Glutathione: This ONE Antioxidant Keeps All Other Antioxidants Performing at Peak Levels

Glutathione: This ONE Antioxidant Keeps All Other Antioxidants Performing at Peak Levels
April 10, 2010 

http://articles.mercola.com/sites/articles/archive/2010/04/10/can-you-use-food-to-increase-glutathione-instead-of-supplements.aspx

By Dr. Mercola, & Ori Hofmekler

Glutathione is your body's most powerful antioxidant and has even been called "the master antioxidant." It is a tripeptide found inside every single cell in your body.
Antioxidants are crucial in eliminating free radicals from your body. Free radicals are basically very reactive particles that bounce all around the cell damaging everything they touch. Most originate during the process of metabolism but they can also arise from exposure to toxins, irradiation, and toxic metals.
Because free radicals are so destructive, cells have a network of defenses designed to neutralize them. This antioxidant network is composed of numerous components that include vitamins, minerals and special chemicals called thiols (glutathione and alpha-lipoic acid).
Glutathione is comprised of three amino acids: cysteine, glutamate, and glycine.
Glutathione is sometimes confused with glutamine and glutamate due to the similarity in names. Although all three molecules are related, they are different in composition and function. When you are healthy, the three are balanced and do a delicate dance within your body.
In a nutshell, this is the difference between the three:

1.      Glutamine: Your body's most abundant amino acid, made in your brain from glutamate; has a major role in various anti-injury processes and muscle repair; a precursor to glutathione.

2.      Glutathione (two types, GSH and GSSG): The "master antioxidant"—most powerful antioxidant in your body, present in every cell. Protects cells, and especially important for liver health; breaks down into free glutamate.

3.      Glutamate (aka glutamic acid or L-glutamate): Monopeptide amino acid neurotransmitter in your brain—required for synaptic activity. You don't want too much of it—it's an excitotoxin. (See also monosodium glutamate, or MSG)

Glutathione is different from other antioxidants in that it is intracellular. It has the unique ability of maximizing the activity of all the other antioxidants, including vitamins C and E, CoQ10,alpha lipoic acid, and the fresh veggies and fruits you (hopefully) eat every day. It removes toxins from your cells and protects you from the damaging effects of radiation, chemicals, and environmental pollutants.
You might think that a miracle molecule such as glutathione might be a good thing to put into supplement form. As usual, science loses to nature when it comes to optimizing this health-promoting little gem.
There is currently a great deal of hype about glutathione supplementation, highly popularized as a "miracle" means to boost health, prevent disease and fight aging.
Let's separate some of the facts from the myths about how glutathione works and look at the right way to build your body's glutathione reserves.

How Glutathione Works

The main function of glutathione is to protect your cells and mitochondria from oxidative and peroxidative damage. As you age, your body's ability to produce glutathione decreases.
Glutathione isn't just an endogenous antioxidant--it is also an essential factor in energy utilization, detoxification, and preventing the diseases we associate with aging. Glutathione deficiency has been linked to:

·        Age-related diseases such as Alzheimer's and Parkinson's

·        Coronary and autoimmune diseases

·        Arthritis, asthma and other inflammatory conditions

·        Cancer

·        Mitochondrial dysfunction

·        Muscle weakness and fatigue

Synthesis of glutathione depends upon adenosine triphosphate (ATP), which is the molecule that provides cellular energy. It follows that glutathione levels are linked to energy deficiency, or low ATP.
This is a major reason why exercise is so beneficial for your overall health—among other things, it boosts your glutathione levels!
If you can enhance internal glutathione production, you will strengthen your immune system in a way that will shield you from many of the adverse effects of aging.

Do Glutathione Supplements Work?

Your body is quite poor at getting glutathione from your digestive system into your blood. Most oral glutathione supplements have been shown to be poorly absorbed and a waste of your hard-earned money.
There has been some success with intravenous glutathione supplementation, but this is certainly not practical and very expensive and should be reserved for extreme situations. Glutathione supplementation can help people with immunodeficiency but only to a certain degree, and only temporarily—kind of like recharging a dead battery.
Ironically, glutathione supplements may actually interfere with your body's own glutathione production.
The human body is programmed to self-produce its own antioxidant enzymes such as glutathione and SOD (superoxide dismutase, the first antioxidant mobilized by your cells for defense). And synthetic supplementation of these compounds actually signal your body to stop its own production – which leaves you dependent on synthetic substances (supplements or drugs).
Glutathione levels can be enhanced somewhat by taking supplements such as alpha lipoic acid, which is known to regenerate glutathione. Alpha lipoic acid also helps to regenerate vitamins C and E so that they remain active longer in your body. Red meat and organ meats are the best dietary source of alpha lipoic acid.
Glutamine can be used as a supplement since it's a direct precursor to glutathione. However, there is quite a bit of evidence it is poorly absorbed.
There is also evidence that vitamin D increases intracellular glutathione. Unless you are a newcomer to my website, you know that I am an enthusiastic fan of vitamin D, and this is yet one more reason it's so important for your health.
Some nutritional authorities recommend taking a form of cysteine known as N-acetyl-cysteine (NAC), but I would advise against using this supplement if you still have mercury amalgam fillings because it could interfere with detoxification of the mercury.
Fortunately, there are natural ways to boost your body's glutathione reserves.
Vitamins and supplements have their uses but are always less desirable than nutrients in their natural form, obtained from the foods you eat. What has been proven beyond a doubt is that whole food based diets--rich in vegetables, fruits, nuts, seeds, and quality protein--promote health and longevity.

What Foods Promote the Highest Glutathione Levels?

Many whole foods contain significant amounts of glutathione or its precursors. Foods richest in sulfur-containing amino acids are usually the best sources of glutathione:

·        The overall top food for maximizing your glutathione is high quality whey protein. It must be cold pressed whey protein derived from grass fed cows, and free of hormones, chemicals and sugar.
Quality whey provides all the key amino acids for glutathione production (cysteine, glycine and glutamate) and contains a unique cysteine residue (glutamylcysteine) that is highly bioactive in its affinity for converting to glutathione.

Glutamylcysteine is a bonded cysteine molecule (cysteine plus glutamate) that naturally occurs in Bovine Serum Albumin – a fragile immune component of the whey. This unique cysteine is exclusive to whey and rarely appears in other protein foods – which makes whey protein the best glutathione-promoting food source.

Furthermore, whey provides critical co-factors, immunoglobulins, lactoferrin and alpha Lactalbumin (also a great source of cysteine), which together help create the right metabolic environment for high glutathione activity.

·        Raw milk products, raw eggs and meat: Glutathione occurs in the highest levels in fresh, uncooked meats and raw milk, but is almost entirely absent in pasteurized dairy products.

·        Fresh fruits and vegetables provide excellent glutathione, but once cooked, values become negligible. Spinach, potatoes, asparagus, avocado, squash, okra, cauliflower, broccoli, walnuts, garlic and tomatoes have the highest glutathione per serving.

·        The herb milk thistle is an excellent source of the antioxidant compound silymarin, which may help to prevent glutathione depletion in the liver. Glutathione is crucial in the liver for detoxification and can become depleted from acetaminophen (Tylenol), alcohol consumption, and general toxic overload.

·        Curcumin may also be useful for increasing glutathione levels.

Keeping your glutathione levels up is a matter of increasing factors that boost your glutathione and decreasing factors that lower it. The things that deplete your glutathione the fastest are chemicals, toxins and sugar.

The Right Whey

If you want to supplement your diet with whey protein products, you have to be careful because not all whey protein products are created equal. Supermarket and nutrition store shelves are lined with protein powder choices, 99 percent of which are loaded with sugar and chemicals that don't support your health goal.
If you're going to supplement, you should only use a high quality whey protein that provides all the necessary nutritional elements for NATURALLY boosting glutathione and also preventing its decline.
Be sure your whey protein supplement has the following features:

1.      The whey comes from grass-fed cows that are not treated with pesticides or hormones

2.      Cold processed, since heat destroys whey's fragile molecular structure

3.      Whey protein concentrate, not protein isolates

4.      Sweetened naturally, not artificially, and low in carbohydrates

5.      Highly digestible—look for medium chain fatty acids (MCTs), not long chain fatty acids

References

·        Bounous G. Whey protein concentrate (WPC) and glutathione modulation in cancer treatment. Anticancer Res. 2000 Nov-Dec;20(6C):4785-92.

·        Bounous G., Gold P. 1991. The biological activity of undenatured dietary whey proteins: role of glutathione. Clin Invest Med. Aug;14(4):296-309.

·        Dickinson D., Iles K., Zhang K., Blank V., and Forman H. (2003) Curcumin alters EpRE and AP-1 binding complexes and elevates glutamate-cysteine ligase gene expression. J FASEB 17, 472.

·        Donnini D., Zambito A.M., Perrella G; Ambesi-Impiombato F.S., Curcio F. Glucose may induce cell death through a free radical-mediated mechanism.Biochem Biophys Res Commun. 219(2):412-7 1996 Feb 15.

·        El-Hawary Z., El-Hawary M.F.S., Morcus S.R. 1977. Blood glucose, glutathione, and total keto-acids levels in alloxan-diabetic rats. Zeitschrift für Ernährungswissenschaft 16(4): 227-230.

·        Fidelus R.K., Tsan M.F. Glutathione and lymphocyte activation: a function of aging and auto-immune disease. Immunology. 1987 61:503-508.

·        Glutathione. 

·        Glutathione White Paper. Richard Van Konynenburg, PhD. 

·        Herbert F.K., Cotonio Bourne M., Groen J. 1930. The effect of glutathione on the determination of blood-sugar. Department of Chemical Pathology, St. Bartholomew's Hospital, London.

·        Higashi T., Tateshi N., Naruse A., Sakamoto Y. (1977) A novel physiological role of liver glutathione as a reservoir of L-cystein. J Biochem. 82, 117.

·        Huh K., Kwon T.H., Kim J.S., Park J.M. Role of the hepatic xanthine oxidase in thyroid dysfunction: effect of thyroid hormones in oxidative stress in rat liver. Arch Pharm Res; 21(3):236-40 Jun 1998.

·        Loven D., Schedl H., Wilson H., Daabees T.T., Stegink L.D., Diekus M., Oberley L. Effect of insulin and oral glutathione on glutathione levels and superoxide dismutase activities in organs of rats with streptozocin-induced diabetes. 

·        Meister A. (1983) Selective modification of glutathione metabolism. Science.220, 472.

·        Meredith M.J., Reed D.J. (1983) Depletion in vitro of mitochondrial glutathione in rat hepatocytes and enhancement of lipid peroxidation by adriamycin and 1,3Bis(2-chloroethyl)-1-nitrosaurea (BCNU). Biochem Pharmacol. 32, 1383.

·        Powell L.A., Warpeha K.M., Xu W., Walker B., Trimble E.R. High glucose decreases intracellular glutathione concentrations and upregulates inducible nitric oxide synthase gene expression in intestinal epithelial cells. Journal of Molecular Endocrinology. December 1, 2004 33:797-803.

·        Seymen, O., Seven A., Candan G., Yigit G., Hatemi S., Hatemi H. The effect of iron supplementation on GSH levels, GSH-Px, and SOD activities of erythrocytes in L-thyroxine administration. Acta Med Okayama. 51(3):129-33 1997 Jun.

·        Stohs S.J., Lawson T., Al-Turk W.A. (1984) Changes in glutathione and glutathione metabolizing enzymes erythrocytes and lymphocytes of mice as a function of age. Gen Pharmacol. 15, 267.

·        Tsan M.F., Danis E.H., Del Vecchio P.J., Rosano C.B. (1985) Enhancement of intracellular glutathione protects endothelial cells against oxidative damage. Biochem Biophys. Res. Commun. 127, 270.

·        Wellner V.P., Anderson M.E., Puri R.N., Jensen G.L., Meister A. (1982) Radioprotection by glutathione ester: transport of glutathione ester in human lymphoid cells and fibroblasts. Proc. Natl. Acad. Sci. U.S.A. 81, 4732.

Vitamin D reduces need for antibiotics in seniors, according to new trial

Posted on October 15, 2013 by Brant Cebulla

A new randomized controlled trial out of Australia suggests that vitamin D reduces the need for antibiotics.
Research to date on vitamin D’s role in the immune system and fighting infection has primarily focused on viral infections. A few small trials have found a reduction in influenza incidence and a reduction in general upper respiratory tract infections for those who took vitamin D compared to those who took placebo.
For bacterial infections, there have been a few trails looking at vitamin D’s effect on tuberculosis, with mixed results. There have also been a few trials looking at vitamin D’s effect on the need for antibiotic use, but the trials have been few and small, although they have shown some promising results.
In the present study, researchers wanted to fill this gap in research and examine vitamin D’s effect on the need for antibiotic use. They wanted to know, if people take vitamin D supplements, does it reduce their need for antibiotics? If yes, this would suggest that vitamin D does have a hand in fighting bacterial infections.
Researchers enrolled 644 people into their study. They randomly assigned one-third of them to take a placebo pill, one-third to take 30,000 IU and one-third to take 60,000 IU once per month for a year.
The researchers measured vitamin D levels at baseline and at the end of study. They kept track of antibiotic use by using Australia’s national administrative health data, so the participants didn’t have to self-report.
At the end of the trial, here is what they found:

• Seventy-five percent of patients were deficient in vitamin D at baseline (level under 20 ng/ml). Mean vitamin D levels in the 30,000 IU group increased from 16.8 ng/ml at baseline to 25.6 ng/ml over the year. Mean vitamin D levels in the 60,000 IU group increased from 16.8 ng/ml at baseline to 31.2 ng/ml. Placebo levels remained the same, with a level around 17 ng/ml.
• People in the 60,000 IU group had a nonsignificant lower risk of having at least one antibiotic prescribed compared to people taking placebo (RR: 0.72; 95% CI: 0.48, 1.07; P = 0.10). The 30,000 IU group also had a nonsignificant lower risk of having at least one antibiotic prescribed, although the association was even weaker (RR: 0.84; 95% CI: 0.57, 1.25; P = 0.40), which makes sense since it was a lower dose.
• When the researchers stratified their results based on age and only looked at seniors over 70 years old, they observed a significantly lower risk of having at least one antibiotic prescribed compared to people taking placebo (RR: 0.53; 95% CI: 0.32, 0.90; P = 0.02). They could not find a statistically significant relationship for younger age brackets.

The researchers concluded,
“Our results lend some support to the hypothesis that vitamin D supplementation might reduce the need for antibiotics, particularly in people aged over 70 years old. Because this was a post hoc analysis and quite possibly because of chance, the results suggest that future trials of vitamin D with antibiotic use or common infections as key outcomes are warranted.”
Prior to looking at the data, the researchers hypothesized that vitamin D would be most beneficial to seniors because of the known progressive decline of immune function as you age. And that’s exactly what they found: vitamin D was of almost exclusive benefit to seniors in protecting against need for antibiotics.
Future research should examine this topic using a larger dose of vitamin D and if possible, a larger population, to try and elucidate the antibiotic effects of vitamin D across all age groups.
Source
Tran B et al. Effect of vitamin D supplementation on antibiotic use; a randomized controlled trial. AJCN, 2013

Vitamin D deficiency prevalent among people with Parkinson's disease, new study says

Vitamin D deficiency prevalent among people with Parkinson’s disease, new study says

Researchers out of Harvard have found that those with Parkinson’s disease are more likely to have vitamin D deficiency compared to healthy adults.
Parkinson’s disease (PD) is a debilitating disease that effects the body’s central nervous system. It gets worse over time, and people with PD often develop tremors, rigidness in movement and poor postural stability.
There are an estimated seven million worldwide and one million in the United States living with PD. Sixty thousand new cases are diagnosed each year in the United States alone.
Vitamin D is important for people with PD, as proper vitamin D intake can reduce falls and fractures, a common and serious concern for patients with PD.
In this recent study, researchers looked at 388 patients with PD and 283 control subjects from the Harvard Biomarker Study. While they measured many things, one of the things they measured were vitamin D levels.
They found that nearly 18% of those with PD were deficient in vitamin D compared to 9% of the control group.
Furthermore, the researchers found a correlation between vitamin D levels and severity of disease. Those with the lowest levels of vitamin D were in more severe stages of PD. This association was stronger among males.
One limitation of the study was that only patients from the Massachusetts General Hospital and Brigham and Women’s Hospital were sampled. Researchers note that future studies should examine minority populations who may be at a greater risk for deficiency.
The study concluded by saying, “These data suggest that patients with PD should be included among the categories of individuals at high risk of vitamin D deficiency who warrant…vitamin D treatment.”

Source
Ding, H. et. al. Unrecognized vitamin D3 deficiency is common in Parkinson disease. American Academy of Neurology, 2013.

Do Vaccines Cause Autism?

Please watch this important short 5 minute video!http://canaryparty.net/index.php/the-news/129-the-canary-partys-new-viral-video-do-vaccines-cause-autism

The Canary Party presents a video on the corrupt Vaccine Injury Compensation Program to show how the federal government and pharmaceutical companies continue to get away with claiming that vaccines don't cause autism in the face of mounting evidence that they are doing just that in a growing number of children.

Do Vaccines Cause Autism?

In the last 30 years, the childhood vaccine schedule has tripled —while the US autism rate has skyrocketed from 1 in 10,000 to 1 in FIFTY. Dozens of published research papers show that YES, vaccines and autism are linked. 

Yet the “debate” rages on in part, because of the 1986 National Childhood Vaccine Injury Act—passed by Congress as a result of pharmaceutical lobbying.  It shields drug companies from liability for injuries and deaths caused by the vaccines they manufacture… vaccines that the federal government admits are “unavoidably unsafe.” 

To see how this tilted the law in big pharma’s favor, let’s look at Eric, a child suffering from vaccine-induced autism.

Had Eric been harmed by a pharmaceutical product other than vaccines, his parents could sue the manufacturer in civil court, entitling them to the standard legal process with a judge, jury, private attorneys, legal precedent and discovery, all within public view.

But for kids like Eric, the National Childhood Vaccine Injury Act says NO.

Instead of suing the pharmaceutical company directly, parents of children like Eric are forced to “petition” the Department of Health and Human Services and, if federal health officials oppose compensation, the case is argued before a special master in the U.S. Claims Court.  Many refer to this as "vaccine court”—though it isn’t a court at all, but rather an "administrative procedure" in which the family asks the government to admit the vaccine caused their child harm, and requests compensation for the child’s care.

Here are some shocking facts about the so-called “vaccine court”:

1.      Pharmaceutical companies do not have to participate in the proceedings at all.  Taxpayers pay for all damages.

2.      The US Department of Justice acts as the government’s lawyer—with taxpayers footing the bill for their defense.

3.      The family's attorney is paid out of the Trust Fund, administered by the Department of Health and Human Services, which has a history of punishing plaintiff’s lawyers by slashing their fees and waiting a decade or more to pay them, leaving some families without any legal representation.

4.      There’s no required discovery process—so potentially incriminating documents stay hidden in the hands of vaccine manufacturers.

5.      Most hearings are off limits: No public, no reporters.

6.      There’s no judge or jury—a special master appointed by the U.S. Court of Federal Claims both presides over the hearings, and issues the rulings, which can limit the chance of an objective verdict

7.      Legal precedent is limited, so the program issues contradictory rulings. In the case of Bailey Banks, a special master ruled the boy's autism was "caused-in-fact" by the MMR vaccine. Yet in later cases, special masters  ruled that vaccines do not cause autism, even though federal compensation has been awarded in at least 83 cases with autism.

Almost unbelievably, the Department of Health and Human Services actually owns vaccine patents. When these vaccines are purchased, HHS profits.

In the words of Eric’s mom, “Government attorneys defend a government program using government-funded science, decided by federal bureaucrats trying to keep their government jobs.  Kids like Eric NEVER had a chance.” 

The passing of the National Childhood Vaccine Injury Act prompted manufacturers to ramp up development of new vaccines, furiously lobbying the CDC to add their new shots to the "recommended schedule."

As a result, a baby today receives more vaccinations by six months than her mother did by the time she graduated high school.

Amazingly, neither HHS nor Congress has ever reviewed the potentially devastating health effects this vaccination surge has had on our children. Today over half of US kids suffer from chronic disease and disability.

At a November 2012 Congressional autism hearing, CDC officials failed to cite even one study backing up vaccine safety claims.

Congress is now planning federal hearings to further investigate the Vaccine Injury Compensation Program. 

The next round of hearings begins in November of 2013. If you’re outraged by the staggering miscarriage of justice exposed in this video, please visit CanaryParty.org now, and register for our mailing list.  Find out how YOU can help hold our government accountable for vaccine safety and bring about justice for our vaccine-injured children.

http://www.vitamindcouncil.org/blog/how-does-vitamin-d-work-in-multiple-sclerosis/

How does vitamin D work in multiple sclerosis?

Posted on October 2, 2013 by Rebecca Oshiro

A reader recently asked, after noticing a plethora of articles on vitamin D and multiple sclerosis (MS), how does vitamin D actually work in this condition? Yes, we see it’s probably important for MS, but why? How does it work? The Vitamin D Council asked me to write on this topic, which I systematically reviewed just this past March.

To start, I’d like to note that while it appears that vitamin D and sunlight play a strong role in preventing the development of (MS), researchers are still trying to pinpoint exactly how it works. Researchers may discover that vitamin D is essential for preventing MS without fully understanding the mechanisms.

MS is an autoimmune condition where the body’s immune system attacks the nerves in the brain and spinal cord. In 1974, Goldberg was the first to suggest a link between vitamin D and MS. He noted that MS was much more common in areas with less sun and proposed that the resulting low vitamin D levels of people in these areas interfered with their ability to properly form nerve cells.

In 1986, Goldberg performed a very small study in which he supplemented MS patients with 5,000 IU of vitamin D per day by giving them cod liver oil. The patients also received magnesium and calcium. There was no placebo group, but those receiving the vitamins had a significantly lower rate of relapses than before treatment.
Since Goldberg’s work, a large amount of research continues to link low sun exposure and vitamin D levels with MS. Several recent clinical trials have yielded promising results, but they include too few people to make solid conclusions about the role of vitamin D in preventing and treating multiple sclerosis.

But just what are the proposed mechanisms for how vitamin D might treat and prevent MS?

The majority of the research linking vitamin D and MS is actually research studying the link between the amount of sun exposure people get and whether or not they develop MS. Because people that report being in the sun more have less risk of developing MS, and because most people get their vitamin D by exposing their bare skin to sunlight, it is assumed that vitamin D is primarily responsible for this protective effect, though we need more research to say for sure.

As mentioned above, multiple sclerosis is an autoimmune disease where the body’s own immune system attacks insulating sheaths of nerve cells in the brain and spinal cord. The result is the body has a hard time communicating with itself. Vitamin D and sunlight – if effective – probably work by smartening the immune system and decreasing inflammation.

Sunlight contains ultraviolet (UV) A and B radiation. UV radiation affects the immune system, making it less inflammatory and less likely to attack other cells of the body. A handful of animal studies show that UVB radiation alone, without any significant vitamin D production, suppresses the symptoms of MS.

Many cells of the immune system have vitamin D receptors and activate vitamin D for their own use. In laboratory studies, when immune cells are exposed to active vitamin D, they become less inflammatory and decrease the amount of antibodies they produce. These changes might mean that the immune system can function more normally and not attack other areas of the body, like the brain and spinal cord.

Cells throughout the brain and spinal cord also have vitamin D receptors. In studies where very large doses of vitamin D are given, the type of nerve cell break down usually seen in MS patients is significantly reduced. Thus it appears that vitamin D works somehow by promoting normal nerve cell development and protecting the cells from attack by an immune system gone awry.

Lastly, researchers are looking at differences in genes that encode for the enzymes that make and break down vitamin D. This could mean inheriting certain genes increases your risk for developing MS because your ability to make and maintain levels of activated vitamin D is altered. The HLA-DRB1*1501 gene is most strongly associated with multiple sclerosis, and in vitro studies show that vitamin D regulates how it expresses itself.

The link between vitamin D deficiency and MS is one of the most exciting areas in vitamin D research, and researchers are scrambling to learn more about the role vitamin D can play in the prevention and treatment of MS. We should have a better idea of just how it is vitamin D works to prevent MS from developing and a better understanding of how much oral vitamin D people with MS should take to treat their condition in the next 5 years or so.

Sources
Goldberg, P. Multiple sclerosis: vitamin D and calcium as environmental determinants of prevalence (A viewpoint) part 1: sunlight, dietary factors and epidemiology. Intern. J. Environmental Studies. 1974;6(1)19-27.
Goldberg P, Fleming MC, Picard EH. Multiple sclerosis: decreased relapse rate through dietary supplementation with calcium, magnesium and vitamin D. Med Hypotheses. 1986;21(2):193-200.
Holmøy T, Kampman MT, Smolders J. Vitamin D in multiple sclerosis: implications for assessment and treatment. Expert Rev Neurother. 2012;12(9):1101-12.
Faridar A, Eskandari G, Sahraian MA, Minagar A, Azimi A. Vitamin D and multiple sclerosis: a critical review and recommendations on treatment. Acta Neurol Belg. 2012;112(4):327-33.
Ho SL, Alappat L, Awad AB. Vitamin D and multiple sclerosis. Crit Rev Food Sci Nutr. 2012;52(11):980-7.

About Melatonin, The Sleep Hormone

About Melatonin, The Sleep Hormone

Have you heard this adage: "I am backwards; I wake up sleepy and go to bed wide awake"? As we age, sleep seems to become a precious commodity.

Much of our ability to sleep is initiated by melatonin, also known as the sleep hormone. Melatonin is produced by the pineal gland in the brain. Light inhibits the production of melatonin. Sleep and darkness are required in order to activate the pineal gland.

Artificial light and length of day also play a part in the production of melatonin, as does exercise and electromagnetic energy. This is why it is suggested when sleeping, one should be in a completely dark room without noise. Melatonin levels are higher in childhood than in adulthood. This is why as we age our sleep is easily disrupted. Disrupted sleep and too much light causes the decrease of melatonin which also affects our immune systems as we age. Those that work over night and sleep during the day tend to have poorer immune systems for this reason.

Melatonin is a powerful antioxidant. When our body cells use oxygen, they naturally produce free radicals (by-products) which can cause damage. Antioxidants act as "free radical scavengers" and hence prevent and repair damage done by these free radicals. Antioxidants also suppress tumors. Low levels of melatonin can not only lead to breast and cervical cancers in women but can cause chronic fatigue and brain fogginess.

Remember, homeopathic care can help your body naturally adjust and correct hormone levels and optimize the detoxification process, which positively impacts brain and immune system function.

Vitamin D most important early in life to prevent type 1 diabetes, says new research

http://www.vitamindcouncil.org/vitamin-d-news/14787/

Vitamin D most important early in life to prevent type 1 diabetes, says new research
Posted on September 18, 2013 by Vitamin D Council

A new meta-analysis published in the journal Nutrients has found that in effort to prevent type I diabetes, vitamin D intake may be most important early in life.

Type I diabetes (T1D) is an autoimmune disease acquired early in life, usually diagnosed during childhood or early adulthood. What happens is the body’s own immune system destroys insulin-producing beta cells, creating a state of insulin deficiency in the body.

Researchers believe vitamin D can help prevent T1D, but they’re still trying to figure out at what stage of development it’s most important. Some studies have shown that vitamin D has a protective association against T1D in offspring if the mother gets enough during pregnancy. And some studies show that if infants get enough vitamin D, they may reduce their risk of T1D later in life.

In the present study, researchers performed a meta-analysis, gathering all studies that examined vitamin D intake during pregnancy or early infancy and compared the intakes to risk of getting T1D later in life.

When all the studies were pooled together, they found that babies that received vitamin D supplements in infancy were 29% less likely to develop T1D later in life compared to the babies that didn’t get vitamin D supplements.

They also observed an effect in pregnant women, though the effect was more modest and not statistically significant. They observed a 5% reduction in risk in offspring getting T1D in the mothers who supplemented during pregnancy compared to those who didn’t. The mothers may not have gotten enough vitamin D in these studies to see a larger effect. The researchers also call for more studies on vitamin D intake during pregnancy and risk of offspring getting T1D, as there were relatively fewer studies of this type compared to supplementation in early infancy.

The researchers concluded, “Our findings suggest that vitamin D intake during early life is associated with a reduced risk of type 1 diabetes.”

Source
Dong JY et al. Vitamin D Intake and Risk of Type 1 Diabetes: A Meta-Analysis of Observational Studies. Nutrients, 2013.

___

MTHFR Gene Mutation: Common in Autism, Autoimmune Diseases, Chronic fatigue, Fibromyalgia, PANDAS , Thyroid Disease

“Holy MTHFR!” from http://www.easytolovebut.com/?p=2782

Posted on December 12, 2012 by Laura Matheos

If I say MTHFR, then Methylenetetrahydrofolate Reductase are the two words that pop into your brain, right? No? Well, hopefully after reading this, you’ll see more than that swear word that caught your attention.
If I next mention bipolar struggles, rapid mood swings, depression, anxiety, heart disease, strokes, macular degeneration, miscarriages – and any of these issues hit home for you, then read on, because you might just want to know about MethyleneTetraHydroFolate Reductase – better known by its abbreviation – MTHFR.
MTHFR is a gene and like all genes, it acts as a light switch – turning on or turning off various body processes. In this case, MTHFR takes folate (vitamin B9) and methylates (converts) it into methylfolate (5-methylTHF). Hardly seems like a big deal, does it? Yet, if you belong to an autism, Pandas, Lyme or chronic fatigue group, you’ve probably noticed a big buzz around this thing called methylation. While the past decade has seen MTHFR studied in terms of cardiovascular disease and cancer, it turns out it might also be a very big deal for those raising kids with developmental, neurological or behavioral symptoms and for those fighting chronic infections.

Methylwhat?
A lot of parents raising kids with challenges are already overwhelmed – too overwhelmed to start stuffing their brains with hard to pronounce words describing hard to understand biochemistry. But you can think of methylation as a kind of metabolism. Imagine the insides of a clock with many cogs, each cog regulating specific chemical reactions. This is an over-simplified diagram of the methylation cycle:

The cogs in this picture turn in your body billions of times per second. But quick, before your eyes glaze over, find the MTHFR in the middle of the picture. Got it? The MTHFR gene sits at a critical point. If you have a glitch that keeps this gene from doing its job, the cogs on both sides of the picture are going to get mucked up. Instead of the light switch being on or off, it’s stuck in some sort of dimmer switch mode, functioning, but not nearly as well as it should be. The proper interaction of methylfolate and Methyl-B12 is what drives your body’s ability to fuel every cell in your body with energy (this is what’s going on in the green and red cogs). Methyl-B12 regulates certain T-cells that may play a role in some autoimmune diseases. Improper methylation can also raise your levels of homocysteine (look to the bottom of the red cog on your right).  This can greatly increase your risks for heart disease, stroke, macular degeneration, dementia and some cancers (e.g. lung, colon and leukemia). It also impedes your ability to manufacture glutathione (bottom right of diagram), the body’s master antioxidant (the “sanitation engineer”) that plays a critical role in autism treatments, chronic Lyme disease and some tic disorders. While there isn’t enough research to say for certain, some MTHFR literature discusses a possible role of MTHFR mutations and increased miscarriages. Insufficient levels of methylfolate are linked to neural tube defects, which is why pregnant women are told to take supplements of folic acid. But if your body has a faulty MTHFR gene and can’t properly convert folate into methylfolate, then this advice may not be having the intended benefits.

So you can see why this one little gene is a big deal. And you can find some pretty decent articles on the web on why treating an MTHFR mutation is so important for many health issues. But there’s one more important role that MTHFR plays. One that doesn’t get nearly enough ink. Look to the left of the MTHFR circle. See the blue cog labeled “BH4 cycle”? MTHFR plays a direct role in how well the BH4 cycle works – and the BH4 cycle controls those two neurotransmitters that are so essential to people with behavioral and emotional challenges – serotonin and dopamine. This has a huge potential impact for how some kids might be helped – kids whose parents are averse to psychotropic medications as well as kids for whom medications have been ineffective or caused serious side effects.

After months of studying everything I could get my hands on, I came to realize that given my long family history of heart disease and depression, this microscopic chemical conductor, aptly named MTHFR, might be the cause of a lot of suffering along my family tree.

Testing MTHFR is actually very simple. Most commercial labs in the U.S. can test for it.  Go to your local lab’s website, find their test menu (usually under the section for doctors) and search on “mthfr” or “methylfolate” or some similar phrase. This should bring you the test code number that you can ask your physician to order. The list price for my test was $150 but my insurance negotiated rate was $50 and since we’d met our annual deductible, my 20% portion of the bill was $10.

The results for one of my children came back normal. So the source of his hurdles lay elsewhere. MTHFR, no matter how important, is certainly not the single root of all evil. But my other child showed one mutation (called a polymorphism) on her MTHFR gene. At least 24 mutations have been identified on the MTHFR gene. Only two are well studied at this point – mutations labeled C677T and A1298T. My daughter had one mutation of C677T, making her heterozygous. (If she had two mutations of C677T, she’d be homozygous).
In the U.S., it’s estimated that roughly 45% of the population may have at least one mutation of MTHFR, though your heritage can increase or decrease your individual risk. While exact numbers are hard to verify, one mutation on C677T means you’re probably methylating (converting) folate into methylfolate at 40-60% efficiency. 

If you have two mutations, that number drops to approximately 10% efficiency.

In my personal experience, this is a pretty big deal when it comes to dealing with anxiety and depression. (I couldn’t find estimates for A1298C mutations and much less is written about this. It seems to play a greater role in gut health. For more details, you’ll need to watch Dr. Amy Yasko’s videos. It’s well beyond my ability to do justice to A1298C.)

By following the green cog counterclockwise to the blue cog, you can see the impact on serotonin and dopamine and why knowing about this gene can be important to those who struggle with mood and behavioral disorders.

So what to do about it?
Those who’ve studied methylation extensively have developed various protocols depending on what ailment they’ve focused on. But the common thread for those with a C677T mutation is that if your body can’t convert folate into methylfolate properly, then you can help your body around this hurdle by taking a supplement that already contains methylfolate (not regular folate) to make up for the shortage.  (Think of using instant mashed potatoes where the hard work has already been done for those of us who are cooking-challenged – except unlike potatoes, methylfolate from a store is just as good as “home-made”).

Because this is an emerging field of research, little guidance is out there regarding dosage and step by step how-to’s. There’s no vetted resource to tell you the proper dosage of 5-methylTHF to give an adult, let alone a child. I know one child who’s doing well at less than 100mcg/day (that’s micrograms) and a teen who’s on 10mg/day (that’s milligrams) of Deplin (a prescription form of methylfolate). This is an enormous range for dosage. Most sources I’ve come across discuss ranges of 100-400mcg for a child and 800mcg-1mg for an adult. But many factors are at play and it’s best to work with a physician if possible. Unfortunately, the whole field of epigenetics is so new that few clinicians have much experience in this area. So you may need to do a lot of research alongside an open-minded doctor. We started out slow – very slow, then gradually built up dosage under the guidance of my daughter’s doctor. Even with a doctor’s help, there was still an element of guesswork involved, in the same way doctors work with any patient to zero in on an ideal dosage for any medication.

Supplementing with methylfolate has made a huge difference for my daughter (and has also helped my own health). Over a few months, my daughter’s anxiety, mood cycling and sadness evaporated. So we kept tweaking. At the two month mark, we unwittingly went too high and endured a period of extreme anger, serious depression, food refusal, rapid mood swings, oppositional defiance and truly ugly times – the very things that drove us to our supplementation trial to begin with. Confused, I was ready to give up. But then, almost by accident, we stumbled onto the problem when I stopped the methylfolate in order to do a lab test. Within 24 hours of being methylfolate-free, my daughter’s issues melted away. Hmmm. She became pretty stable – for about a week. Had we been on the wrong path? Then things started to head south again. That feeling of panic returned to the pit of my stomach – that feeling just before you plunge over the peak of the rollercoaster track and you start screaming for your life.

So I re-started the methylfolate at a low dose – and things got good again. It felt like the sun had come back out from behind the clouds. So we built back up once more, not as high as before but just to the point where things got a little dicey again. When warning signs of a meltdown showed on the horizon, I used the advice from one of the MTHFR researchers and gave a small dose of niacinamide (vitamin B3), which has the effect of using up methyl groups (think of it as a sponge mopping up a spill). Within the hour, things were calm again – and stayed that way. Over the course of a few weeks, we zeroed in on the dose of methylfolate that seemed to work best. It will inevitably change as my daughter grows and when her body may need extra resources, like when she’s fighting an illness. It will always be a little bit of an experiment, in the same way that dosing of an SSRI or psychotropic medication is never carved in stone. After all, what fun would parenting be if you were allowed to figure things out and then get on with your life?

Our experiment has been going on for awhile now and I’m happy to report that things have stayed pretty stable. I did find that in addition to methylfolate, my daughter also needs methyl-B12, because both are necessary to keep the methylation cycle functioning properly. If you only take one without the other, you can develop what’s called a folate trap and you can end up thinking you’re on the wrong track when you’re really not. I’ve also tried to keep my daughter away from things fortified with regular folate – things like cereals and multi-vitamins. Her body just can’t handle the regular stuff and if she consumes too much, we end up paying for it with glimpses of the bad old days. Things we once used to help with anxiety have gone by the wayside. My own methylfolate supplement has lowered my blood pressure to the point where I may be able to stop taking prescription medication. I’ll never know if I’ve averted some other ailment, such as the macular degeneration that robbed my father of his eyesight or the strokes that crippled my grandmother or the congestive heart disease that killed my uncle. But I know that both my daughter and I have improved our own odds significantly. Best of all, as winter brings shorter days, it isn’t bringing the depression and sense of dread that has often come with it. Is this all because of a supplement? Hard to say. I’m sure having a happy child plays a role in many ways. But unless things take a dramatic change for the worse, I’m feeling like we’ve found a key piece of our behavioral and health puzzles.

MTHFR is by no means the Holy Grail. The entire field of epigenetics promises to bring even greater gifts and ideas and more than a few dead ends. But for now, this one little gene has proven to be one big deal in my family.

• Dr. Amy Yasko http://www.dramyyasko.com/ ,
• Rich Van Konynenburg  http://forums.phoenixrising.me/index.php?threads/documents-by-rich-van-konynenburg-parts-1-7.11488/ and
• Dr. Ben Lynch http://mthfr.net/
• Dr. Bill Walsh has also written extensively on the subject of methylation. His latest explanation of the role methylation plays in emotional health can be found in his book Nutrient Power http://www.walshresearch.mybigcommerce.com/nutrient-power-book/
• Many other informative discussions can also be found online.

Vitamin D beneficial against lung cancer, says new large cohort study

Vitamin D beneficial against lung cancer, says new large cohort study

http://www.vitamindcouncil.org/vitamin-d-news/vitamin-d-beneficial-against-lung-cancer-says-new-large-cohort-study/

Recent research published in the American Journal of Clinical Nutrition suggests that vitamin D may protect against lung cancer in never-smoking postmenopausal women.

Researchers took a look at the Women’s Health Initiative, a cohort of 128,779 postmenopausal women. Among the entire cohort, 1,771 had lung cancer between the years of 1993-2010.

They found that for those who took more than 800 IU of vitamin D per day had a 63% decreased risk of developing lung cancer among never-smokers compared to those who took less than 100 IU/day.

Furthermore, the researchers looked at a specific portion of participants among the cohort that enrolled in a trial of taking 1,000 mg/day of calcium and 400 IU/day of vitamin D or daily placebos. There were about 38,000 participants in this subset trial.

While there was no benefit against lung cancer in taking calcium plus vitamin D in initial analysis, when the researchers only looked at participants that took less than 1,000 IU/day of vitamin A (retinol form), they did indeed find benefit in calcium + vitamin D. There was a 31% decreased risk of developing lung cancer if you took calcium and vitamin D and kept your retinol intake down compared to taking placebo and keeping your retinol intake down.

What does this mean? Researchers believe that if you take too much vitamin A in retinol form, it may negate any benefit in taking vitamin D and calcium, particularly for lung cancer.

Source
Cheng TY et al. Vitamin D intake and lung cancer risk in the Women’s Health Initiative. Am J Clin Nutr, 2013

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Vitamin D: A role in eating disorders?

http://www.vitamindcouncil.org/blog/vitamin-d-a-role-in-eating-disorders/

Anorexia nervosa (AN) and bulimia nervosa are two common eating disorders.

AN is characterized by food restriction and irrational fear of gaining weight, as well as a distorted body self-image. Those suffering from AN often view themselves as “too fat” even if they are often emaciated. Recent studies show the onset age has recently decreased from an average of 15 years of age to 10 years of age. It occurs in ten times more females than males. The average caloric intake in AN is 500–800 calories per day, but extreme cases of complete self-starvation require intravenous feeding.

AN is a serious mental illness with a high incidence of comorbidity (especially autism and depression) and mortality similar to other serious psychiatric disorders. People suffering from AN have extremely high levels of ghrelin (the hunger hormone that signals a physiological desire for food) in their blood. The high levels of ghrelin suggest that their bodies are desperately trying to make them hungry; however, that hunger call is being ignored or suppressed.

AN is more prevalent in the upper social classes and it is thought to be rare in less-developed countries. It is more common at higher latitudes and some studies show emergency admissions for AN are seasonal.

Bulimia nervosa (BN) is an eating disorder characterized by binge eating and purging, or consuming a large amount of food in a short amount of time followed by an attempt to rid oneself of the food consumed (purging), typically by vomiting, taking a laxative, diuretic, or stimulant, and/or excessive exercise, because of an extensive concern for body weight.

Like most psychiatric disorders, there is a distinct seasonality of Google searches for eating disorders, searches peaking in the winter.

Recently, Doctor Karina Allen and colleagues, working under senior author Professor Andrew Whitehouse, all of the University of Western Australia, were the first to discover that low 25(OH)D levels during pregnancy increase the risk of eating disorders in their offspring in later adolescence.

Allen KL, Byrne SM, Kusel MM, Hart PH, Whitehouse AJ.  Maternal vitamin D levels during pregnancy and offspring eating disorder risk in adolescence. Int J Eat Disord. 2013 Jun 26.

The researchers looked at a cohort of 526 Caucasian mothers who had their 25(OH)D levels measured at 18 weeks of pregnancy and whose offspring were studied up to 20 years of age. The authors assessed eating disorder symptoms at ages 14, 17 and 20 years. Core analyses were limited to female offspring (n=308).

At 18 months gestation, quartile one’s 25(OH)D was between  6 –18 ng/ml;  quartile 2 between 18–24 ng/ml; quartile 3 between 24–29 ng/ml and quartile 4 between 29–62 ng/ml.

At 20 years of age, eating disorders had been diagnosed in 98 of the 526 offspring studied, making the prevalence rate 18% by age 20.

Maternal 25(OH)D concentrations in the lowest quartile of 25(OH)D were associated with a significant two-fold increase in eating disorder risk in women, relative to concentrations in the highest quartile of 25(OH)D. Female participants born in spring were also significantly more likely to experience an eating disorder by age 20 years than participants born in winter, but this association did not hold up under multivariate analysis. No relationships were found for males.

The authors concluded:

“This study has provided new data to link low gestational 25(OH)D to increased eating disorder risk in female offspring of Caucasian mothers. This association may account for the season of birth effects observed in eating disorder groups previously. Ongoing research is required to extend our findings and to clarify the role of vitamin D in the pathogenesis of eating disorders. We recommend that our findings are viewed as preliminary, and as a basis for further research in this area.”