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.

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.

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 proteins ³²
• Decreases the harmful effect of beta-amyloid on brain cell function ^39-41
• Reduces levels of alpha synuclein , another protein that accumulates and causes damage in Parkinson’s disease ⁴²
• Prevents the loss of dopamine-producing brain cells in a model of Parkinson’s disease ^43,44
• Improves motor coordination in a mouse model of Parkinson’s ⁴⁵

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.

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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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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The January 2016 issue of the journal Diabetes Care reported the outcome of a randomized trial that revealed a beneficial role for testosterone treatment in men with diabetes.

“We hypothesized that testosterone may be an anti-inflammatory and insulin sensitizing agent since it has been known for some time that testosterone reduces adiposity and increases skeletal muscle,” remarked lead researcher Paresh Dandona, MD, PhD, who is a Distinguished Professor at the State University of New York and chief of endocrinology, diabetes and metabolism in the Department of Medicine in the Jacobs School of Medicine and Biomedical Sciences at the University of Buffalo. “Our previous work has shown that obesity is associated with oxidative stress and inflammation, and inflammatory mediators are known to interfere with insulin signaling.”

The trial included 94 type 2 diabetic men, among whom 44 had low testosterone levels and reduced insulin signaling genes indicative of decreased insulin sensitivity. Participants with low testosterone received a weekly testosterone injection or a placebo for 24 weeks. Body weight, body fat, markers of inflammation, insulin sensitivity and other factors were assessed before and after treatment.

At the end of the trial, men who received testosterone experienced a more than six pound average loss of body fat and an equal increase in muscle mass. They also had lower levels of the inflammatory markers C-reactive protein, interleukin-1b and tumor necrosis factor-a. “Most importantly, we saw a dramatic increase in insulin sensitivity, demonstrated by a 32 percent increase in the uptake of glucose by tissues in response to insulin,” Dr Dandona reported.

“Testosterone treatment for men, where indicated, will improve sexual function and increase skeletal muscle strength and bone density,” Dr Dandona noted. “This is the first definitive evidence that testosterone is an insulin sensitizer and hence a metabolic hormone.”

Article Source: http://www.lifeextension.com/WhatsHot/2015/11/November-Whats-Hot-Articles/Page-01#test

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We aimed to evaluate the efficacy of tadalafil 5 mg once-daily treatment on testosterone levels in patients with erectile dysfunction (ED) accompanied by the metabolic syndrome. A total of 40 men with metabolic syndrome were evaluated for ED in this study. All the patients received 5 mg tadalafil once a day for 3 months. Erectile function was assessed using the five-item version of the International Index of Erectile Function (IIEF) questionnaire. Serum testosterone, follicle-stimulating hormone and luteinising hormone levels were also evaluated, and blood samples were taken between 08.00 and 10.00 in the fasting state. All participants have three or more criteria of metabolic syndrome. At the end of 3 months, mean testosterone values and IIEF scores showed an improvement from baseline values (from 3.6 ± 0.5 to 5.2 ± 0.3, from 11.3 ± 1.9 to 19 ± 0.8 respectively). After the treatment, serum LH levels were decreased (from 5.6 ± 0.6 to 4.6 ± 0.5). There was significantly difference in terms of baseline testosterone and luteinising hormone values and IIEF scores (p < .05). Based on our findings, we recommend tadalafil 5 mg once daily in those men with erectile dysfunction especially low testosterone levels accompanied by metabolic syndrome.

Article Source: https://www.ncbi.nlm.nih.gov/pubmed/28295481

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WHAT VITAMIN DO WE need in amounts up to 25 times higher than the government recommends for us to be healthy?

What vitamin deficiency affects over half of the population, is almost never diagnosed, and has been linked to many cancers, high blood pressure, heart disease, diabetes, depression, fibromyalgia, chronic muscle pain, bone loss, and autoimmune diseases like multiple sclerosis?

What vitamin is almost totally absent from our food supply?

What vitamin is the hidden cause of so much suffering that is so easy to treat?

The answer to all of these questions is vitamin D.

Over the last 10 years of my practice, my focus has been to discover what the body needs to function optimally. And I have become more interested in the role of specific nutrients as the years have passed.

Two recent studies in The Journal of Pediatric s found that 70 percent of American kids aren’t getting enough vitamin D, and this puts them at higher risk of obesity, diabetes, high blood pressure, and lower levels of good cholesterol. Low vitamin D levels also may increase a child’s risk of developing heart disease later in life.

Overall, 7.6 million, or 9 percent, of American children were vitamin D deficient, and another 50.8 million, or 61 percent, had insufficient levels of this important vitamin in their blood.

Over the last 5 years, I have tested almost every patient in my practice for vitamin D deficiency, and I have been shocked by the results. What’s even more amazing is what happens when my patients’ vitamin D status reaches optimal levels. Having witnessed these changes, there’s no doubt in my mind: vitamin D is an incredible asset to your health.

That is why in today’s blog I want to explain the importance of this essential vitamin and give you 6 tips on how to optimize your vitamin D levels.

Let’s start by looking at the massive impact vitamin D has on the health and function of every cell and gene in your body.

How Vitamin D Regulates Your Cells and Genes

Vitamin D has a huge impact on the health and function of your cells. It reduces cellular growth (which promotes cancer) and improves cell differentiation (which puts cells into an anti-cancer state). That makes vitamin D one of the most potent cancer inhibitors — and explains why vitamin D deficiency has been linked to colon, prostate, breast, and ovarian cancer.

But what’s even more fascinating is how vitamin D regulates and controls genes.

It acts on a cellular docking station ,called a receptor, that then sends messages to our genes. That’s how vitamin D controls so many different functions – from preventing cancer, reducing inflammation, boosting mood, easing muscle aches and fibromyalgia, and building bones.

These are just a few examples of the power of vitamin D. When we don’t get enough it impacts every area of our biology, because it affects the way our cells and genes function. And many of us are deficient for one simple reason …

For example, one study found that vitamin D supplementation could reduce the risk of getting type 1 diabetes by 80 percent.

Your body makes vitamin D when it’s exposed to sunlight. In fact, 80 to 100 percent of the vitamin D we need comes from the sun. The sun exposure that makes our skin a bit red (called 1 minimum erythemal dose) produces the equivalent of 10,000 to 25,000 international units (IU) of vitamin D in our bodies.

The problem is that most of us aren’t exposed to enough sunlight.

Overuse of sunscreen is one reason. While these product help protect against skin cancer – they also block a whopping 97 percent of your body’s vitamin D production.

If you live in a northern climate, you’re not getting enough sun (and therefore vitamin D), especially during winter. And you’re probably not eating enough of the few natural dietary sources of vitamin D: fatty wild fish like mackerel, herring, and cod liver oil.

Plus, aging skin produces less vitamin D — the average 70 year-old person creates only 25 percent of the vitamin D that a 20 year-old does. Skin color makes a difference, too. People with dark skin also produce less vitamin D. And I’ve seen very severe deficiencies in Orthodox Jews and Muslims who keep themselves covered all the time.

With all these causes of vitamin D deficiency, you can see why supplementing with enough of this vitamin is so important. Unfortunately, you aren’t really being told the right amount of vitamin D to take.

The government recommends 200 to 600 IU of vitamin D a day. This is the amount you need to prevent rickets, a disease caused by vitamin D deficiency. But the real question is: How much vitamin D do we need for OPTIMAL health? How much do we need to prevent autoimmune diseases, high blood pressure, fibromyalgia, depression, osteoporosis, and even cancer?

The answer is: Much more than you think .

Recent research by vitamin D pioneer Dr. Michael Holick, Professor of Medicine, Physiology, and Dermatology at Boston University School of Medicine, recommends intakes of up to 2,000 IU a day — or enough to keep blood levels of 25 hydroxy vitamin D at between 75 to 125 nmol/L (nanomoles per liter). That may sound high, but it’s still safe: Lifeguards have levels of 250 nmol/L without toxicity.

Our government currently recommends 2,000 IU as the upper limit for vitamin D — but even that may not be high enough for our sun-deprived population! In countries where sun exposure provides the equivalent of 10,000 IU a day and people have vitamin D blood levels of 105 to 163 nmol/L, autoimmune diseases (like multiple sclerosis, type 1 diabetes, inflammatory bowel disease, rheumatoid arthritis, and lupus) are uncommon.

Don’t be scared that amounts that high are toxic: One study of healthy young men receiving 10,000 IU of vitamin D for 20 weeks showed no toxicity.

The question that remains is: How can you get the right amounts of vitamin D?

6 Tips for Getting the Right Amount of Vitamin D

Unless you’re spending all your time at the beach, eating 30 ounces of wild salmon a day, or downing 10 tablespoons of cod liver oil a day, supplementing with vitamin D is essential. The exact amount needed to get your blood levels to the optimal range (100 to160 nmol/L) will vary depending on your age, how far north you live, how much time you spend in the sun, and even the time of the year. But once you reach optimal levels, you’ll be amazed at the results.

For example, one study found that vitamin D supplementation could reduce the risk of getting type 1 diabetes by 80 percent. In the Nurses’ Health Study (a study of more than 130,000 nurses over 3 decades), vitamin D supplementation reduced the risk of multiple sclerosis by 40 percent.

I’ve seen many patients with chronic muscle aches and pains and fibromyalgia who are vitamin D deficient – a phenomenon that’s been documented in studies. Their symptoms improve when they are treated with vitamin D.

Finally, vitamin D has been shown to help prevent and treat osteoporosis. In fact, it’s even more important than calcium. That’s because your body needs vitamin D to be able to properly absorb calcium. Without adequate levels of vitamin D, the intestine absorbs only 10 to 15 percent of dietary calcium. Research shows that the bone-protective benefits of vitamin D keep increasing with the dose.

So here is my advice for getting optimal levels of vitamin D:

1. 1. Get tested for 25 OH vitamin D. The current ranges for “normal” are 25 to 137 nmol/L or 10 to 55 ng/ml. These are fine if you want to prevent rickets – but NOT for optimal health. In that case, the range should be 100 to 160 nmol/L or 40 to 65 ng/ml. In the future, we may raise this “optimal” level even higher.

1. 2. Take the right type of vitamin D. The only active form of vitamin D is vitamin D3 (cholecalciferol). Look for this type. Many vitamins and prescriptions of vitamin D have vitamin D2 – which is not biologically active.

1. 3. Take the right amount of vitamin D. If you have a deficiency, you should correct it with 5,000 to 10,000 IU of vitamin D3 a day for 3 months — but only under a doctor’s supervision. For maintenance, take 2,000 to 4,000 IU a day of vitamin D3. Some people may need higher doses over the long run to maintain optimal levels because of differences in vitamin D receptors, living in northern latitudes, indoor living, or skin color.

1. 4. Monitor your vitamin D status until you are in the optimal range. If you are taking high doses (10,000 IU a day) your doctor must also check your calcium, phosphorous, and parathyroid hormone levels every 3 months.

1. 5. Remember that it takes up to 6 to 10 months to “fill up the tank” for vitamin D if you’re deficient. Once this occurs, you can lower the dose to the maintenance dose of 2,000 to 4,000 units a day.

1. 6. Try to eat dietary sources of vitamin D. These include:

1. • Fish liver oils, such as cod liver oil. One tablespoon (15 ml) = 1,360 IU of vitamin D

1. • Cooked wild salmon. (3.5) ounces = 360 IU of vitamin D

1. • Cooked mackerel. (3.5) ounces = 345 IU of vitamin D

1. • Sardines, canned in oil, drained. (1.75) ounces = 250 IU of vitamin D

1. • One whole egg = (20) IU of vitamin D

You can now see why I feel so passionately about vitamin D. This vitamin is critical for good health. So start aiming for optimal levels – and watch how your health improves.

By: Mark Hyman, MD

Article Source: http://drhyman.com/blog/2010/08/24/vitamin-d-why-you-are-probably-not-getting-enough/

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Article Source: http://www.worldhealth.net/news/poor-oral-health-may-signal-prostate-issues/

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Testosterone replacement therapy (TRT) is associated with a lower risk of adverse cardiovascular (CV) events among men with testosterone deficiency, according to a new study.

Researchers led by T. Craig Cheetham, PharmD, MS, of the Southern California Permanente Medical Group, identified a retrospective cohort of 44,335 men aged 40 years and older with evidence of testosterone deficiency. The cohort included 8808 men who had ever been dispensed testosterone (ever-TRT group) and 35,527 men never dispensed testosterone (never-TRT group). The primary outcome was a composite of cardiovascular endpoints that included acute myocardial infarction (AMI), coronary revascularization, unstable angina, stroke, transient ischemic attack (TIA), and sudden cardiac death (SCD).

After a median follow-up of 3.2 years in the never-TRT group and 4.2 years in the ever-TRT group, the rates of the composite endpoint were significantly higher in the never-TRT than ever-TRT group (23.9 vs 16.9 per 1000 person-years), Dr Cheetham and colleagues reported online ahead of print in JAMA Internal Medicine . After adjusting for potential confounders, the ever-TRT group had a significant 33% lower risk of the primary outcome compared with the never-TRT group. The investigators found similar results when looking separately at combined cardiac events (AMI, SCD, unstable angina, coronary revascularization) and combined stroke events (stroke and TIA). The ever-TRT group had a significant 34% and 28% lower risk of cardiac events and stroke events compared with the never-TRT group, respectively.

“While these findings differ from those of recently published observational studies of TRT, they are consistent with other evidence of CV risk and the benefits of TRT in androgen-deficient men,” the investigators wrote.

Previous studies have found an association between low serum testosterone levels in aging men and an increased risk of coronary artery disease as well as an inverse relationship between serum testosterone and carotid intima thickness, Dr Cheetham’s team pointed out.

The never-TRT and ever TRT groups had a mean age of 59.8 and 58.4 years, respectively. In the never-TRT group, 13,824 men (38.9%) were aged 40 to 55 years, 10,902 (30.7%) were aged 56 to 65 years, and 10,801 (30.4%) were older than 65 years. In the ever-TRT group, 3746 men (42.5%) were aged 40 to 55, 2899 (32.9%) were aged 56 to 65 years, and 2163 (24.6%) were older than 65 years. The groups were similar with respect to race and ethnicity composition.

The researchers defined testosterone deficiency as a coded diagnosis and/or a morning serum total testosterone level below 300 ng/dL.

With regard to study limitations, the investigators noted that their criterion for identifying men with testosterone deficiency (a diagnosis or at least 1 morning testosterone measurement) does not meet the strict criteria established by the Endocrine Society. “Therefore some individuals in the study could be misclassified as being androgen-deficient.” In addition, as the study was observational in design, “unmeasured confounding may have had an influence on the results; unmeasured confounders could possibly influence clinicians to selectively use testosterone in healthier patients.”

In an accompanying editorial, Eric Orwoll, MD, of Oregon Health & Sciences University in Portland, commented that while the study by Dr Cheetham’s group “provides reassuring data concerning the effects of testosterone on cardiovascular health, convincing answers about this question—and other safety issues like prostate health—remain elusive and will require large, prospective randomized trials.

“At this point, clinicians and their patients should remain aware that the cardiovascular risks and benefits of testosterone replacement in older hypogonadal men have not been adequately resolved.”

Reference

1. Cheetham TC, An JJ, Jacobsen SJ et al. Assocation of testosterone replacement therapy with cardiovascular outcomes among men with androgen deficiency. JAMA Intern Med 2017; published online ahead of print. doi: 10.1001/jamainternmed.2016.9546

Jody A. Charnow, Editor

Article Source: http://www.renalandurologynews.com/hypogonadism/testosterone-deficiency-treated-trt-may-reduce-cardiovascular-events/article/639486/

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