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.


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.


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.


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.


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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Mitochondria, Telomeres, Strength Training & What It Means For Something To Qualify As An “Anti-Aging” Activity

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In his excellent article series on anti-aging, anti-aging fitness expert Clarence Bass highlights this study showing that six months of progressive resistance training made the gene expression pattern of aging mitochondria appear significantly younger. 

Muscles can become smaller and weaker with age (a process known as sarcopenia), and evidence suggests that a key part of the decline occurs in a component of muscle cells called the mitochondria, the primary engine of energy production.

From the study, which was done on men at an average age of 70 years old, researchers reported that “…the older individuals were able to improve strength by approximately 50%, to levels that were only 38% less than that of young individuals…”. This means that seniors engaged in weight training closed the strength gap between themselves and their counterparts who were nearly 40 years younger from 59% to 38%, which is an improvement of almost 36% in a mere six months of the study.

Muscle biopsies from the study showed “a remarkable reversal of the expression profile of 179 genes associated with age and exercise training…Genes that were down-regulated with age were correspondingly up-regulated with exercise, while genes that were up-regulated with age, were down-regulated with exercise.”

The researchers summed things up by reporting that “healthy older adults show a gene expression profile in skeletal muscle consistent with mitochondrial dysfunction and associated processes such as cell death, as compared with young individuals. Moreover, following a period of resistance exercise training in older adults, we found that age-associated transcriptome expression changes were reversed, implying a restoration of a youthful expression profile.”

So when it comes to mitochondria, weight training reversed nearly 40 years of aging!

But exercise doesn’t only affect mitochondria.  Two more studies show how exercise protects DNA from the wear and tear of aging, and how the addition of fast-twitch muscle fibers precipitate fat loss and improve metabolic function – primarily by acting on telomeres.

Telomeres cap the DNA chromosomes in your cells and protect these chromosomes from damage. As you age, telomeres progressively wear and shorten from repeated cell division, oxidative stress, inflammation, and other metabolic processes, eventually leaving the cell’s chromosomes unprotected. When the caps are completely eroded or disappear, the wear and tear begins to cut into your genes, causing cells to become damaged and discarded as you grow older.

In this next study, scientists measured telomeres in twins to gauge the effect of exercise on aging, hypothesizing that “telomere dynamics might chronicle the cumulative burden of oxidative stress and inflammation and, as such, serve as an index of biological age” and that “physical activity level may have an [independent] effect on telomere attrition”.

They studied 2401 twins (2152 women and 249 men, aged 18 to 81), used questionnaires on physical activity level, smoking status, disease status, and socioeconomic status, and extracted DNA from blood samples.

So what did they find in this study on twins?

Telomere length decreased with age. No surprises there. But both the women and men who were physically active had longer telomeres than those who were sedentary, even after adjusting for the influence of age, weight, disease, socioeconomic status, and smoking.

In addition, the study participants who spent more than 3 hours each week engaged in vigorous physical activity (such as lifting weights) had longer telomeres than subjects 10 years younger, suggesting that individuals who eschew placing a vigorous load on their body may wind up biologically older by 10 years.

Obviously, since they were studying twins, these differences weren’t due to genes, but rather due to the lifestyle factor of exercise. When one twin exercised significantly more than the other, they had longer, more durable telomeres.

In the next study, researchers found that replacing slow-twitch type I muscle fibers with stronger and faster type II muscle fibers produced a significant reduction of fat mass and insulin resistance. Endurance training develops slow-twitch fibers, but strength training builds fast-twitch fibers.

For this study, researchers used a genetically engineered mouse that contained a muscle-growth regulating gene called Akt1 that could be turned on and off by the researchers. Activating Akt1 caused the mice to grow type II fibers, without exercise (important to note, since mice don’t really lift weights that well, even when commanded to by scientists in white lab coats). When the Akt1 gene was turned on, the mice took on the characteristics of a lean and powerful sprinter or weight lifter, and when the gene was turned off, the mice reverted to a predominance of type I muscle fibers, along with becoming more obese and insulin resistant (notably, this was without an actual change in diet!).

The researchers reported that “remarkably, type II muscle growth was associated with an overall reduction in body mass, due to a large decrease in fat mass. In addition, blood tests showed that these mice became metabolically normal [with no insulin resistance]. This work shows that type 2 muscle just doesn’t allow you to pick up heavy objects, it is also important in controlling whole body metabolism. It appears that the increase in type 2 muscle fiber orchestrates changes in the body through its ability to communicate with other tissues”.

Beyond the age of 30, we lose approximately six pounds of muscle mass per decade, and these findings indicate that interventions designed to increase skeletal muscle mass (such as weight training) may prove to be critical weapons in the fight against obesity and obesity-related ailments, including diabetes, heart disease, stroke, hypertension, and cancer.

The key point here of course is that weight training, due to it’s recruitment of type II muscle fibers, appears to be more effective than cardio, endurance and aerobics for fat loss, weight control, essentially converting the cells into a fat-burning machine.

Finally, yet another study on strength training effects on telomere length in human skeletal muscle looked into reports of a phenomenon of abnormally short telomeres in skeletal muscle of athletes who had overtraining and exercise-associated fatigue. This important study looked into the question of whether long-term hard exercise might have deleterious effects on muscle telomeres. So, using muscle biopsies, the researchers compared telomere length of a group of power lifters who had trained for an average of eight years against that of a group of healthy, active subjects who had no history of strength training.

There was absolutely no abnormal shortening of telomeres in the power lifters. As a matter of fact, telomere lengths in the power lifters were significantly higher than those of the control group, and telomere length was positively correlated to the power lifters’ individual records in the squat and deadlift!

These results show for the first time that long-term weight training is not associated with an abnormal shortening of skeletal muscle telomere length, and that the heavier the load you put on your muscles, the longer your telomeres will tend to be.

Written by: Ben Greenfield

Article Source: https://bengreenfieldfitness.com/2016/05/the-fittest-old-people/

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The Big Picture: 5 Fundamentals of Lifetime Health

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Discover what you can start doing now to prepare for your healthiest, most vibrant future.

Elaine Hooker was a trailblazer. As a newspaper reporter and editor in the 1960s, she excelled in a challenging field dominated by men. What’s more, she shouldered the added pressure of caring for four children at a time when there was little institutional or cultural support for working women.

“There was no tolerance for staying home with sick kids,” recalls Hooker, now 70. “I didn’t even dare keep photos of my children on my desk for fear I’d be considered not as serious as the guys.”

Still, even as Hooker was going through one of the most stressful times of her life, she took good care of herself. Exercise and meditation were part of her routine. And she is now enjoying a healthy and active retirement.

More of us would do well to follow Hooker’s example, looking beyond momentary circumstances and time pressures to see the bigger picture — namely, how the daily habits we form now can dictate our health for a lifetime.

When functional-medicine gynecologist Sara Gottfried, MD, met Hooker a few years ago for a checkup, Gottfried witnessed Hooker’s hardiness at a cellular level.

Gottfried checked Hooker’s telomeres — the protective tips on the chromosomes that keep them from fraying and sticking to each other. Functional physicians often examine the length of telomeres to assess how well a patient is aging.

“She had the telomeres of a woman 20 years younger,” Gottfried says. “Despite a very stressful life, she had practices in place that are associated with a better health span.”

We’d all like to have a “health span” that equals our life span. And the new science of epigenetics confirms that we have a significant say in how long we stay in fighting shape.

Epigenetics shows that lifestyle choices (like nutrition, activity, and how we manage stress) can trump our genetic heritage by controlling which of our genes actually turn on.

There are also new tools that can track tiny alterations in cellular function — such as the test Gottfried used to check Hooker’s telomeres — to help doctors evaluate how well our bodies are withstanding the test of time.

“These biomarker tools help us better understand and optimize the health of the cells throughout our body,” says Jeffrey Bland, PhD, FACN, CNS, cofounder of the Institute for Functional Medicine.

These tools are also definitively showing what we’ve suspected all along: that the choices we make on a daily basis He— about our food, exercise, sleep, and stress — all make a huge difference in how well we age at a biochemical, structural, and neurological level.

Read on to discover the factors that are affecting your rate of aging now and how some simple adjustments can help set the stage for a healthier, more vital, more vibrant future.


We tend to think of inflammation as the angry red swelling around a splinter or mosquito bite. Indeed, that acute inflammatory response is a critical part of the body’s healing process — a good thing. “If we didn’t have an inflammatory response, we could die from a minor injury such as a paper cut,” says Robert Rountree, MD, a functional-medicine practitioner at Boulder Wellcare in Colorado and the chief medical officer of Thorne Research.

Chronic inflammation, which can be caused by “injuries” to the body like poor nutrition and excessive stress, is something else entirely: It’s a slow-boil systematic disturbance that affects many parts of the body and injures cells. Over time, it can play a huge role in major afflictions like heart disease, type 2 diabetes, dementia, cancer, and more.

Here’s how it works: Inflammation creates atoms called free radicals. These carry at least one unpaired electron that damages cells in its reckless pursuit of another electron with which to pair. Free radicals traumatize tissues throughout the body and can even harm DNA, leaving cells to malfunction or die.

We might feel the effects of systemwide inflammation when it causes ongoing pain in a knee, for instance, but are less likely to notice when that same inflammatory process wreaks silent havoc in other areas, such as the brain. We may detect some fogginess and forgetfulness, but we don’t connect it to inflammation.

“We don’t have pain receptors in the brain and we certainly can’t tell that it’s turning red like that area around the mosquito bite, but it’s the same exact process,” says neurologist David Perlmutter, MD, author of Brain Maker. “We measure inflammatory markers in the brains of individuals with things like Parkinson’s, Alzheimer’s, multiple sclerosis, and a variety of brain-related disorders, and we can see that these are the same markers of inflammation that are elevated in your arthritic knee.”


Embrace an anti-inflammatory lifestyle, and be proactive about addressing inflammatory health conditions.

Your doctor can assess your inflammation level with a blood test for high-sensitivity C-reactive protein (hs-CRP), a substance the body produces when inflammation is present.

A high reading could indicate that your lifestyle is contributing to bodywide inflammation, or that a more localized problem -— such as gum disease or leaky gut — is triggering an inflammatory cascade.

“You want to get that hs-CRP lower,” says Bland, “because it’s a marker for biological aging and it’s increasing your risk for a variety of chronic illnesses.” One key area of focus is the intestinal tract, he says, because over 50 percent of the immune system is clustered around our intestines: “An unfriendly intestinal tract activates the immune system and that produces hs-CRP in your liver.”


“Genes play an absolutely pivotal role in human health,” states Perlmutter. “But 99 percent of the genes and 99 percent of the DNA in our body are not ours.”

The majority of genes in the body belong to the microbiota in our guts — and they have a big influence on how we age, he explains.

“In terms of healthy aging, the bacterial DNA carries the biggest sword,” Perlmutter says, noting that, in his view, Alzheimer’s, Parkinson’s, and other aging-related diseases are influenced to some degree by negative changes to the bacterial population in our guts. (For more on the gut-brain connection, see “Healthy Gut, Healthy Brain“.)

Indeed, one of the most revolutionary  areas of health research — carried on  notably by the National Institutes of Health’s Human Microbiome Project — has to do with our microbiome, that -collection of tiny organisms living in and on our body that are our essential partners in good health.

According to the Human Microbiome Project, these microbes “produce some vitamins that we do not have the genes to make, break down our food to extract nutrients we need to survive, teach our immune systems how to recognize dangerous invaders, and even produce helpful anti-inflammatory compounds that fight off other disease-causing microbes.”

Growing numbers of studies have linked changes in the composition of our microbiomes to various diseases. Perlmutter points to a 2015 study in the Journal of Neuroinflammation showing that chronic inflammation of the gut causes a decrease in the formation of new brain cells in the hippocampus, a process that normally continues throughout adulthood and is linked to cognition and mood.

Among other roles, our friendly gut bacteria maintain the lining of the gut — only a single cell thick — and keep dangerous compounds from circulating throughout the body. Factors like poor diet, stress, toxins, and infections can damage the gut lining. And when the intestinal wall is breached, inflammatory compounds seep into the rest of the body, promoting a variety of premature-aging and chronic-disease factors. (For more on leaky-gut syndrome, check out “How to Heal a Leaky Gut“.)


Be on the lookout for the symptoms of microbiome imbalance and leaky gut, including diarrhea, constipation, intestinal pain and bloating, chronic joint pain, psoriasis, and headaches.

When gut distress is suspected, many progressive physicians recommend their patients try an elimination diet. (For more on elimination diets, see “The Institute for Functional Medicine’s Elimination Diet Comprehensive Guide and Food Plan“.) Getting rid of allergenic foods is often enough to quell the disturbance and restore balance in the gut.

When it’s not, practitioners can order a stool analysis to help clarify what else might be disrupting intestinal bacteria, like yeast overgrowth, parasites, or viruses.

To support the microbiome over time, Perlmutter recommends a diet rich in probiotic foods like yogurt, kefir, kimchi, kombucha, and sauerkraut, all of which are full of microbial life.

In addition, he recommends consuming plenty of prebiotic foods that contain the fibers our microbes love to eat. These include onions, jicama, raw dandelion greens, bananas, and Jerusalem artichokes.


“None of the interventions that we talk about in the anti-aging field work unless you exercise,” says Rountree. He is especially impressed by the impact of exercise on our cells’ mitochondria, those powerhouses that generate the cells’ energy and are involved in other vital functions.

We inherit all our mitochondria and can’t make new ones from scratch, but those that we possess can split and make copies of themselves. This intracellular revitalization is called mitochondrial biogenesis, and recent research indicates that one way to stimulate it is through vigorous exercise. (For more on mitochondria, see “The Care and Feeding of Your Mitochondria“.)

Exercise also helps mitigate the aging effects of stress. “If we don’t have activity as a regular part of life, those stress hormones can’t get properly metabolized and they build up,” says Bland. “When you get regular exercise, your hormones improve, your energy improves, and your cell viability improves.”

On the other hand, a sedentary lifestyle can promote the production of inflammatory cytokines, which accelerate aging and endanger bone health. “There are bone cells that break down bone,” says Rick Mayfield, DC, a faculty staff doctor at the Institute for Functional Medicine, and these get activated when the body experiences systemwide inflammation.

But note: While regular exercise is essential, exercising too often or aggressively without adequate recovery can actually cause you to age faster.


Rountree says the best exercise for mitochondrial biogenesis is high-intensity interval training (HIIT), in which you push really hard for a short while, recover, then push hard again. (For details on HIIT workouts, see “HIIT It“.)

Still, any exercise you do -regularly, whether that’s yoga, strength training, or cycling, will help you metabolize stress -hormones, maintain better energy, and offset chronic inflammation.


As we age, our hormones shift. For men, testosterone tends to drop 1 to 2 percent every year after age 30, though research shows this can be related to lifestyle factors (typically weight gain) rather than aging alone.

Women, meanwhile, see decreases in estrogen and fluctuations in thyroid hormones during and after menopause. They may be 10 times as likely as men to have thyroid problems, with a resulting impact on their energy, mood, and weight. And everyone’s cortisol patterns tend to shift over time, which can be linked to disrupted sleep, shorter telomeres, and accelerated aging.

Keeping stress in check supports the health of the adrenal glands, and vice versa. “Imbalance in your adrenal function can accelerate aging,” says Gottfried, “so it’s important to keep cortisol in the optimal range.”

Gottfried uses a blood test to evaluate all of her patients’ cortisol, estrogen, and thyroid levels, and then works with her patients on lifestyle and treatment plans to get their levels within an optimal range.


Adjust your eating, exercise, stress management, and sleep cycles in ways that help optimize your hormone levels. And if you suspect your hormones might be out of whack, ask your doctor for a hormone panel. Just keep in mind that most imbalances are best addressed by lifestyle adjustments.

For example, while overconsuming carbs spikes insulin, avoiding them altogether can increase cortisol production, Gottfried notes. She recommends focusing on protein, fat, and nonstarchy vegetables for breakfast and lunch, and enjoying some quality carbohydrates at dinner. “Cycling” carbohydrates this way helps rein in cortisol at night, when it’s most likely to disrupt sleep.

And don’t underestimate the role stress might be playing in your hormonal fluctuations. “High perceived stress -— that overwhelmed feeling that you’re a victim and it’s all just happening to you — can be disastrous for your hormonal balance,” she explains. “Things like yoga, meditation, mindfulness, and exercise can really help us adjust our mindset.”

Sleep helps, too, but many people find it more elusive as they age because of disrupted cortisol patterns. Gottfried recommends moderating circadian rhythms by dimming lights in the evening and timing carbohydrate consumption.


Some of the best predictors of a good health span may not sound especially scientific. They involve words like “community” and “passion,” says Nortin Hadler, MD, professor of microbiology/immunology at the University of North Carolina at Chapel Hill. But they have a real and measurable effect on how long and how well you live.

Hadler has spent years as a medical iconoclast, arguing that while certain drugs and procedures may be indispensable for treating diseases, community and social engagement are equally crucial for maintaining overall good health. And there’s plenty of science to back him up.

In 2014, University of Chicago researchers reported that feelings of loneliness represent a major health risk for older adults and can increase their risk of premature death by 14 percent. They also referenced a 2010 meta-analysis that found that loneliness has twice the impact on early death as obesity does. But you don’t have to be old to have your health negatively affected by a lack of social support and connection.

Numerous studies have shown that feeling a strong sense of social and emotional connection helps reduce the biochemical markers of stress, lowers inflammation, improves immunity, supports healthy hormonal balance,
and can even affect gene expression.

In his best-selling book The Blue Zones, National Geographic explorer Dan Buettner named having a strong sense of community as one of the top factors dictating not just one’s chances of living to 100, but of living to 100 as a reasonably healthy and happy person.

And in the big picture, that’s really what aging well is all about: enjoying a high-vitality, rewarding life both now and later. Starting wherever you are, right here, today.


Make some space for real, live human interaction and significant relationships. Start by looking at your calendar. Do you have plans for social activities that feel rich, rewarding, and fun? Are you visiting with friends and family, volunteering on projects, participating in group activities, going on dates?

All of these things make a big difference in how connected you feel, and that feeling of connection keeps you vital at all levels. “You want to be engaged, you want to feel valued, you want to have a community,” says Hadler. “If you don’t, it will take years off your life.”

7 Key Anti-Aging Ingredients For Your Skin And Hair

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There Are Certain Supplements Which You Can Buy, Ingredients And Or Substances Which Your Body Produces And Others Found In Your Food That Have Important Anti-Aging Properties For Your Skin And Hair. We’ve Identified Seven Key Anti-Aging Ingredients That Will Help You Look Better, For Longer


Amino acids are compounds that combine to form proteins. Along with proteins, they are considered to be the building blocks of life. According to AminoStudies.org, amino acids help our body to break down food, grow, repair body tissue and perform a number of other body functions. Amino acids are classified as: essential amino acids (these cannot be made by our body, so we need to get them through food); non-essential amino acids (our body produces these, even if we don’t get them from our food); and conditional amino acids (these are usually not essential, except during times of illness and stress).

HOW IT WORKS ON YOUR SKIN:  Creatine is considered to be one of the most important amino acids for skin, as it not only keeps skin functioning properly, but also plays an important role in the production of collagen. Creatine is formed from arginine (conditional amino acid) and carnitine. Creatine also ensures that the body stays hydrated. It surrounds the cells of the skin with a thin layer of water, which protects them from being damaged by heat, UV rays and other pollutants.

HOW IT WORKS ON YOUR HAIR:  Methionine (an essential amino acid) plays a role in the health of your hair, helping to build stronger hair structures. Plus, research shows that methionine can assist in the reduction of hair loss. L-Lysine (also an essential amino acid) has been shown to positively affect the synthesis of collagen, which increases the strength of your hair. This is also believed to play a role in repairing the mechanisms of your hair, which can assist in the reduction of daily hair loss.


These are natural and man-made substances that help to protect your cells from free radicals, explains Paula Begoun, an internationally recognised consumer expert for the cosmetic industry, and author of bestsellers Don’t Go to the Cosmetic Counter without Me and The Original Beauty Bible. Sun, smoke and pollution all cause oxidative damage that in turn results in cell death. It is impossible to avoid free radicals completely, as the body produces them. By adding antioxidant-rich fruits, vegetables and vitamins to your diet, you can boost your body’s ability to fight infection, diseases and even premature aging. Some of the most powerful antioxidants are green tea, blueberries and grapeseed extract.

HOW IT WORKS ON YOUR SKIN: Glutamine (which is also an essential amino acid) is an antioxidant, so it aids in combating the effects of aging on the skin. If you are not getting enough of this amino acid in your diet, your body tries to pull it from your muscles. This means reduced muscle mass and less elasticity in your skin, which in turn results in sagging, wrinkles and a dull appearance. Vitamins E and D are also beneficial for skin health, is well known for it’s anti-aging properties and will help to preserve the youthful look of skin.

HOW IT WORKS ON YOUR HAIR: Hair’s keratin-based structures are susceptible to oxidative damage, which can lead to split ends, broken hairs, rough cuticles, frizz, tangling, lack of lustre, and even loss of colour (both natural and artificial). The sun is the biggest culprit for oxidative damage, as the rays penetrate the hair shaft and deplete the natural stores of melanin, found in the hair cortex. This also alters the protein structures of both the hair cuticle and cortex. Chemical processes (in particular, bleaching and permanent dyeing) tend to deplete the natural melanin, therefore creating oxidative damage. Treatments such as relaxers, perms, keratin treatments and heat styling all contribute to the formation of free radicals, which in turn negatively affect the lipids and proteins in the cuticle. Environmental factors such as pollutants, tobacco smoke, certain substances in our water and radiation all add to this free-radical damage. The good news is that evidence indicates that antioxidants are found in formulations for rinse-off products, leave-in conditioners and styling agents. Also look for vitamins and vitamin precursors, such as vitamin E, C and beta carotene, as these have been found to have protective effects.


Scientifically speaking, hyaluronic acid (also known as hyaluronan) is a glycosaminoglycan, a type of molecule composed partly of sugars, says Begoun. “Hyaluronic acid is a natural structural component of skin, and, in fact, is present in connective tissue throughout the human body.” Hyaluronic acid is found in the greatest concentrations in skin tissue (with almost 50% of the body’s hyaluronic acid found here), in both the deep underlying dermal tissue and the visible epidermal top layers. Begoun adds: “The true magic of this special anti-aging ingredient is its ability to retain moisture. In fact, one gram of of hyaluronic acid is able to hold up to six litres of water!”

HOW IT WORKS ON YOUR SKIN: As we age, so our skin loses moisture, which in turn affects its elasticity and pliability. Begoun explains that this doesn’t mean that all skin becomes dry with age; it simply means that your skin can lack the amount of moisture you had in your youth, due to sun damage and other environmental factors. “Without question, you can still have oily skin in your 60s (perhaps just not as oily as it was in your 20s).” Hyaluronic acid helps to improve the skin’s moisture content, while also strengthening the skin’s barrier, which results in a softer, smoother, plumper looking skin. “We know that just about everything, from sun damage and acne to sensitive skin and rosacea, can lead to a damaged barrier, so repairing the skin’s barrier with skin-identical ingredients, such as hyaluronic acid, can go a long way towards fixing, or at least minimising, those issues, which means it’s helpful for all skin types. Its lightweight texture isn’t an issue for oily skin, and it’s gentle enough that it isn’t a problem for sensitive skin,” notes Begoun.

HOW IT WORKS ON YOUR HAIR: Hyaluronic acid hydrates deep within the hair fibre, due to its small molecular size. Plus, it acts like a sponge, and has the ability to retain moisture, build volume and even fill in rough or cracked parts of your hair shaft.


This is the term given for the entire vitamin A molecule, explains Begoun. It is a beneficial cell communicating ingredient and antioxidant. In skincare and beauty products, it is found in the form of retinol, retinyl palmitate and retinaldehyde. In prescription-only skincare products, it is in the form of retinoic acid or tretinoin.

HOW IT WORKS ON YOUR SKIN:  It is believed that, when applied to skin, it assists in creating better, healthier skin cells, and increases the number of skin-support substances, adds Begoun. “Retinol has been shown to increase the skin’s collagen production and glycosaminoglycan content, resulting in firmer skin with an improved texture and enhanced barrier function.” According to numerous published dermatology studies, retinol also functions as an antioxidant, and can interrupt the free-radical damage that results in the most obvious signs of aging. Plus, it promotes collagen production, fades discolouration from sun damage, and helps to build elastin. With retinol, you need to start slowly. Begoun suggests that you apply it every other day, or mix it in with your usual moisturiser to buffer against redness, flaking and irritation. This allows your skin to gradually acclimatize to this potent ingredient. You also need to be diligent with applying sun protection.

HOW IT WORKS ON YOUR HAIR: Retinyl palmitate provides free-radical protection, while nourishing your hair and scalp. It also adds a healthy sheen to your hair, in addition to body and suppleness. If your hair has been damaged through over processing, retinyl palmitate can help to improve texture.


HOW IT WORKS ON YOUR SKIN: As CoQ10 is found in the mitochondria of cells, it can help to prevent the formation of matrix metalloproteinases (MMPs). MMPs are known to damage or destroy collagen and elastin, which in turn leads to saggy skin and the formation of wrinkles. CoQ10 also assists in the production of cellular energy. According to research conducted by the Mayo Clinic, studies have found that C0Q10, combined with other antioxidants and minerals, can improve skin roughness and fine wrinkles.

HOW IT WORKS ON YOUR HAIR: When used topically (such as through shampoo or a hair treatment), it is believed to enhance scalp circulation, and may even increase the rate at which hair grows. It also helps to restore shine and lustre to mature, fine or fragile hair. Plus, a 2009 study published by the Society of Cosmetic Scientists and the Société Française de Cosmétologie in the International Journal of Cosmetic Science found that CoQ10 has anti-aging effects on your hair.

COQ10 According to the University of Maryland School of Medicine, Co-enzyme Q10 is a powerful antioxidant that is found in almost every cell in the body. This substance helps to convert food into energy. As it is an antioxidant, it fights free radicals which damage cell membranes, tamper with DNA and can even cause cell death. These free radicals also contribute to the aging process (in addition to a number of health concerns, including heart disease and cancer). CoQ10 is believed to aid in reducing, or even preventing, this damage and is considered an important ingredient and


Research out of Rockefeller University reveals that adult stem cells reside in most tissues in the body. These stem cells are remarkable, as they can survive long-term, and can regenerate both themselves and their resident tissues during normal wear and tear, and following injury. The researchers explain that they exist in two distinct states: a quiescent state, in which they are not making tissue, and an active state, in which they are making tissue. When activated, they produce shorter-lived progenitors that divide rapidly and then progress to terminally differentiate, to form their respective tissue cells. Plants also have stem cells, reports lead researcher David Schmid and his team in their research paper Plant Stem Cell Extract for Longevity of Skin and Hair. However, unlike humans, adult plants contain potent stem cells with the potential to regenerate a whole plant. These stems cells are being researched and developed into skin and hair products.


HOW IT WORKS ON YOUR SKIN: The plant stem cells are, more often than not, obtained from rare Swiss apple trees. They are starting to be incorporated into anti-aging skin formulas, to repair DNA damage and protect against environmental aggressors.

HOW IT WORKS ON YOUR HAIR:  Research reveals that, when incorporated into hair products, stem cells can assist in maintaining healthy follicle cells, to delay the effects of aging on hair and scalp. Again, apple stem cells (the most common variety used in haircare products) contain the right characteristics to aid in hair growth. They work at a cellular level to maintain cellular renewal, and apple stem cells are believed to stimulate the activity of dormant hair follicles.


Resveratrol, a potent antioxidant found in red grapes, has been found to have preventive and therapeutic effects, according to a 2011 paper, The Grape Antioxidant Resveratrol for Skin Disorders: Promise, Prospects and Challenges. Lead author Mary Ndiaye and her team reported that studies have shown protective effects of resveratrol against ultraviolet radiation, oxidative stress and cutaneous damages, including skin cancer. “Because many of the skin conditions stem from ultraviolet radiation and oxidative stress, this antioxidant appears to have promise and prospects against a wide range of cutaneous disorders, including skin aging.”


HOW IT WORKS ON YOUR SKIN:  Researchers have found that resveratrol as an ingredient can have an anti-aging and inflammatory effect. This extract protects against UV and free-radical damage, helping to improve skin tone, the appearance of wrinkles and skin discolouration.

HOW IT WORKS ON YOUR HAIR: Resveratrol plays a role in protecting hair from free-radical damage and stimulating cell regeneration. The antioxidant feeds new cells that are forming at the root, to keep the follicle strong. This in turn creates healthier hair. Resveratrol also helps to re-balance the pH of the scalp and reverse the damage caused by environmental aggressors, resulting in healthier, shinier and stronger hair.

Article Source: http://www.longevitylive.com/key-anti-aging-ingredients-skin-hair/

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Keeping older muscles strong

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As we grow older, we lose strength and muscle mass. However, the cause of age-related muscle weakness and atrophy has remained a mystery.

Scientists at the University of Iowa have discovered the first example of a protein that causes muscle weakness and loss during aging. The protein, ATF4, is a transcription factor that alters gene expression in skeletal muscle, causing reduction of muscle protein synthesis, strength, and mass. The UI study also identifies two natural compounds, one found in apples and one found in green tomatoes, which reduce ATF4 activity in aged skeletal muscle. The findings, which were published online Sept. 3 in the Journal of Biological Chemistry, could lead to new therapies for age-related muscle weakness and atrophy.

“Many of us know from our own experiences that muscle weakness and atrophy are big problems as we become older,” says Christopher Adams, MD, PhD, UI professor of internal medicine and senior study author. “These problems have a major impact on our quality of life and health.”

Previously, Adams and his team had identified ursolic acid, which is found in apple peel, and tomatidine, which comes from green tomatoes, as small molecules that can prevent acute muscle wasting caused by starvation and inactivity. Those studies set the stage for testing whether ursolic acid and tomatidine might be effective in blocking the largest cause of muscle weakness and atrophy: aging.

In their latest study, Adams’ team found that ursolic acid and tomatidine dramatically reduce age-related muscle weakness and atrophy in mice. Elderly mice with age-related muscle weakness and atrophy were fed diets lacking or containing either 0.27 percent ursolic acid, or 0.05 percent tomatidine for two months. The scientists found that both compounds increased muscle mass by 10 percent, and more importantly, increased muscle quality, or strength, by 30 percent. The sizes of these effects suggest that the compounds largely restored muscle mass and strength to young adult levels.

“Based on these results, ursolic acid and tomatidine appear to have a lot of potential as tools for dealing with muscle weakness and atrophy during aging,” Adams says. “We also thought we might be able to use ursolic acid and tomatidine as tools to find a root cause of muscle weakness and atrophy during aging.”

Adams’ team investigated the molecular effects of ursolic acid and tomatidine in aged skeletal muscle. They found that both compounds turn off a group of genes that are turned on by the transcription factor ATF4. This led them to engineer and study a new strain of mice that lack ATF4 in skeletal muscle. Like old muscles that were treated with ursolic acid and tomatidine, old muscles lacking ATF4 were resistant to the effects of aging.

“By reducing ATF4 activity, ursolic acid and tomatidine allow skeletal muscle to recover from effects of aging,” says Adams, who also is a member of the Fraternal Order of Eagles Diabetes Research Center at the UI and a staff physician with the Iowa City Veterans Affairs Medical Center.

The UI study was done in collaboration with Emmyon, Inc., a UI-based biotechnology company founded by Adams, that is now working to translate ursolic acid and tomatidine into foods, supplements, and pharmaceuticals that can help preserve or recover strength and muscle mass as people grow older.


In addition to Adams, the UI team included Michael Dyle, Steven Bullard, Jason Dierdorff, Daryl Murry, Daniel Fox, Kale Bongers, Vitor Lira, and David Meyerholz, as well as Scott Ebert and John Talley at Emmyon, Inc.

The study was funded by a Small Business Innovation Research (SBIR) grant to Emmyon, Inc. from the National Institute on Aging, as well as grants from the Department of Veterans Affairs and the Fraternal Order of Eagles Diabetes Research Center at the University of Iowa.

Source: http://www.eurekalert.org/pub_releases/2015-09/uoih-kom090815.php

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The below was issued on February 18, 2014 in response to the flawed TRT studies recently published.  Unfortunately the main stream media only seeks to fan the flames of any salacious stories rather than focus on the hundreds of studies that prove otherwise.  The media also ignores all the physicians, PhD’s and Harvard Medical School Professors who disagree with the failed study.

It is very important to note that these studies, while causally flawed, also found that there was no excess risk at all to men under 65 years old without a prior history of heart attacks.  

For more information call Boston Testosterone Partners at 855.617.6337 or visit our webpage at http://www.BostonTestosterone.com.


 A4M responds to Finkle W, et al “Increased risk of nonfatal myocardial infarction following testosterone therapy prescription in men” PLOS One 2014; DOI: 10.1371/journal.pone.0085805.

In response to William Finkle, et al. in PLOS One (29 Jan. 2014) the A4M finds the statistical study fails to represent an actual causal relationship between Testosterone therapy (TT) and myocardial infarction (MI).

Dr. Abraham Morgentaler, Associate Clinical Professor in the Department of Urology at Harvard University, writes the following regarding the statistical results of the study:  “It is possible that the men’s heart attacks in this study were caused by their underlying medical problems not testosterone…most heart attacks occurred in the first 90 days after a prescription was written.  It is unlikely that heart attacks could develop in such a short period of time.” (Featured interview:  USA Today Jan 29, 2014).

This statistical study is a manipulation of data, and does not represent an actual causal relationship between testosterone therapy and myocardial infarctions. These researchers’ statistical findings are extremely flawed as they don’t accurately account for any phenotypical variability or the fact that multi-factorial variables were not examined in their research project.  There was not any form of analysis of various serum parameters, ekg, exercise tolerance, muscle to fat ratio, the particular nature of testosterone therapy as well as dosing and administration of other drug interactions.  It is possible for any researcher to a manipulate a particular database and exhibit a correlational relationship between testosterone therapy and non-fatal myocardial infarctions.  It is also likely that the succinct population used in this study may have a greater disposition to cardiovascular events as compared to another cohort population of males over 65.

William Finkle et.  al. writes in their discussion that there are difficulties with this study.  The homogeneous database employed in this study is definitely not representative of other global heterogeneous databases, and most likely in terms of the correlational outcome of this study cannot be generalized to a larger population configuration.  This study should not have ever been published due to its methodological limitations, and Finkle et. al., did not review any of the other variables which needed to be analyzed in order to make an accurate assessment in terms of the relationship between exogenous testosterone normalization and cardiovascular morbidities.  The comparison that was employed in this study using the PDE5I group clearly makes this study invalid.  PDE5I induces vasodilation and therefore is not a valid control group.   What this study does point out is that actual research investigations should be conducted, in the rodent model as well as humans, about how higher levels of testosterone in the older phenotype impacts transcriptional and translation activities which eventuates in modifications in the cardiovascular system.  Furthermore, William Finkle et. al. did not consider any kind of epigenetic factors in his insufficient data analysis.  He is raising certain issues as to criteria which needs to be considered prior to a clinician prescribing testosterone for older males, such as certain phenotypes that should be excluded, based on their pathophysiology from receiving exogenous testosterone replacement.

Finkle et. al. states the following regarding the shortcomings of his study:  “Further study is needed to examine the risk of a variety of specific serious adverse cardiovascular events in relation to TT dose and duration, and to assess if the risks of TT vary by level of serum testosterone and presence or absence of hypogonadal disease”.  Paradoxically, these researchers discuss elsewhere “low endogenous testosterone levels may also be positively associated with cardiovascular events.”  This article makes salient many issues regarding this therapeutic protocol for the treatment of andropause in men.  Finkle  et.  al. does state that this therapy is pathophysiological, however, his correlational analysis as mentioned is flawed.  Clinicians should consider when prescribing testosterone to the older phenotype whether his overall health status or way of living should warrant this therapeutic protocol.
Finkle et. al.  did discuss some of the recognized side effects of testosterone therapy “increase of blood pressure, polycythemia, reduction in HDL cholesterol and hyper viscosity of blood and platelet aggregation.”  These pathophysiological parameters can be readily alleviated by a competent clinician with the employment of medicinal protocols.  It is not likely that polycythemia if regulated by a physician could engender cardiovascular events in the older phenotypes who have been placed on testosterone therapy. There have been a plethora of studies which have demonstrated that exogenous testosterone replacement to physiological levels does, in fact, mitigate the risk of cardiovascular morbidities.

Should a lethargic, obese, and hypertensive patient who is a borderline type 2 diabetic over 70 be prescribed exogenous testosterone therapy?  The physiological parameters of a male patient that is highly educated and involved in cardiovascular exercise programs, and who has an optimal fat to muscle ratio with an exquisite BMI is very different from an obese, hypertensive, pathogenic 65 year old male phenotype.  There is certainly more risk associated with the prophylaxis of a pathophysiological male compared to those optimally conditioned older cohorts.  In the hands of a highly qualified Anti-Aging physician, practicing preventative endocrinological therapies aka Anti-Aging Medicine (see http://www.worldheath.net),  testosterone replacement therapy can be used in conjunction with exercise, dietary manipulation and other cardiovascular risk factor reductions including the routine monitoring of hematocrit, blood viscosity, platelet counts and other indicators of polycythemia.  It is also common practice to remove 100-200cc of whole blood in individuals who are on long-term testosterone therapy to maintain optimal indices.

This article has caused unwarranted and exaggerated fears in the media and in the non-medically trained public. It has already induced unwanted trepidation regarding this medicinal therapy which has for the preceding 50 years improved the quality of life in millions of males and females.  The popular media will interpret the results of this skewed correlational study, which is unrepresentative of the overall older male population, as causing myocardial infarctions in patients being titrated with this therapeutic strategy.  However, physicians have the responsibility to judiciously manage patients in older phenotypes with multiple co morbidities.

At the most recent ENDO 2013 Annual Meeting (sponsored by The Endocrine Society), many of the speakers from the international endocrinology community lauded Testosterone therapy as an extremely viable prophylaxis for the mitigation of the symptomology associated with aging-related declines in male hormones.  There was no discussion of increased risk of cardiovascular morbidity with properly administered and monitored Testosterone therapy.  The speakers at the Winter 2013 Session of the 22nd Annual Congress on Anti-Aging Medicine, sponsored by the American Academy of Anti-Aging Medicine (A4M; http://www.worldhealth.net & http://www.a4m.com), held December 2013, also lectured on this topic.  These speakers cited overwhelming evidence of benefits of Testosterone therapy; and this protocol for the treatment of Testosterone decline reduced the risk of myocardial infarction.

Submitted by:
Ron Shane, PhD., O.M.D.
Tina Miranda, M.D., M.B.A., Diplomate ABIM
Karan Pandar
Ronald Klatz, M.D., D.O., President, A4M
Sharon McQuillan, M.D.
Jeffry S. Life, M.D. Ph.D.

Welcome to the 50 year old club Brad Pitt!

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aaabrad-pitt-300x400Welcome to the 50+ club, Brad.

Wondering why everyone in Hollywood looks 10-15 years younger?

Hormone and Regenerative medicine is not just for the elite. Contact us through our “Get Started” page at www.BostonTestosterone.com today to learn more about how our regenerative medicines can help you regain your natural state of health, balance & youthfulness.

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