Understanding Inflammation

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

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

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

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

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


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

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

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

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

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

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

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

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

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

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

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


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

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

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

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

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

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

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

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


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

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

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

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

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

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

Written By: Michael Anft

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

 

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Will Metformin Become the First Anti-Aging Drug?

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

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

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

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

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

Broad-Spectrum Effects

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

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

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

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

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

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

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

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

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

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

WHAT YOU NEED TO KNOW

Metformin as an Anti-Aging Drug

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

Cancer Protective Effects of Metformin

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

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

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

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

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

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

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

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

Metformin Prevents Cardiovascular Disease

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

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

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

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

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

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

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

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

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

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

FDA APPROVES FIRST ANTI-AGING STUDY

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

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

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

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

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

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

Metformin Reduces Body Weight and Fat Mass

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

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

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

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

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

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

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

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

Metformin as Neuroprotectant

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

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

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

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

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

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

PRECAUTIONS AND USEFUL SUGGESTIONS WITH METFORMIN USE

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

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

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

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

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

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

Summary

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

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

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

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

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

Written By: Raegan Linton

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

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Why glutathione is important to us

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

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

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

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

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

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

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

How glutathione works

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

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

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

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

Key benefits of glutathione

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

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

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

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

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

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

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

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

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

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

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

 

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

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Jane Fonda reveals testosterone is the secret behind her sex success at 73

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She has attributed her youthful looks to a healthy love life and given hope to millions by saying she had the best sex of her life at 71.

So it is something of a let down to find out that even sex symbol Jane Fonda needs artificial help.

The Barbarella star has revealed she took the male sex hormone testosterone from the age of 70 to boost her libido.

Miss Fonda said it made ‘a huge difference’.

Advising other women of a certain age how to pep up their love lives, three-times married actress, political activist and fitness guru said: ‘Here’s something I haven’t said publicly yet: I discovered testosterone about three years ago, which makes a huge difference if you want to remain sexual and your libido has dropped.

‘Use testosterone, it comes in a gel, pill or patch.’

Earlier this year, Robbie Williams shocked his legions of female fans by admitting he was injecting himself with testosterone to boost his sex drive.

Although testosterone is usually thought of as a male hormone, it is also made by women, but in much smaller amounts.

Levels drop off after the menopause, leading to some doctors prescribing testosterone alongside more traditional hormone replacement therapy.

It is relatively cheap, costing around £50 for six months’ supply and comes in patches, implants and gels.

But a reinvigorated love life can come at a cost.

Miss Fonda, now 73, and in a relationship with music producer Richard Perry, who is four years her junior, told the Sunday Telegraph: ‘I had to stop because it was giving me acne.

‘It’s one thing to have plastic surgery, but it is quite another to have adolescence acne. That is going too far.’

Two years ago, she created envy in millions of bedrooms by telling how she was having the best sex of her life, despite having had spinal surgery and boasting an artificial knee and a titanium hip.

She said: ‘How do I still look good?  I owe 30 per cent to genes, 30 per cent to good sex, 30 per cent because of sports and healthy lifestyle with proper nutrition and for the remaining ten per cent, I have to thank my plastic surgeon.

But I’m happier, the sex is better and I understand life better. I don’t want to be young again.’

More recently, she has devoted 50 pages of her new autobiography to explaining how couples can keep the passion alive long after the vigour of their youth has failed.

However, her use of testosterone has remained secret until now.

British experts welcomed the revelation.

Professor John Studd, of the London PMS and Menopause Clinic has been prescribing testosterone for women for 30 years.

He said: ‘It is not just about libido.  The benefits include more energy, more self-confidence, better mood and all of those things.’

He added that carefully balancing the dose should remove the risk of side-effects such as acne and excessive bodily or facial hair.

Dr John Stevenson chairman of the charity Women’s Health Concern, said: ‘Jane Fonda clearly thinks there should be no time limit to being sexually active, which is fine. Good for her.’

However, the Royal College of Obstetricians and Gynaecologists warns that the long-term consequences of the treatment are unknown.

THE TRUTH BEHIND TESTOSTERONE

Testosterone can be part of the hormone replacement therapy given to menopausal women.

Gels that are rubbed into the skin are the most popular.  But patches, creams and implants are also available.

Topping up levels of the hormone can give a woman in her 50s or 60s the libido of someone half her age, as well as boost energy and mood.

But too high a dose carries the risk of acne and greasy skin and hair.

‘Masculine’ side-effects such as excessive bodily and facial hair and a deepened voice are also possible.

Testosterone pills aren’t given to women but can raise cholesterol, increasing the odds of heart attacks and strokes.

The Royal College of Obstetricians and Gynaecologists urges caution when prescribing the libido-boosting treatment to women other than those who have had their ovaries removed.

It advises: ‘Testosterone replacement may be associated with adverse clinical and metabolic side effects and long-term consequences are unknown.

Written By: Fiona Macrae

Read more: http://www.dailymail.co.uk/femail/article-2028544/Jane-Fonda-reveals-testosterone-secret-sex-success-73.html#ixzz4cj0r8L4x

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Break for BP

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A midday nap may help to lower blood pressure, among hypertensive men and women.

In today’s 24/7/365 society, few of us take time to tend to our health and well-being; a midday nap may seem completely elusive.  Manolis Kallistratos, from Asklepieion Voula General Hospital (Greece), and colleagues assessed the effect of midday sleep on blood pressure among a group of 386 men and women, average age 61.4 years), with arterial hypertension.  The team collected these measurements for all subjects: midday sleep time (in minutes), office blood pressure, 24 hour ambulatory blood pressure, pulse wave velocity, lifestyle habits, body mass index (BMI) and a complete echocardiographic evaluation including left atrial size. After adjusting for confounding factors, the researchers found that midday sleepers had 5% lower average 24 hour ambulatory systolic blood pressure (by 6 mmHg), as compared to patients who did not sleep at all midday. Their average systolic blood pressure readings were 4% lower when they were awake (by 5 mmHg) and 6% lower while they slept at night (by 7 mmHg), as compared to non-midday sleepers.  As well, in midday sleepers pulse wave velocity levels were 11% lower and left atrium diameter was 5% smaller. The lead investigator comments that: “midday naps seem to lower blood pressure levels and may probably also decrease the number of required antihypertensive medications.”

Article Source: http://www.worldhealth.net/news/break-bp/

 

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Do We Need to Give Up Alcohol to Lose Weight? Not Necessarily

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People trying to lose weight — or not gain weight — are frequently advised to “lay off the booze.” Although organizations like Weight Watchers offer ways to drink wisely within their plans, alcohol, with seven calories a gram and no compensating nutrients, is commonly thought to derail most efforts at weight control.

After the winter holidays, I often hear people blame alcohol for added pounds, not just from its caloric contribution but also because it can undermine self-control and stimulate the appetite and desire for fattening foods.

Yet you probably know people who routinely drink wine with dinner, or a cocktail before it, and never put on an unwanted pound. Given that moderate drinkers tend to live longer than teetotalers, I’d love a glass of wine or a beer with dinner if I could do so without gaining, so I looked into what science has to say about alcohol’s influence on weight.

Despite thousands of studies spanning decades, I discovered that alcohol remains one of the most controversial and confusing topics for people concerned about controlling their weight.

I plowed through more than two dozen research reports, many with conflicting findings on the relationship between alcohol and weight, and finally found a thorough review of the science that can help people determine whether drinking might be compatible with effective weight management.

The review, published in 2015 in Current Obesity Reports, was prepared by Gregory Traversy and Jean-Philippe Chaput of the Healthy Active Living and Obesity Research Group at the Children’s Hospital of Eastern Ontario Research Institute in Ottawa, Ontario.

The reviewers first examined so-called cross-sectional studies, studies that assessed links between alcohol intake and body mass index among large groups of people at a given moment in time. The most common finding was that, in men on average, drinking was “not associated” with weight, whereas among women, drinking either did not affect weight or was actually associated with a lower body weight than among nondrinkers.

Their summary of the findings: Most such studies showed that “frequent light to moderate alcohol intake” — at most two drinks a day for men, one for women — “does not seem to be associated with obesity risk.” However, binge drinking (consuming five or more drinks on an occasion) and heavy drinking (more than four drinks in a day for men, or more than three for women) were linked to an increased risk of obesity and an expanding waistline. And in a departure from most of the other findings, some of the research indicated that for adolescents and (alas) older adults, alcohol in any amount may “promote overweight and a higher body fat percentage.”

Prospective studies, which are generally considered to be more rigorous than cross-sectional studies and which follow groups of people over time, in this case from several months to 20 years, had varied results and produced “no clear picture” of the relationship between alcohol and weight. Several found either no relationship or a negative relationship, at least in women, while others found that men who drank tended to risk becoming obese, especially if they were beer drinkers.

The conclusion from the most recent such studies: While heavy drinkers risked gaining weight, “light to moderate alcohol intake is not associated with weight gain or changes in waist circumference.”

The studies Dr. Chaput ranked as “most reliable” and “providing the strongest evidence” were controlled experiments in which people were randomly assigned to consume given amounts of alcohol under monitored conditions. One such study found that drinking two glasses of red wine with dinner daily for six weeks did not result in weight gain or a greater percentage of body fat in 14 men, when compared with the same diet and exercise regimen without alcohol. A similar study among 20 overweight, sedentary women found no meaningful change in weight after 10 weeks of consuming a glass of wine five times a week.

However, the experimental studies were small and the “intervention periods” were short. Dr. Chaput noted that even a very small weight gain over the course of 10 weeks can add up to a lot of extra pounds in five years unless there is a compensating reduction in food intake or increase in physical activity.

Unlike protein, fats and carbohydrates, alcohol is a toxic substance that is not stored in the body. Alcohol calories are used for fuel, thus decreasing the body’s use of other sources of calories. That means people who drink must eat less or exercise more to maintain their weight.

Dr. Chaput said he is able to keep from gaining weight and body fat despite consuming “about 15 drinks a week” by eating a healthy diet, exercising daily and monitoring his weight regularly.

Big differences in drinking patterns between men and women influence the findings of alcohol’s effects on weight, he said. “Men are more likely to binge drink and to drink beer and spirits, whereas women mostly drink wine and are more likely than men to compensate for extra calories consumed as alcohol.”

Genetics are also a factor, Dr. Chaput said, suggesting that alcohol can be more of a problem among people genetically prone to excessive weight gain. “People who are overweight to begin with are more likely to gain weight if they increase their alcohol intake,” he said.

Furthermore, as I and countless others have found, alcohol has a “disinhibiting” effect and can stimulate people to eat more when food is readily available. “The extra calories taken in with alcohol are stored as fat,” he reminded drinkers.

Here’s the bottom line: Everyone is different. The studies cited above average the results among groups of people and thus gloss over individual differences. Even when two people start out weighing the same and eat, drink and exercise the same amount, adding alcohol to the mix can have different consequences.

The critical ingredient is self-monitoring: weighing yourself regularly, even daily, at the same time of day and under the same circumstances. If you’re a moderate drinker and find yourself gradually putting on weight, try cutting down on, or cutting out, alcohol for a few months to see if you lose, gain or stay the same.

Or, if you’re holding off on drinking but gradually gaining weight and have no medical or personal reason to abstain from alcohol, you might try having a glass of wine on most days to see if your weight stabilizes or even drops slightly over the coming months.

You might also consult a reliable source on the sometimes surprising differences in calorie content among similar alcoholic drinks. The Center for Science in the Public Interest recently published such a list, available at http://www.nutritionaction.com. Search for “Which alcoholic beverages have the most calories?” While you’ll find no difference in calories between white and red wines, depending on the brand, 12 ounces of beer can range from 55 to 320 calories.

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Article Source: https://www.nytimes.com/2017/03/13/well/do-we-need-to-give-up-alcohol-to-lose-weight-not-necessarily.html?rref=collection%2Fsectioncollection%2Fwell&action=click&contentCollection=well&region=stream&module=stream_unit&version=latest&contentPlacement=10&pgtype=sectionfront

 

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Vitamin D – Why You are Probably NOT Getting Enough

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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 Pediatrics 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. 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.
    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.
    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.
    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.
    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.
    6. Try to eat dietary sources of vitamin D. These include:
      • Fish liver oils, such as cod liver oil. One tablespoon (15 ml) = 1,360 IU of vitamin D
      • Cooked wild salmon. (3.5) ounces = 360 IU of vitamin D
      • Cooked mackerel. (3.5) ounces = 345 IU of vitamin D
      • Sardines, canned in oil, drained. (1.75) ounces = 250 IU of vitamin D
      • 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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