Free Radical Biology & Medicine.

Leafy greens are full of nitrate, which the body needs to create nitric oxide. According to a March 2017 study published in the African Journal of Traditional Complementary and Alternative Medicines, greens such as spinach, kale, and arugula contain a significant amount of nitrates.

Watermelon is a rich source of citrulline, an amino acid the body converts to arginine before converting to nitric oxide. In a January 2017 study in Current Opinion in Clinical Nutrition & Metabolic Care, watermelon supplementation was shown to reduce resting blood pressure and improve exercise performance.

Nuts and seeds have a high concentration of the amino acid arginine. A May 2016 study published in Nutrients found that there is a strong association between dietary intake of L-arginine and serum levels of nitric oxide because l-arginine promotes nitric oxide production.

Nitrates to Include In Your Diet

Nitrates tend to be most concentrated in plant foods that are closest to the source; the roots. As such, fruits tend to contain significantly fewer nitrates than, say, root vegetables or leafy greens. Nevertheless, a few fruits provide dietary nitrate. Apples are among these.

Although they do not contribute to nitrates directly, research shows that the unique, potent natural antioxidants in pomegranate and pomegranate juice help to enhance the biological functions of nitric oxide. They accomplish this by preventing the oxidative loss of NO.

Like other fruits, bananas cannot come close to vegetable sources of nitrates, such as beetroot, or even spinach. But as a fruit, they have relatively higher amounts of nitrate.

Supplements That Can Help

Another amino acid called citrulline also impacts nitric oxide because it is used to produce arginine. Citrulline may increase the amount of arginine in your blood plasma better than taking arginine supplements, reports Huntington College of Health Sciences.

Your body produces a sufficient supply of citrulline, which is good because it is not found in many foods. Watermelon is an excellent source, as well as one of the few foods containing citrulline. You’ll also get a small amount from walnuts, cucumbers, cantaloupe, and the milk protein casein.

Not too many people know about nitric oxide and how it promotes cardiovascular health. But our body’s production of nitric oxide actually plays a crucial role in keeping our blood vessels flexible to increase blood flow.

While it is best to eat foods that support nitric oxide production supplements can help. The supplement we have seen the best results from is Cardio Cocktail. It is in a liquid form which makes for optimal absorption and the taste is actually quite good. This is unusual for a nitric oxide supplement. Most are produced as a powder and have been unable to produce a great tasting supplement in liquid form.

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Poop Transplant for Cancer Patients

For some cancer patients, a “poop transplant” could boost the positive effects of immunotherapy, a treatment designed to rally the immune system against cancer cells.

Not all cancer patients respond to immunotherapy drugs. For example, only about 40% of patients with advanced melanoma, a type of skin cancer, reap long-term benefits from the drugs, according to recent estimates. In trying to pinpoint the differences between patients who respond well to immunotherapy and those who don’t, scientists have zeroed in on a likely suspect: the microorganisms living in their guts.

Now, a new study, published Feb. 4 in the journal Science, adds to the growing evidence that having the right gut bugs can improve a patient’s response to immunotherapy, helping to stop disease progression or even shrink tumors.

In the study, scientists collected stool from melanoma patients who responded well to immunotherapy and then transplanted their feces (and microbes) into the guts of 15 patients who had never previously responded to the drugs. After the transplant, six of the 15 patients responded to immunotherapy for the first time, showing either tumor reduction or disease stabilization that lasted more than a year.

Related: 7 odd things that raise your risk of cancer (and 1 that doesn’t)

“The microbes really appear to drive the immunological … changes we see in patients, ” said study author Dr. Hassane Zarour, a cancer immunologist, co-leader of the Cancer Immunology and Immunotherapy Program at the University of Pittsburgh Medical Center Hillman and a professor of medicine at the University of Pittsburgh. The team linked the changes in gut bugs to changes in both tumor growth and the immune system; for instance, some of the participants showed an increase in specific immune cells and antibodies that appeared in their blood.

Despite the positive changes seen in some patients, fecal transplants likely won’t help all patients whose cancer resists immunotherapy, Zarour said. In the new study, for instance, nine of the 15 patients did not benefit from the treatment. As part of their research, the team began to sift through the differences between those who improved after the transplant and those who didn’t.

Gut bugs as a Cancer Treatment

The idea for combining fecal transplants with immunotherapy first came from studies in mice with tumors, in which the rodents responded differently to the drugs depending on which gut microbes they carried, according to Science Magazine. By tweaking the mice’s gut microbiomes — the collection of bacteria, viruses and other microbes in their digestive tracts — scientists found that they could improve this response, but they weren’t sure which microbes made the difference.

That said, mice’s responses to immunotherapy improved after they were given fecal matter from human cancer patients whose tumors had shrunk under immunotherapy. “When they took non-responding mice and gave them the right bugs … they could convert non-responding mice into responding mice, ” Zarour said.

Other research showed that when human patients took antibiotics, which alter the gut microbiome, they were less likely to respond to immunotherapy, providing more evidence that gut bugs make a big difference in people, too.

Having seen the positive effects of fecal transplants in mice, scientists began testing the treatment in humans, starting with a few small clinical trials.

In two such trials, led by researchers at Sheba Medical Center in Ramat Gan, Israel, patients received both fecal transplants and oral pills containing dried stool. The patients then took immunotherapy drugs called “checkpoint blockades, ” which essentially rip the brakes off of immune cells and help amplify their activity against tumors. A subset of these patients, who had previously not responded to the drugs, suddenly began responding.

The new study by Zarour and his colleagues echoes these positive results, but it also starts to address a crucial question: How do gut bugs boost the effects of immunotherapy?

To answer this question, the team closely analyzed the microbes present in the donor stool samples and the recipients, before and after fecal transplants. The team also collected blood and tumor cell samples to assess the patients’ immune responses over time, and computed tomography (CT) scans, to track tumor growth. They then used artificial intelligence to find connections between all these data points.

Out of the 15 patients, nine still didn’t respond to immunotherapy after their transplant. But of the six who did respond, one showed a complete response to checkpoint blockade drugs, meaning their tumors shrunk so much they were no longer detectable; two others showed a partial response, meaning their tumors shrunk but did not disappear, and three have shown no disease progression for over a year. In all six of these patients, the microbes from the donor’s stool quickly colonized their guts, and several of the newcomer bugs that were previously linked to positive immunotherapy outcomes increased in number.

Related: 11 surprising facts about your immune system

This change in gut bacteria triggered an immune response in the six patients, as their bodies began building antibodies that recognized the new bugs; these antibodies showed up in their blood. While the link between bacteria-specific antibodies and cancer is not well understood, it’s thought that some of these antibodies can help prime the immune system to hunt down tumor cells, Zarour said.

“The bugs that increased in the responders were really correlated with positive immunological changes, ” he said. These patients also built up a larger arsenal of activated T cells — immune cells that can target and kill cancer cells — while substances that suppress the immune system decreased. For example, a protein called interleukin-8 (IL-8) can summon immunosuppressive cells to tumor sites and therefore blunt the effects of immunotherapy; but IL-8 decreased in the six responsive patients.

Links between the gut and immune system

By comparison, cells that secrete IL-8 increased in the nine patients who didn’t respond to the fecal transplant. Based on this new data, “IL-8 seems to really play a critical role in regulating patients’ responses” to the two-part treatment, Zarour said.

Compared with the six responsive patients, the nine others also showed less pronounced immune responses to the transplant and lower levels of the noted beneficial bacteria; some even had dissimilar gut microbiomes to their fecal donors, suggesting the bacteria didn’t take over their guts as seen in responsive patients.

In general, “the gut microbiome may be just one of the many reasons we don’t respond to a specific treatment, ” Zarour said, so fecal transplants wouldn’t be expected to work for everyone. That said, the immune changes seen in the six responders, including the decline in IL-8, provide hints as to why it works for some people.

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In the future, these results will need to be validated in larger groups of melanoma patients, as well as other cancer patients whose disease resists immunotherapy, Zarour said.

Though small, the new trial provides “firm evidence that manipulating the microbiome can yield benefit when added to immunotherapy for cancer, ” said Dr. Jeffrey Weber, a medical oncologist and co-director of the Melanoma Research Program at New York University Langone Health, who was not involved in the research. Assuming these results hold up in other patients, though, fecal transplants may not be the best way to deliver helpful microbes into the gut, Weber said in an email.

The future may lie in ingesting the bacteria orally after they’ve been freeze-dried, Weber said. This approach could include something similar to the oral pills used in other trials, for example. Either that or scientists could isolate specific metabolites produced by the helpful bacteria and use those as drugs, Weber said. “The big question is, what metabolites from the ‘favorable’ bacterial species are actually responsible for benefit, ” he said.

Originally published on Live Science. 

 

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Debating the Connection Between Herpesvirus Infection and Alzheimer's Disease

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The role of persistent infection in the development of Alzheimer's disease is much debated these days, particularly now that the amyloid cascade hypothesis is under attack, following the continued failure of trials for therapies that clear amyloid-β. The biggest challenge in understanding Alzheimer's disease is the question of why only some people develop the condition, even given very similar lifestyle choices relating to weight, exercise, and other well-known influences on health. If the burden of persistent infection is an important contributing factor, it would very conveniently explain this otherwise puzzling outcome.

Herpesviruses and other persistent pathogens are hypothesized to contribute to the development of Alzheimer's via (a) greater chronic inflammation, and (b) greater generation of amyloid-β in its role as a part of the innate immune system response. The mechanisms make sense, but the data for herpesviruses in particular is contradictory, indicating that while herpesvirus infection may contribute to Alzheimer's disease, it likely isn't the major cause. Perhaps other persistent infections are also important. Or perhaps Alzheimer's is in fact a collection of distinct conditions with quite different roots that converge on the same situation of amyloid-β and inflammation in the brain.

New Data Questions Herpes-Alzheimer's Connection

The virus-Alzheimer's tug of war continues. New data across several studies weaken the proposed, and much-debated, association; its proponents are holding fast. A new epidemiology study reports a weak link between herpes and dementia. Researchers combed through four European population-wide healthcare databases and describe equivocal data. In Denmark and Wales, short-term antiviral drug use came with slightly fewer future dementia cases. Alas, in Germany and Scotland, this association did not hold. The opposite was also true; infected people who were not prescribed an antiviral had a slightly higher risk of dementia - but only in the German cohort. "The results are not very encouraging. Some of these associations held no matter what type of dementia or virus was considered. Because neither dementia subtype nor herpes subtype modified the association, the small but significant decrease in dementia incidence with antiherpetic administration may reflect confounding and misclassification."

Twenty-five years ago, researchers linked herpes simplex virus type 1 (HSV-1) infection with an increased risk of Alzheimer's disease (AD). She later spotted the virus hiding in amyloid plaques in brain tissue, and postulated that it may trigger the deposits. Since then, other connections have emerged. Scientists linked viral DNA in the brain to expression changes of genes involved in amyloid metabolism; others proposed that amyloid acts as an antimicrobial peptide.

Still, compelling evidence that viruses, particularly herpesviruses, cause AD remains elusive, although some researchers believe that the teeny irritants could speed disease along. The debate has taken on a new sense of urgency since reports that COVID-19 causes long-term neurological symptoms in a fraction of people who contract the disease. Scientists are just beginning to study this aspect of the infection. "Heterogeneous results are not terribly surprising given the complex nature of AD etiology and pathogenesis, which, so far, does not exclude an infectious component."

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source https://www.fightaging.org/archives/2021/02/debating-the-connection-between-herpesvirus-infection-and-alzheimers-disease/

An Example of Automating Nematode Lifespan Studies

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The growth of interest in targeting mechanisms of aging has led to the development of a variety of approaches to automating nematode life span studies, some of which are already available as commercial services. Researchers use the nematode species C. elegans in screening studies, searching for compounds that have effects on life span, or that interact with specific aging mechanisms of interest. Running ten thousand compounds through ten thousand dishes of nematode worms is a daunting prospect if it has to be carried out manually, and automation allows a great deal more screening to be accomplished for a given cost.

Despite being an extremely simple animal, C. elegans has differentiated organs such as nerves, skeletal muscles, and a digestive tract, and many mammalian animal-related genes are conserved. It is very useful for cutting-edge research in fields like genetics and molecular biology. However, while lifespan analysis of this nematode provides a great deal of useful information, previous lifespan studies had many limitations including 1) sensitivity to various stimuli at room temperature, 2) a long experimental time required for daily measurements, 3) a lack of objectivity due to a tendency for results to be dependent on experimental technique, and 4) the small number of samples that can be processed at one time making it unsuitable for simultaneous measurement of many samples.

The researchers attempted to resolve these issues by developing a new healthy lifespan assessment system that maintained the advantages provided by nematodes. They focused on determining the optimal conditions in a live cell imaging system for automatically measuring nematode survival, such as counting the number of nematodes in a sample, incubation temperature, medium thickness, feeding conditions, imaging interval, and survival determination method. This became C. elegans Lifespan Auto-monitoring System (C-LAS), a fully automated lifespan measurement system that can non-invasively measure a large number of samples (currently up to 36 samples). C-LAS uses overlapping images of nematodes to identify those that are moving, meaning they are alive, and those that are not moving, meaning they are dead.

The researchers performed a mini-population analysis of nematode healthy lifespan using a combination of C-HAS and statistical analysis on common nematodes with the same genetic background. They found that about 28% of the population had average lifespans, about 30% had long and healthy lifespans, about 35% had healthy lifespans but died prematurely, and about 7% had a long period of frailty. They also found that activating - either genetically - or through administration of the drug metformin - AMP-activated protein kinase (AMPK), which is closely associated with healthy life expectancy, dramatically increased the population with healthy longevity and reduced the population with long periods of frailty. Metformin is thought to increase healthy life expectancy in humans, and the present study supports this idea. Currently, clinical trials are underway to ascertain its association with healthy longevity.

Link: https://ewww.kumamoto-u.ac.jp/en/news/429/

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source https://www.fightaging.org/archives/2021/02/an-example-of-automating-nematode-lifespan-studies/

Further Investigations of Partial, Transient Cellular Reprogramming

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Reprogramming cells from old tissues into induced pluripotent stem cells has the effect of reversing many of the epigenetic changes that are characteristic of age, thus restoring mitochondrial function and other aspect of cell behavior. This is a limited rejuvenation: it can't do much about DNA damage, and nor can it make cells clear persistent molecular waste that even youthful cells struggle with. Nonetheless, applying reprogramming to living mice has produced benefits to health, suggesting that if the process can be sufficiently controlled, then it may be a useful basis for therapy - perhaps globally forcing cells to behave more as though they are in young tissues. Groups such as Turn.bio are investigating the use of partial and transient reprogramming, in search of a balance point at which cells are rejuvenated without losing their cell type or radically changing their behavior. Here, another groups reports on early results from their analogous efforts to develop a methodology of safe transient reprogramming.

Ageing is the gradual decline in organismal fitness that occurs over time leading to tissue dysfunction and disease. At the cellular level, ageing is associated with reduced function, altered gene expression and a perturbed epigenome. Somatic cell reprogramming, the process of converting somatic cells to induced pluripotent stem cells (iPSCs), can reverse these age-associated changes. However, during iPSC reprogramming somatic cell identity is lost, and can be difficult to reacquire as re-differentiated iPSCs often resemble foetal rather than mature adult cells. Recent work has demonstrated that the epigenome is already rejuvenated by the maturation phase of reprogramming, which suggests full iPSC reprogramming is not required to reverse ageing of somatic cells.

Here we have developed the first "maturation phase transient reprogramming" (MPTR) method, where reprogramming factors are expressed until this rejuvenation point followed by withdrawal of their induction. Using dermal fibroblasts from middle age donors, we found that cells reacquire their fibroblast identity following MPTR, possibly as a result of persisting epigenetic memory at enhancers. Excitingly, our method substantially rejuvenated multiple cellular attributes including the transcriptome, which was rejuvenated by around 30 years as measured by a novel transcriptome clock. The epigenome, including H3K9me3 histone methylation levels and the DNA methylation ageing clock, was rejuvenated to a similar extent.

The magnitude of rejuvenation instigated by MTPR is substantially greater than that achieved in previous transient reprogramming protocols. MPTR fibroblasts produced youthful levels of collagen proteins, suggesting functional rejuvenation. Overall, our work demonstrates that it is possible to separate rejuvenation from pluripotency reprogramming, which should facilitate the discovery of novel anti-ageing genes and therapies.

Link: https://doi.org/10.1101/2021.01.15.426786

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source https://www.fightaging.org/archives/2021/02/further-investigations-of-partial-transient-cellular-reprogramming/

Cellvie Seed Funded to Develop Mitochondrial Transplantation as a Therapy

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Mitochondria are the power plants of the cell, producing chemical energy store molecules to power cellular processes. They are also embedded deeply into may core functions of the cell, from replication to programmed cell death. Mitochondrial function declines throughout the body with age, for reasons that are likely downstream of other more fundamental damage. Mitochondrial dynamics change in ways that make mitochondria more resilient to removal via mitophagy when worn or broken, and mitophagy itself loses efficiency. This may or may not be connected to mitochondrial DNA damage. It is unclear as to whether the progressive accumulation of mutations in mitochondrial DNA has a broad effect on function in most cells, or only results in a small number of highly dysfunctional cells.

Regardless, is it possible to effectively address mitochondrial dysfunction by delivering new mitochondria in large volumes into the body? It is clearly the case that cells ingest whole mitochondria and put them to work when given the opportunity. This option hasn't been aggressively pursued to date by the core rejuvenation biotechnology community, as it seems likely that it could only have a short term benefit. One can argue that functional mitochondrial placed into a dysfunctional environment will soon go the way of their predecessors, and for the same reasons: altered dynamics and diminished mitophagy. Similarly cells overtaken by dramatically broken mitochondria are overtaken because those mitochondria have a replication advantage over their functional peers. In both cases we suspect that transplanted mitochondria wouldn't last in their pristine state.

Now, however, a number of groups are working on practical approaches to mitochondrial transplantation, including today's example, focused initially on applications in medicine in which short term benefits are sufficient. It will be interesting to see how these efforts progress. If it is possible to restore mitochondrial function broadly in the body for at least months, that may prove to be worth the effort in the context of aging. There are other interesting questions to answer along the way, as well. For example, what happens when you replace a large fraction of native mitochondria with mitochondria that contain a different mitochondrial DNA haplogroup? Possibly nothing bad. Perhaps one can swap out any mammal's mitochondrial genome for a better, more efficient, more resilient, artificially augmented mitochondrial genome without any downside - a worthy long-term goal if it is straightforwardly attained. But we just don't know in certainty.

Link: Harvard spin-off Cellvie Inc closes $5M seed round

Cellvie was founded in the US in 2018 and is headquartered close to Zürich, Switzerland. The founders pioneered the approach of mitochondria augmentation and replacement and the team has now set out to leverage the therapeutic potential of mitochondria for a new treatment modality in ischemia-reperfusion injury, aging and beyond. Mitochondria play a crucial role in the aging process, activating factors and metabolic pathways involved in longevity. Their dysfunction impacts on both lifespan and healthspan. "But treating mitochondria has proven to be an arduous challenge. That is why we turned to introducing healthy, viable mitochondria into cells where these organelles are impaired. To great effect. We can sustainably reinvigorate cells' failing energy metabolism."

The potential of therapeutic mitochondrial transfer was recently demonstrated in a clinical investigation at Boston Children's Hospital; paediatric patients on heart-lung-support after suffering a cardiogenic shock received the treatment to revitalise their heart muscle. 80% of these children experienced myocardial recovery, which compares with an expected 29%. "The investment will enable us to pursue the platform broadly, including a first application in aging, where the need for mitochondria-recovery is particularly dear."

To date, Cellvie has focused primarily on ischemia-reperfusion injury (IRI), which manifests itself whenever the blood flow to a part of the body is interrupted and subsequently reintroduced. Well-known medical conditions causing IRI include heart attacks, strokes, and organ transplantation. Cellvie is also pursuing an indication in organ transplantation, for which the FDA awarded orphan drug designation in 2020. The capital injection will be employed for preparing for market, expanding Cellvie's product pipeline and to prepare an IND submission for a clinical study in kidney transplantation.

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source https://www.fightaging.org/archives/2021/02/cellvie-seed-funded-to-develop-mitochondrial-transplantation-as-a-therapy/

MOTS-c Upregulation Mimics Exercise to Improve Health and Extend Life in Mice

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Upregulation of MOTS-c improves mitochondrial function and has other less well explored influences on stress responses in cells. This might be considered a form of exercise mimetic therapy, given that MOTS-c upregulation is one of the outcomes of exercise. The result of artificial upregulation of MOTS-c in mice is improved health, greater exercise capacity, and extended life span. We should probably not expect life span effects produced by this sort of intervention to translate well to longer-lived mammals, given what we know of the effects of calorie restriction, exercise, and similar interventions that upregulate stress response mechanisms. Benefits to health are certainly plausible, however.

The study looked at the role of MOTS-c, one of several recently identified hormones known to mimic the effects of exercise. However, MOTS-c is unique because it is encoded in the small genome of mitochondria rather than the larger genome in a cell's nucleus. The research team tested how injections of MOTS-c affected mice of different ages by measuring physical capacity and performance in young (2 months), middle-aged (12 months), and old (22 months) mice. When the mice were presented with physical challenges - including maintaining balance on a rotating rod and running on an accelerating treadmill - mice of all ages who had received MOTS-c treatment fared significantly better than untreated mice of the same age.

Even groups of mice that had been fed a high-fat diet showed marked physical improvement after MOTS-c treatment and less weight gain than untreated mice. These findings echo previous research on MOTS-c treatment in mice, which also found that it reversed diet-induced obesity and diet- and age-dependent insulin resistance. Additionally, treating the oldest mice nearing the end of their lives with MOTS-c resulted in marked physical improvements. This late-life treatment improved grip strength, gait (measured by stride length) and physical performance, which was assessed with a walking test (running was not possible at this age)."The older mice were the human equivalent of 65 and above and once treated, they doubled their running capacity on the treadmill. They were even able to outrun their middle-aged, untreated cohorts."

To measure the effects of exercise on MOTS-c levels in people, the researchers collected skeletal muscle tissue and plasma from sedentary, healthy young male volunteers who exercised on a stationary bicycle. Samples were collected before, during and after the exercise as well as following a 4-hour rest. In muscle cells, levels of MOTS-c significantly increased nearly 12-fold after exercise and remained partially elevated after a four-hour rest, while MOTS-c levels in blood plasma also increased by approximately 50% during and after exercise and then returned to baseline after the rest period. The findings suggest that the exercise itself induced the expression of the mitochondrial-encoded regulatory peptides.

Link: https://gero.usc.edu/2021/01/20/exercise-protein-running-capacity-mice-mots-c/

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source https://www.fightaging.org/archives/2021/02/mots-c-upregulation-mimics-exercise-to-improve-health-and-extend-life-in-mice/

Longevity Gene INDY is Involved in Blood Pressure Control

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The INDY gene has been known to affect longevity in a range of species for quite some time, as I noted at length back in 2015. It is more than 20 years now since INDY was first discovered to affect fly aging, and work continues to link the outcomes on life span to specific effects on aging and cell function. INDY has effects on metabolism that look a lot like those connected to calorie restriction. A such, it tends to improve every aspect of aging, making it challenging to sort out what is cause, what is consequence, what is important, and what is a side-effect. The research noted here is a representative example of incremental progress in understanding the effects of INDY on aging. I doubt this to be a path that leads to any practical outcome for human health and longevity.

Researchers have presented data showing that the longevity gene mammalian Indy (mINDY) is involved in blood pressure regulation. Reduced expression of mINDY, which is known to extend life span in lower organisms and to prevent from diet induced obesity, fatty liver, and insulin resistance in mice, has now been shown to lower blood pressure and heart rate in rodents.

The authors provided mechanistic insights for the underlying physiological mechanism based on in vivo data in a genetic knock out model as well as microarray and in vitro studies. Furthermore, the hypothesis is supported by confirming critical effects in vitro using a small molecule inhibitor of mINDY. The authors conclude that deletion of mIndy recapitulates beneficial cardiovascular and metabolic responses to caloric restriction, making it an attractive therapeutic target.

mIndy deletion attenuates sympathoadrenal support of blood pressure and reduced arterial blood pressure and heart rate in a murine knockout model. Blood pressure was assessed invasively using intra-arterial pressure probes over several days. Urinary analysis for catecholamines and metanephrines as well as unbiased transcriptomic analysis of adrenal glands identified the affected biosynthetic pathways. Indeed, catecholamine biosynthesis was attenuated in mINDY-knockout adrenals, whereas plasma steroids and steroid hormone synthesis were unaffected.

In vitro studies on an adrenal cell line supported this hypothesis. mIndy codes for a carboxylic acid transporter protein expressed in plasma membrane. Citrate, the main substrate of the mINDY transporter, increased catecholamine content, while pharmacological inhibition of mINDY by a small molecule inhibitor blunted the effect.

Link: https://www.eurekalert.org/pub_releases/2021-01/dzfd-tlg012621.php

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source https://www.fightaging.org/archives/2021/02/longevity-gene-indy-is-involved-in-blood-pressure-control/

Amyloidosis Contributes to Muscle Aging, and NAD+ Upregulation Reduces Amyloid Burden

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Amyloids are misfolded proteins that can cause other molecules of the same protein to misfold in the same way, linking together into solid deposits that are disruptive to normal cell and tissue function. There are only a score or so of different types of amyloid in the human body, and most are conclusively linked to at least one age-related condition. In today's open access research materials, the scientists involved report on the involvement of amyloid-β (and potentially other amyloids) in muscle aging, connecting loss of mitochondrial function with the growing presence of amyloids.

In order to test the direction of causation in this relationship, the researchers first boosted mitochondrial function in old animals by increasing NAD+ levels. NAD+ is essential to mitochondrial function, but declines with age for a variety of reasons. The proximate causes are fairly well mapped, meaning a loss of efficiency in NAD synthesis and NAD recycling pathways, but connections to the underlying causes of aging remain to be discovered. In this study, improved mitochondrial function reduced the burden of amyloid in muscle tissue. Separately, the researchers also removed amyloid from tissues in a targeted way, and found that this improved mitochondrial function. Thus the relationship appears bidirectional. Amyloid degrades mitochondrial function, while forcing an improvement in mitochondrial function gives cells a greater ability to clear amyloid.

NAD+ can restore age-related muscle deterioration

The older we grow, the weaker our muscles get, riddling old age with frailty and physical disability. Researchers have now looked at the issue through a different angle: the similarities between muscle aging and degenerative muscle diseases. In the study, the scientists identify amyloid-like protein aggregates in aged muscles from different species, from the nematode C. elegans all the way to humans. In addition, they also found that these aggregates also impair mitochondrial function. Although aggregated proteins have been suggested to contribute to brain aging, this is the first time that they have been shown to contribute to muscle aging and to directly damage mitochondria.

But can the formation of the protein aggregates be reversed? To answer this, the researchers fed worms the vitamin nicotinamide riboside and the antitumor agent Olaparib, both of which boost the levels of nicotinamide adenine dinucleotide (NAD+), a biomolecule that is essential for maintaining mitochondrial function, and whose levels decline during aging. In the worms, the two compounds turned on the defense systems of the mitochondria, even when provided at advanced age. Turning on the so-called "mitochondrial quality control system" of mitophagy reduced the age-related amyloid protein aggregates and improved the worms' fitness and lifespan.

The scientists then moved on to human muscle tissue taken from aged subjects. Turning on the same mitochondrial quality control systems produced similar improvements in protein and mitochondrial homeostasis. The encouraging results led the researchers to test nicotinamide riboside in aged mice. The treatment also activated the mitochondrial defense systems and reduced the number and size of amyloid aggregates in different skeletal muscle tissues.

NAD+ boosting reduces age-associated amyloidosis and restores mitochondrial homeostasis in muscle

Due to the fact that mitochondrial function and proteostasis are essential to ensure cellular homeostasis, are functionally interconnected, and decline in aging, it is not surprising that mitochondrial dysfunction and abnormal proteostasis are involved in chronic age-associated neuromuscular proteinopathies, such as Alzheimer's disease (AD), and inclusion body myositis (IBM), a debilitating age-associated muscle disease. Although affecting different organs, AD and IBM are both protein aggregation diseases characterized by the accumulation of amyloid protein deposits. IBM is the most common muscle proteinopathy affecting the elderly; however, it is generally considered a rare disorder, with its overall prevalence still under debate. Skeletal muscle decay instead is one of the most prominent features of aging, characterized by loss of muscle mass and function and by a decline in mitochondrial function. In addition, muscle aging is also typified by dysfunctional proteostasis pathways, including altered ubiquitin-proteasome system (UPS) activity and defective autophagy. Currently, the mechanism underlying the collapse of proteostasis in the aging muscle is not fully elucidated, and it is furthermore unclear whether amyloid deposition, a hallmark of IBM, is also at play in the aging muscle.

Here, we report that, during natural aging, muscle tissues accumulate amyloid-like deposits, a process which is evolutionary conserved in C. elegans, in mouse and human muscle cells and tissues, with molecular features recapitulating some aspects of IBM. Moreover, we also discovered the reversible nature of these deposits, which can be reduced by interventions aimed at restoring mitochondrial homeostasis, such as by enhancing nicotinamide adenine dinucleotide (NAD+) metabolism, even at the onset of aging. Importantly, we show that reduction of the accumulation of amyloid-like deposits in aging is sufficient to improve muscle mitochondrial homeostasis.

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source https://www.fightaging.org/archives/2021/02/amyloidosis-contributes-to-muscle-aging-and-nad-upregulation-reduces-amyloid-burden/

Towards a Universal Epigenetic Clock for Mammals

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Epigenetic marks are constantly added to and removed from CpG sites on the genome, controlling gene expression and thus cell behavior. The pattern of epigenetic marks in any given cell shifts in response to environment and circumstances, and some of those changes are characteristic of the presence of the underlying molecular damage of aging. Epigenetic clocks can thus be constructed from weighted combinations of epigenetic mark status at various CpG sites in order to measure biological age. Existing epigenetic clocks are specific to a given species, but here researchers process an enormous amount of data from many species to produce epigenetic clocks that are universal to all placental mammals. If this result holds up well in further testing, then such universal clocks could help to speed up the development of therapies that target the mechanisms of aging.

Aging is often perceived as a degenerative process caused by random accrual of cellular damage over time. In spite of this, age can be accurately estimated by epigenetic clocks based on DNA methylation profiles from almost any tissue of the body. Since such pan-tissue epigenetic clocks have been successfully developed for several different species, it is difficult to ignore the likelihood that a defined and shared mechanism instead underlies the aging process.

To address this, we generated 10,000 methylation arrays, each profiling up to 37,000 cytosines in highly-conserved stretches of DNA, from over 59 tissue-types derived from 128 mammalian species. From these, we identified and characterized specific cytosines, whose methylation levels change with age across mammalian species. Genes associated with these cytosines are greatly enriched in mammalian developmental processes and implicated in age-associated diseases.

From the methylation profiles of these age-related cytosines, we successfully constructed three highly accurate universal mammalian clocks for eutherians, and one universal clock for marsupials. The universal clocks for eutherians are similarly accurate for estimating ages of any mammalian species and tissue with a single mathematical formula. Collectively, these new observations support the notion that aging is indeed evolutionarily conserved and coupled to developmental processes across all mammalian species - a notion that was long-debated without the benefit of this new and compelling evidence.

Link: https://doi.org/10.1101/2021.01.18.426733

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source https://www.fightaging.org/archives/2021/02/towards-a-universal-epigenetic-clock-for-mammals/

Evidence for Microglia to be Involved in the Depression Accompanying Neurodegenerative Conditions

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Chronic inflammation and activation of microglia in the brain may contribute to the depression that can accompany neurodegenerative conditions, as well as other diseases that feature persistently raised inflammation. Researchers here provide supporting evidence for that hypothesis. Microglia are innate immune cells of the central nervous system, and increased inflammatory behavior and senescence in this cell population is implicated in age-related neurodegeneration. Clearing senescent microglia can reduce inflammation and reverse tau pathology in animal models of tauopathies, for example.

Research has shown that microglial cells are activated in several neurological diseases, such as Alzheimer's disease, Parkinson's disease, and stroke. People who are affected by these conditions also often fall into a negative mood. Other previous research has suggested that inflammatory processes also play a role in the development of depression. This led the researchers behind the new study to examine more closely whether microglial cells are involved in regulating mood during inflammation. "The study showed that animals feel sick and uneasy when we activate the microglial cells. We demonstrate that two signal molecules, interleukin-6 and prostaglandin E2, are particularly important in these processes. It's not surprising that these signal substances are central, but we were a bit surprised that it is the microglial cells that release these molecules."

During inflammation, many processes are initiated in several cell types. One of the challenges in determining the role played by a specific cell type in the body, therefore, is to isolate its effects. In this study, the scientists used a technique known as chemogenetics, which enabled them to switch on the activity specifically in microglial cells in mice. The researchers activated the microglial cells when the mice were being kept in a certain type of surroundings. The mice subsequently avoided this type of surroundings, which the researchers interpret as showing that the animals disliked the experience. The mice also became less interested in a sweet solution, which they normally find very tempting.

In order to investigate whether the microglial cells are an important link between the immune system and mood, the researchers investigated what happened when microglial cells are inhibited. When the microglial cells were not available for activation, the mice did not feel poorly, even when they had inflammation. This reinforces the idea that these cells are necessary for the process. If further research demonstrates that the biological mechanism described in the study functions in the same way in humans, it may be possible in the long run to reduce symptoms of depression by inhibiting this mechanism.

Link: https://liu.se/en/news-item/hjarnans-immuncell-ligger-bakom-nedstamdhet-vid-inflammation-

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source https://www.fightaging.org/archives/2021/02/evidence-for-microglia-to-be-involved-in-the-depression-accompanying-neurodegenerative-conditions/