Benefits of Sermorelin w/GHRP2 in the First Six Months

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Sermorelin and GHRP2 both stimulate the patient’s own pituitary gland by binding to specific receptors that increase production and secretion of endogenous Human Growth Hormone (HGH).  GHRP2 also acts as an appetite suppressant allowing for increased weight loss.

First Month

Weight loss/Body fat reduction

Vivid dreams

Better, sounder sleep

Improved stamina

Optimistic attitude

 

Second Month 

Improved muscle tone

Increased strength

Improved skin tone

Improved nail growth

Better digestion

Weight loss/Body fat reduction

Improved vision

Enhanced sexual function

 

Third Month

Improved mental process

Enhanced productivity

Faster wound healing

Hair re-growth

Increased libido

Increased muscle size

Faster recovery from muscle soreness

Reduced PMS symptoms

Greater body flexibility

Reduced pain

 

Fourth Month

Heightened improvements with all of the above

At times improvements may seem to diminish or plateau

Rejuvenation is still a process. Benefits should resume with continued improvements

 

Fifth Month

Improved weight loss and reduction of inches

Improved skin texture and appearance

Skin thickening and greater elasticity

Reduction of skin wrinkles

Thickening of hair with a shiny, healthy appearance

Continuation of improved muscle tone

 

Sixth Month

Diminished cellulite

Improved resistance to colds, flu and other illnesses

Improved eyesight

Healing of old wounds

Disappearance of pain and soreness

Improved body contour

 

Contact us today for more information on Sermorelin/ghrps

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Understanding Inflammation

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Inflammation has been found to be an underlying cause in many diseases, making it a hot topic in the health media. But what do we really know about chronic inflammation and its effects on the body?

As scientists have searched for the mysteries behind the diseases most likely to afflict us, they have alighted on one factor common to virtually all of them: inflammation. Chronic inflammation, headlines now regularly state, has a role in a host of common and often deadly diseases, including Alzheimer’s, arthritis, cancer, diabetes, heart disease, and possibly even depression.

Unsurprisingly, this news brings with it a raft of self-proclaimed remedies purporting to fight inflammation. Diets, herbs, supplements, and exercise regimens have flooded the market with promises to keep inflammation in check and improve overall health.

But is there evidence that over-the-counter products or sweeping lifestyle changes will reduce inflammation’s damaging effects? Scientists caution that despite its current high profile, inflammation remains a mystery. “Basic science hasn’t yet answered the major questions about inflammation,” says Michelle Petri, a rheumatologist and a director of the Johns Hopkins Lupus Center. Researchers like Petri have been studying low-level inflammation as a culprit in a number of diseases for decades. What they have discovered has led to an emerging understanding of how lifestyle choices—like diet, dental health, and exercise—may influence inflammation and its potentially damaging downsides.

Despite its current high profile, Petri says, inflammation remains a mystery.


Inflammation is a vital part of the human immune system. When harmful bacteria or viruses enter your body, when you scrape or twist your knee, the body’s defense system kicks into high gear. Chemicals ramp up the body to fight, bathing the damaged area with blood, fluid, and proteins; creating swelling and heat to protect and repair damaged tissue; and setting the stage for healing.

Sentinel cells first alert the immune system to the presence of invaders. Another set of cells releases chemicals that signal the capillaries to leak blood plasma, which surrounds and slows down trespassers. Another group of sentinels, called macrophages, releases cytokines, which are specialized germ fighters. Immunizing B- and T-cells join in, destroying both the pathogens and the tissues they have damaged. Finally, a last wave of cytokines is released to end the job and signal the immune system that its work is done. Its mission completed, the immune system calls off its dogs.

When our body’s powers of correction go wrong, however, they can work against us. Think of the acute heat and swelling that protect us during a normal immune response—a fever, or the redness and pain that surround a new injury, for example—and you can get a hint of what chronic inflammation is. Unlike the inflammation that follows a sudden infection or injury, the chronic kind produces a steady, low level of inflammation within the body that can contribute to the development of disease. It’s the result, in part, of an overfiring immune system. Low levels of inflammation can get triggered in the body even when there’s no disease to fight or injury to heal, and sometimes the system can’t shut itself off. Arteries and organs break down under the pressure, leading to other diseases, including cancer and diabetes.

Scientists don’t fully understand how the immune system becomes short-circuited, but they have long known that some diseases, such as lupus and rheumatoid arthritis, emerge after the immune system has gone awry and attacked healthy tissue. Increasingly, as Americans and other Westerners live longer and get larger (35 percent of Americans are obese), researchers have also found that low-level immune responses triggered by extra weight and a lack of exercise can contribute to the development of other illnesses.

“For a long time, we had the idea that inflammation was involved in certain autoimmune diseases, but now we’re seeing this lower level of inflammation in people who are obese and people who are sedentary,” says Kimberly Gudzune, a physician at Johns Hopkins and a clinical researcher who focuses on obesity. “We see a link between obesity and some diagnostic markers for inflammation, but we don’t know what causes them. We worry that there’s something brewing for these people, that they are at higher risk for heart disease, cancer, and diabetes.”

‘We see a link between obesity and some diagnostic markers for inflammation, but we don’t know what causes them. We worry that there’s something brewing for these people, that they are at higher risk for heart disease, cancer, and diabetes.’

Researchers have discovered that fat cells can trigger the release of a steady, low hum of cytokines that, in lieu of an invader to attack, go after healthy nerves, organs, or tissues. As we gain weight, the release becomes prolific, affecting our body’s ability to use insulin, sometimes leading to type 2 diabetes.

They have also learned that inflammatory cells can have an effect elsewhere in the body—for example, chronically infected and inflamed gums in the mouth can cause damage that leads to heart attack and stroke. And they know that inflammation contributes to congestive heart failure and uncontrolled hypertension, and that it somehow has a role in the tangled cells that are the hallmarks of Alzheimer’s disease.

Researchers continue to find answers about how inflammation contributes to cancer. Inflammatory cells produce free radicals that destroy genetic material, including DNA, leading to mutations that cause cells to endlessly grow and divide. More immune cells are then called in, creating inflammation that feeds the growth of tumors.

The link between inflammation and cancer can sometimes be direct. When too much stomach acid—a feature of the immune system that evolved to fight foodborne bacteria—creeps up the esophagus, it causes inflammation and chronic heartburn. Extended exposure to this acid changes the nature of the cells lining the esophagus, increasing the risk of cancer.

In colon cancer patients, certain communities of bacteria associated with diarrhea can create cancer with help from inflammatory cytokines. Cells protected by mucus can become inflamed when that mucus wall is breached by bacteria, says Cynthia Sears, a doctor who specializes in infectious disease research at Johns Hopkins. “The lining in the colon makes peptides”—short chains of amino acids that act to protect the lining of the organ—“to thwart bacteria. If there aren’t enough peptides, bacteria can get a foothold, which means even more bacteria,” Sears says. As inflammation ramps up to fight it, so does the risk of cancer.


If inflammation is the behind-the-curtain factor in so many diseases, what can we do to keep it at bay? Researchers admit that they’re still figuring this out.

Petri has studied lupus for more than three decades and has been investigating the effects of chronic inflammation. “Lupus is basically friendly fire,” Petri explains. “We can’t get the immune system to calm itself down.”

Treating chronic inflammation, whether for lupus or other chronic ailments, is a challenge. Researchers have an idea that inflammation exists as part of a self-reinforcing loop system. If they could figure out how to interrupt or reverse one stage in that loop, then they might be able to develop drugs to stop it. But how do you tone down the immune response enough to control the inflammation but not so much that a body can’t fight disease?  “We’ve done 20 to 25 years of clinical trials on lupus drugs,” Petri says, by way of example. “We’ve had maybe one success and 30 failures.”

Finding a drug that both interrupts the immune cycle and maintains a healthy immune response is important not just for people battling illness but for all of us as we age.

Currently, there are no prescription drugs that specifically target chronic inflammation. (There are, of course, over-the-counter medications that treat the minor and temporary inflammation and accompanying pain caused by injuries or procedures, such as surgery. These are not meant to treat chronic inflammation.) Some drugs, such as hydroxychloroquine, once used to battle malaria, are useful in treating some lupus patients, but they don’t cure the disease. Aspirin and statins have shown promise in reducing inflammation in some people, but researchers aren’t sure how broadly useful such drugs are in that role. With the exception of far-from-perfect anti-inflammatory drugs, such as prednisone, a corticosteroid that brings with it a slew of side effects, scientists are still researching how best to contain inflammation. “We need something that can work broadly and quickly, and without a lot of side effects,” says Petri.

Finding a drug that both interrupts the immune cycle and maintains a healthy immune response is important not just for people battling illness but for all of us, because as we age, inflammation increases in the body. Scientists aren’t sure how and why, but interestingly, the study of HIV is offering some insight.

HIV triggers chronic inflammation in the body, even after medications have rendered levels of the virus undetectable in blood tests. Certain cytokines involved in that inflammation process can profoundly decrease testosterone levels, leading to muscle loss. “It’s possible that the chronic inflammation in people with HIV is similar to the chronic inflammation we see in aging,” says Todd Brown, an endocrinologist who researches the link between bodily markers for inflammation and chronic diseases found in people with HIV. If researchers can understand that process and create treatments to disrupt it in people with HIV, they could potentially translate their findings into treatments for similar muscle loss in aging.

Jeremy Walston is a Johns Hopkins geriatrician who investigates immune system response and muscle function in the elderly. He has been searching for markers that highlight the early signs of inflammation. Some blood tests for inflammation markers exist, but the researchers have uncovered two new markers that they believe may predict mortality and mark signs of late-in-life decline. “These are powerful inflammatory molecules that, when chronically expressed, lead to declines in stem cells and a remodulation of the immune system,” says Walston. “They also contribute to cell death,” particularly in the elderly, he says.


As the quest for diagnostic measures and therapies continues, researchers point to simple lifestyle measures we can all take to help prevent chronic inflammation. Scientists are skeptical of cure-all claims found in the new crop of anti-inflammation diet books, but they do recommend dropping pounds (and the harmful fat cells that come with obesity) and avoiding the now common American diet high in fats and sugars.

“Losing weight can have profound effects on lowering inflammation,” says Brown, who adds that eating a diet rich in fruits and vegetables and low in fats, processed foods, and sugars is generally a good idea, though more study needs to be done to determine how it might affect inflammation. Exercising, which causes an acute inflammatory response in the short term, but an anti-inflammatory one when we regularly get moving, is another strong step to take, he adds.

For most of us, keeping inflammation in check comes down to common sense basics: eat well, don’t smoke, get moving, get more rest, and see your doctor for regular physicals, which could help stop chronic inflammation before it becomes rampant.

Other researchers advise getting plenty of sleep, lowering stress levels, and seeking out treatment for inflammation-inducing culprits, such as gum disease and high cholesterol levels. Avoid contact with heavy metals such as mercury, which is found in dangerous amounts in some large fish, and limit exposure to substances, such as diesel exhaust and cigarette smoke, that can set off the immune system. Additional studies by Brown and his colleagues have also shown some advantage in increasing our intake of omega-3 fatty acids and vitamin D, though more research is needed.

Walston and others caution against popping dietary supplements touted as anti-inflammatory cures. Some so-called remedies, such as turmeric, taken in large amounts, may actually be toxic to the liver and other organs.

For most of us, keeping inflammation in check comes down to common sense basics: eat well, don’t smoke, get moving, get more rest, and see your doctor for regular physicals, which could help stop chronic inflammation before it becomes rampant. “All of the things our grandmothers told us were good for us are actually good for us,” says Brown. “Until we have a more nuanced understanding of what inflammation does, that’s what we have to fall back on.”

Written By: Michael Anft

Article Source: http://www.johnshopkinshealthreview.com/issues/spring-summer-2016/articles/understanding-inflammation

 

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A Man’s Body by Decade

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Heart

The problem: As men age, blood pressure and cholesterol levels often increase. The fix: Eat a heart-healthy diet, exercise, and have your blood pressure and cholesterol levels checked annually. Consider a coronary calcium scan above age 50, if heart disease runs in the family.

Skin

The problem: Men ignore their skin more often than women. The fix: Get an annual head-to-toe skin screen by a dermatologist to evaluate suspicious moles and other skin conditions.

Muscle

The problem: Men begin losing muscle mass by age 30. The fix: Incorporate muscle training into your fitness routine to help increase bone density, metabolism, and muscle-fat ratio, while maintaining flexibility and balance.

Colon

The problem: Colon cancer is the third most common cancer in men. The fix: Eat a diet high in vegetables, fruits, and whole grains, and low in red meat and alcohol. Consider a colon­oscopy at age 50, particularly if colon cancer runs in the family.

Prostate

The problem: Benign prostatic hyperplasia (an enlarged prostate) affects about 50 percent of men between the ages of 51 and 60 and up to 90 percent of men older than 80. The fix: Eat a low-fat diet, exercise, and undergo a prostate exam by age 50 or sooner if at high risk for prostate cancer.

Testosterone

The problem: Levels typically decrease with age, with about 20 percent of men having low T by their 60s. The fix: See a doctor to get your testosterone levels checked, if experiencing a drop in libido, energy level, unexplained weight gain, or ongoing depression.

Article Source: http://www.johnshopkinshealthreview.com/issues/spring-summer-2017/articles/a-users-guide-to-mens-health

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Will Metformin Become the First Anti-Aging Drug?

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A committed group of scientists is seeking to validate metformin as the first-ever anti-aging medication.1,2

In this day of staggering drug prices, metformin is available as a low-cost generic.

One mechanism by which metformin works is by activating AMPK, an enzyme inside cells that lowers blood sugar by promoting energy utilization.

Activating AMPK has broad-ranging effects that extend far beyond blood sugar control. Studies show that boosting AMPK activity can prevent—and even reverse—the life-shortening effects of aging, such as cardiovascular disease, diabetes, neurodegenerative diseases, cancer, and more.3

In this article, we’ll review data that persuaded the FDA to allow metformin to be studied in humans as the first anti-aging drug.1

Broad-Spectrum Effects

The most commonly prescribed antidiabetic drug is metformin. It has been in use in England since 1958 and in the United States since 1995.

Derived from a compound found in the French Lilac, metformin has a track record of safety and effectiveness at routine doses of up to 2,000 mg daily.4-7

So what evidence is there for the FDA to consider this drug as an anti-aging medication? The reason is simple:

Metformin can block or diminish many of the fundamental factors that accelerate aging.8-12

These include protecting against DNA damage glycation, poor mitochondrial function, and chronic inflammation. Metformin has been shown to facilitate DNA repair, which is critical for cancer prevention.

By attacking these fundamental degenerative processes, metformin can prevent the development of aging’s most troubling diseases.

Metformin has also been shown to increase the production of known longevity-promoting signaling molecules in cells, such as mTOR and AMPK—all of which reduce fat and sugar storage and increase youthful functioning at the cellular level.11,13

Studies have shown that by activating AMPK, metformin specifically impacts lifespan. For example, roundworms treated with metformin have higher AMPK activity and live about 20% longer than untreated control animals.14 Mice treated with metformin have been found to live nearly 6% longer than controls.11 And most impressively, diabetics taking metformin were shown to live 15% longer than healthy individuals without diabetes!15

AMPK activity declines with age,16 making us more vulnerable to many of the diseases associated with aging. Fortunately, a wealth of recent studies show that by activating AMPK, metformin plays a major role in preventing age-related disorders including cancer, cardiovascular disease, obesity, and neurocognitive decline.

By combatting many of the underlying causes of aging—and by activating AMPK—metformin can be considered a broad-spectrum anti-aging drug.

WHAT YOU NEED TO KNOW

Metformin as an Anti-Aging Drug

  • Metformin has been a staunch workhorse against diabetes for more than 50 years.
  • Studies show that metformin acts by boosting the activity of AMPK, a master metabolic regulator that favors fat- and sugar-burning and prevents their accumulation.
  • Because AMPK is relevant in all tissues, this makes metformin extremely important in reducing metabolic imbalances in the entire body.
  • Strong evidence suggests that metformin, through its protective effects and AMPK-activating properties, can help prevent cancer, cardiovascular disease, obesity and its consequences, and even neurodegenerative disorders.

Cancer Protective Effects of Metformin

Diabetics have an increased risk of cancer. In a study of head and neck cancers, researchers were surprised to find that diabetic patients had a 46% reduction in risk of developing these cancers compared to non-diabetic patients.17 What was the reason for this unexpected reduction? The diabetic patients were taking metformin.

Similar effects have been seen for the risk of gastric (stomach) cancers as well, with metformin users experiencing a 55% decrease in the risk of stomach cancer compared with nonusers.18 Important studies like these have helped to confirm a decade-long trend suggesting that metformin has anti-cancer properties.17

While these studies show that metformin has the potential to reduce the risk of developing cancer, others show its benefits for those who already have cancer.

A study encompassing 27 clinical trials representing more than 24,000 patients found that in people with early-stage cancers of the colon and rectum, metformin use improved recurrence-free survival by 37%, overall survival by 31%, and cancer-specific survival by 42%.19

The same study reported similar results for men with early-stage prostate cancer, with metformin use increasing recurrence-free survival by 17%, overall survival by 18%, and cancer-free survival by 42% compared with non-metformin users.19

By now, metformin has been studied in the context of total tumor incidence in 17 different target organs, 21 strains of mice, and four strains of rats. It has been studied in cancers that occur spontaneously, and in those induced by 16 different chemical carcinogens from multiple classes, ionizing radiation, viruses, genetic modifications, and high-fat diets, using five different routes of administration.20

A whopping 86% of such studies showed that metformin clearly inhibited cancer development and showed zero evidence of cancer stimulation by the drug.20

Indeed, as one expert recently put it, maybe it’s time “to make this long story short” about metformin: It works to prevent cancer.20

Metformin Prevents Cardiovascular Disease

Despite billions of dollars spent on drugs such as Crestor and Lipitor, cardiovascular disease remains the single biggest killer in America. While there are multiple causes of cardiovascular disease, most boil down to the development of atherosclerosis, or “hardening of the arteries.”

Atherosclerosis is promoted by factors such as oxidation of LDL cholesterol, accumulation of that oxidized fat in arterial walls, and damage to the endothelium, which is the thin layer of cells lining those arterial walls.21

Metformin is now known to prevent these early steps in atherosclerosis development.

One of the key ways it does this is by activating the metabolic regulator AMPK. By activating AMPK, metformin:

  • Mitigates LDL oxidation and the resulting endothelial dysfunction, which slows the development of atherosclerosis.21
  • Reduces the conversion of harmless immune system cells (monocytes) into fat-laden macrophages, an action that reduces their accumulation in vessel walls.22 It also increases cholesterol export out of those cells, while also suppressing the inflammatory stimulus they normally produce.23,24
  • Offers critical protection to endothelial cells that line coronary arteries, which supply blood to the heart muscle itself. Specifically, metformin enhances the resistance of endothelial cells to “fat poisoning,” the death of endothelial cells in the presence of high fat concentrations.25 This is highly protective against heart attacks, which occur when coronary arteries, blocked by atherosclerotic plaques laden with fat and inflammatory cells, fail to provide enough blood to the hard-working heart muscle.

Metformin has also been shown to prevent the fragmentation of mitochondria in endothelial cells.26 Such fragmentation is closely associated with the dysfunction of endothelial cells and is now considered an important precursor of atherosclerosis.26

The results of these protective effects have been seen in numerous human studies. In one study, heart attack patients taking metformin had a significant 75% reduction in the risk of dying after 30 days, and a 68% reduction in their risk of dying 12 months after the attack.27

Several studies have also demonstrated that metformin reduces the risk of heart attack, and is associated with reduction in stroke, atrial fibrillation (an arrhythmia), and death from all causes.28

Finally, a 2016 study showed significant reductions in systolic (top number) blood pressure in nondiabetic people taking metformin. The largest reductions were seen in those having impaired glucose tolerance or obesity.29

Obesity itself appears ready to yield to metformin treatment, as we’ll now see.

FDA APPROVES FIRST ANTI-AGING STUDY

The FDA has approved a study that will determine if metformin can do more than lower blood sugar—it will evaluate metformin’s ability to slow aging. This is the first ever anti-aging study approved by the FDA.

Studies have shown that metformin can block or diminish many of the underlying factors that accelerate aging, and it has also been shown to extend lifespan in animals. Dr. Nir Barzilai from the Albert Einstein College of Medicine, along with researchers from the American Federation for Aging Research (AFAR), want to find out if metformin can extend lifespan in humans as well.

The study, called Targeting Aging with Metformin (TAME), will evaluate 3,000 people over a course of six years. Half of the participants will receive metformin, and the other half will receive a placebo. Since aging is largely characterized by the development of disease, the success of the study will be determined by whether or not the drug delays the onset of typical age-related diseases, such as cardiovascular disease, cancer, and cognitive decline.

This groundbreaking study has the potential to change the future of how we treat disease. Developing a single drug designed to treat multiple conditions would dramatically reduce the number of drugs a typical person would need, which would reduce overall drug side effects, eliminate contraindications, and of course, save money.

None of this is good for Big Pharma’s bottom line—which is likely why no company has agreed to fund the study. Until that happens, this important study is on hold.

But you can help. AFAR is seeking individual contributions to get the TAME study started. To learn more, and make a donation if you like, visit http://www.afar.org/donate/

Metformin Reduces Body Weight and Fat Mass

Metformin’s ability to activate AMPK makes it especially beneficial in combatting obesity. This is because AMPK is a metabolic regulator that stimulates youthful cellular behaviors such as burning fat (instead of storing it), taking sugar out of the blood, and recycling cellular contents to eliminate toxic proteins.30

As a result, metformin can be expected to have important effects on body weight and fat deposits. And indeed, studies show that metformin fights obesity and reduces body fat mass, even in non-diabetic patients.

This is true in some of the most challenging populations, such as women with polycystic ovary syndrome, a major cause of obesity and endocrine problems in premenopausal women.

In one study, women with polycystic ovary syndrome were treated with 850 mg of metformin or a placebo twice daily for 6 months. During that time, those in the placebo group experienced increases in weight and blood sugar, as expected. Those taking metformin, on the other hand, had significant decreases in weight and blood sugar—with metformin-treated women losing an average of 9.24 pounds. The metformin group also had significant increases in beneficial HDL cholesterol.31

Metformin has been found to significantly reduce body weight, body mass index (BMI), and insulin resistance in patients taking modern antipsychotic medications such as olanzapine, aripiprazole, risperidone, and quetiapine.32-35 These are impressive results, since major side effects of these drugs include rapid weight gain, loss of insulin sensitivity, and other features of metabolic syndrome.36

But by far, the largest group of people fighting obesity are simply aging individuals who are otherwise healthy (nondiabetic). Metformin shows promise for this population as well.

An important study in a group of such people—all women with midlife weight gain but normal blood sugars—showed that taking metformin for 12 months reduced mean body weight by 11.6 pounds.37 In addition, treated subjects had significant decreases in their body fat percentage, a favorable change that can reduce many of the long-term consequences of obesity.

Metformin is showing promise in obese but otherwise healthy young people as well. A group of 10-16- year-olds took 2,000 mg of metformin per day or a placebo for 18 months. Those taking metformin lost nearly half a pound in fat mass. By contrast, the placebo group gained almost 4.5 pounds in fat mass.38

Metformin as Neuroprotectant

There is rapidly growing literature on metformin’s potential role in preventing neurodegenerative disorders such as Alzheimer’s and Parkinson’s diseases. Once again, much of this literature focuses on metformin’s ability to activate AMPK, the youth-promoting energy regulator in all of our cells.

One major effect of AMPK activation is the cleanup of accumulated misfolded proteins in brain cells. The accumulation of proteins, such as tau and beta-amyloid, contributes to brain cell death and dysfunction in neurodegenerative diseases.

Thus, it makes sense that metformin might be effective in preventing disorders associated with those proteins. Numerous animal and laboratory studies show that metformin does indeed have such effects. These studies demonstrate that metformin:

  • Reduces levels of an enzyme that generates beta-amyloid proteins32
  • Decreases the harmful effect of beta-amyloid on brain cell function39-41
  • Reduces levels of alpha synuclein, another protein that accumulates and causes damage in Parkinson’s disease42
  • Prevents the loss of dopamine-producing brain cells in a model of Parkinson’s disease43,44
  • Improves motor coordination in a mouse model of Parkinson’s45

In 2016, a human study showed that taking 1,000 mg of metformin twice daily for 12 months improved memory recall in a group of older adults with a condition called amnestic mild cognitive impairment (a memory-stealing predecessor of Alzheimer’s).39

Given the close connections between Alzheimer’s and diabetes (it’s been called “Type III diabetes”), there is every reason to believe that metformin, through its AMPK-activating properties, will help in the long fight to retain our minds and personalities as we age.

PRECAUTIONS AND USEFUL SUGGESTIONS WITH METFORMIN USE

Although metformin has an outstanding track record in the fight against diabetes, cancer, obesity, neurodegenerative and cardiovascular diseases, there are some precautions to be aware of with its use.

Metformin is known to interfere with the absorption of B12, increasing the risk of vitamin B12 deficiency.46,47 Low B12 levels contribute to higher concentrations of artery-clogging homocysteine—an independent risk factor for cardiovascular disease.48,49 The tiny amounts of vitamin B12 and other B-vitamins found in commercial supplements is usually not enough to offset this problem. Individuals using metformin should ensure that they are taking higher doses of B-vitamins (at least 300 mcg of methylcobalamin, the active form of vitamin B12) and checking their homocysteine levels to ensure proper protection.

Some studies have shown that metformin reduces free and total testosterone levels in men.50Testosterone is especially important in male diabetics as it enhances insulin sensitivity.51 Life Extension has previously published clinical data on the importance of maintaining youthful testosterone levels in diabetic men to improve glucose utilization.52

If a blood test shows low testosterone, applying a topical testosterone cream can restore levels of this vital hormone to youthful ranges.

Side effects associated with metformin use include gastrointestinal distress or a slight taste disturbance, usually a metallic taste. Rarely, metformin may cause a potentially serious lactic acidosis, a buildup of lactic acid in the blood.53

If you use or are considering metformin, consult your physician, take your B-vitamins, and periodically check your kidney function, homocysteine levels, and in men, free and total testosterone.

Summary

The world’s first clinical trial of a true “anti-aging” drug may be about to begin. But while the study is new, the drug is more than half a century old.

Metformin has been used for more than 50 years to treat type II diabetes. A wealth of recent studies now supports a major role for metformin in preventing age-related disorders including cancer, cardiovascular disease, obesity, and neurocognitive decline.

The American Federation for Aging Research (AFAR) has a long uphill road to get this study (called TAME, or the Targeting Aging with Metformin trial) started. They face almost-certain opposition from Big Pharma companies for whom treating—not preventing—aging is a lucrative business.

The good news is that we don’t have to wait for this new metformin study to get off the ground. Metformin is already available as a prescription medication. And many thoughtful physicians who are presented with the evidence will prescribe it based on its recognized benefits against specific age-related disorders.

There are also nutrients that have been shown to boost AMPK activity and function to lower blood glucose similar to metformin.54-57

Written By: Raegan Linton

Article Source: http://www.lifeextension.com/Magazine/2017/4/Metformin-Slashes-Cancer-Risks/Page-01

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Why glutathione is important to us

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 One important protein that appears in every human cell is a tripeptide known as glutathione.

Found in the highest concentrations in the liver, it consists of three amino acids: glutamic acid, L-cysteine and L-glycine.

The first record of glutathione was in 1888, but it was not until 1984 that its function in the body began to be researched in detail.

It turns out that glutathione serves as an antioxidant and detoxifier that protects cells from free radicals and oxidative stress, thus, improving the immune system.

But glutathione levels in human cells begin to decline after you turn 20. In order to produce more glutathione, supplementation of L-cysteine is recommended.

In the absence of glutathione, the body will experience several things. All the cells in the body would face premature death, causing the liver, which cleanses your body of toxic materials, to malfunction.

Worse, the entire immune system will break down – in other words, without glutathione, humans would cease to exist.

How glutathione works

Glutathione is the only antioxidant that is intracellular, meaning that it acts inside the cells. This helps to resist disease by neutralising free radicals and keeping other antioxidants like vitamins C and E in their active form.

Many scientists believe there is a link between low glutathione levels and cell death, which could be why the levels of glutathione in patients with serious diseases such as AIDS and cancer, are typically very low.

On the other hand, clinical observations of people aged 100 and more in various countries like Poland, Italy and Denmark, have found very high levels of glutathione in their cells.

Other functions of this protein include helping to process toxins in the liver; DNA and protein synthesis; and regulating the nitric oxide cycle and the metabolism of iron.

Key benefits of glutathione

Decreased levels of glutathione have several consequences that are linked to a number of age-related illnesses. This includes:

Alzheimer’s disease and macular degeneration – A University of Alabama study in the United States revealed that the red blood cells in male Alzheimer’s patients indicated a significant lack of glutathione.

Heart disease – A study of patients with heart disease found that the lower their levels of glutathione, the higher the likelihood of them experiencing a heart attack.

Cancer – While glutathione is not able to cure cancer, several studies suggest that the growth of new cancer cells may be reduced. Its strong antioxidant properties make it suitable as a supplement.

This is why some doctors recommend it as a supplement to treat cancer, as it improves the effectiveness of chemotherapy drugs and reduces their side effects.

Psychiatric illnesses, including bipolar disorder, schizophrenia and depression – These have been linked to low levels of glutathione. The lack of antioxidant abilities in the brain can cause oxidative stress.

Glutathione has also been used to treat Parkinson’s disease, sickle cell anaemia, idiopathic pulmonary fibrosis and poisoning, as it is able to cleanse the body of unhealthy metals such as mercury.

Glutathione has been found to improve the quality of the human male sperm. This is achieved by the lowering of blood pressure and decreasing oxidative stress on the sensitive sperm cells, hence, minimising damage to their DNA cargo.

Couples who are trying to conceive should look for micronutrient supplements, especially n-acetyl-cysteine (NAC), which is used in the body to produce L-glutathione.

The aspiring father could also benefit from consuming scientifically-proven nutrients such as arginine, carnitine and pine bark extract.

Because it is a protein, a fair amount of glutathione that you ingest is broken down in your gut and eliminated before reaching the cells.

 

Article Source: http://www.star2.com/living/viewpoints/2016/05/29/why-glutathione-is-important-to-us/#v9QZZBkX3X5BqJzk.99

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Weight-Bearing Exercises Promote Bone Formation in Men

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Human hormone and protein linked to bone mass are impacted by 12 months of targeted exercise

COLUMBIA, Mo. – Osteoporosis affects more than 200 million people worldwide and is a serious public health concern, according to the National Osteoporosis Foundation. Now, Pamela Hinton, associate professor in the Department of Nutrition and Exercise Physiology, has published the first study in men to show that long-term, weight-bearing exercises decrease sclerostin, a protein made in the bone, and increase IGF-1, a hormone associated with bone growth. These changes promote bone formation, increasing bone density.

“People may be physically active, and many times people know they need to exercise to prevent obesity, heart disease or diabetes,” Hinton said. “However, you also really need to do specific exercises to protect your bone health.”

In the study, men 25- to 60-years-old who had low-bone mass were split into two groups. One group performed resistance training exercises such as lunges and squats using free weights. The other group performed various types of jumps, such as single-leg and double-leg jumps. After 12 months of performing the exercises, Hinton then compared the levels of bone proteins and hormones in the blood.

“We saw a decrease in the level of sclerostin in both of these exercise interventions in men,” Hinton said. “When sclerostin is expressed at high levels, it has a negative impact on bone formation. In both resistance and jump training, the level of sclerostin in the bone goes down, which triggers bone formation.”

The other significant change Hinton observed was an increase in the hormone IGF-1. Unlike sclerostin, IGF-1 triggers bone growth. The decrease of harmful sclerostin levels and the increase in beneficial IGF-1 levels confirmed Hinton’s prior research that found both resistance training and jump training have beneficial effects on bone growth.

To increase bone mass and prevent osteoporosis, Hinton recommends exercising specifically to target bone health. While exercises such as swimming and cycling are beneficial to overall health, these activities do not strengthen the skeleton. Hinton suggests also doing exercise targeted for bone health, such as resistance training and jump training.

The study, “Serum sclerostin decreases following 12 months of resistance- or jump-training in men with low bone mass,” was published in Bone.

https://www.eurekalert.org/pub_releases/2017-03/uom-wep032217.php

 

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Testosterone Does Not Appear to Increase The Risk For Cardiovascular Disease

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Testosterone replacement therapy does not appear to increase the risk for cardiovascular disease or thromboembolic events in middle-aged men.

In fact, the risk for a cardiovascular event was lower in men taking supplemental testosterone than in those who were not, said lead investigator Julian Hanske, MD, from Ruhr University Bochum in Herne, Germany, who collaborated on the study during a fellowship at Brigham & Women’s Hospital in Boston.

But physicians should know whether a patient suffers from obstructive sleep apnea before prescribing testosterone, Dr Hanske said here at the European Association of Urology 2017 Congress.

Cohort studies of the cardiovascular and thromboembolic consequences of supplemental testosterone have generally relied on sources such as the Surveillance, Epidemiology, and End Results Medicare database, which is limited to an older population, he told Medscape Medical News.

To get a better handle on the relative risks associated with testosterone replacement therapy in a younger population, Dr Hanske and his team searched the TRICARE American military insurance database, which covers all retired and active-duty military personnel and their dependents.

They looked for men 40 to 65 years of age treated for low levels of testosterone. Patients were excluded if they had a history of heart disease, thromboembolism, prostate cancer, or obstructive sleep apnea.

For the final cohort, 3422 men who took testosterone were matched with 3422 control subjects who did not by year of birth, then by date of first testosterone prescription, and then by race and baseline comorbidities.

The study outcomes were event-free survival and absolute risk for cardiovascular disease, thromboembolism or obstructive sleep apnea.

We have so many fears of testosterone replacement therapy.

Cardiovascular event-free survival was significantly better in the testosterone group than in the control group (P = .0085), and risk for coronary artery disease was lower in the testosterone group (P = .0082).

There was no difference in thromboembolic event-free survival between the testosterone and control groups (P = .0998).

These findings are reassuring, said session comoderator Raanan Tal, MD, head of the male infertility program at Rambam Medical Center in Haifa, Israel.

“We have so many fears of testosterone replacement therapy, and actually what they showed is that so many beliefs that we have cannot be supported,” he told Medscape Medical News.

“The fact that you don’t have an increase in cardiovascular events or thrombotic events is an important message — more important than the risk of increased obstructive sleep apnea,” he explained.

But the other comoderator said he thinks the findings would be more compelling if the investigators had used propensity-score matching or a similar statistical method to ensure a close case–control match.

“Age is a risk factor,” Andrea Salonia, MD, from the Vita-Salute San Raffaele University in Milan, pointed out. “The younger the patient, the lower the probability of having difficulties sleeping at night, and they did not adjust for that specific issue, or at least they did not find any kind of difference according to this specific variable.”

“At the same time, the number of patients they considered was amazing, and it is probably one of the most important studies in terms of the huge cohort they selected,” Dr Salonia told Medscape Medical News.

Dr Hanske, Dr Tal, and Dr Salonia have disclosed no relevant financial relationships.

European Association of Urology (EAU) 2017 Congress: Abstract 256. Presented March 25, 2017.

Article Source: http://www.medscape.com/viewarticle/877786

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