Vitamin D Research Controversy. Vitamin D is beneficial

You've seen the news headlines surrounding the recent study which claimed that vitamin D has minimal benefit to health.
Now, watch this interview from GrassrootsHealth where Carole Baggerly and Dr. Cedric Garland discuss the study, as well as other studies, in length:
Here is a short text by Dr. Cedric Garland about the Autier paper, Vitamin D status and ill health: a systematic review.
"This meta-analysis is nothing new and is already obsolete, since it is mainly based on old papers that used too little vitamin D to expect any effect. A New Zealand study saying we should only supplement people with vitamin D deficiency and evidence of bone loss is equally wrong. Virtually everyone in New Zealand, and most adults in the US, are vitamin D deficient by modern criteria, being below 32 ng/ml. The reality is that we now know that they are deficient with regard to extraskeletal effects of 25(OH)D if their serum level is below 40 ng/ml.
These papers should be disregarded as obsolete work. We are moving into a new era of using vitamin D3 in doses no less that 4,000 IU/day for people aged 9 years and older (The NAS-IOM total upper level intakes [TULI's] that are safe for daily use per NAS-IOM monograph, 2011). Studies using less than 4000 IU/day are on the verge of obsolescence.
It does not matter much that giving 400 IU/d in the meta-analysis being cited did not achieve very much -- the amount given to the subjects was less than a tenth the effective dose. The authors of this review did not use any epidemiological research and they appear to have paid no attention in their conclusions to the only RCT that was relevant, that of Lappe et al. in 2007.
Lapper et al. used 1100 IU/day of vitamin D3 and 1500 mg/day of calcium. They achieved a serum level of approximately 40 ng/ml. It reported a 77% reduction in incidence of all invasive cancer combined, after a 1-year run-in period. The benefit was 60% less cancer without a run-in period. These cancers included breast, colon, lung and others. The women in the Lappe et al. RCT were very compliant. The result was statistically significant.
The Lappe et al, study and the many supportive epidemiological studies that preceded and followed it should prove to even the most ill-informed skeptic that vitamin D prevents most cancer. It is incredible that the authors of this review virtually disregarded all of the relevant epidemiology this randomized controlled clinical trial.
Several scientists have informed the editors of the journal, that published the review, presenting their objections to the conclusions this study reached, they were based on obsolete low-dose vitamin D studies, and that they virtually totally neglected the work of the entire science of epidemiology.
Doctors and their patients should not be discouraged by this obsolete review. Patients aged 9 years and older can take 4,000 IU/day of vitamin D3 safely according to the National Academy of Sciences-Institute of Medicine (2011 monograph). The benefits of such a dose will be substantial. The scientific data already accumulated is easily strong enough to support this. Serum 25(OH)D should be monitored regularly in any event, and serum calcium in older adults or anyone where there is a concern about hypercalcemia. It is true that the current NAS-IOM RDA is 600-800 IU/day of vitamin D3, but higher doses seem far more logical and safer now for most people based on studies and the Lappe et al RCT of 1100 IU/day of vitamin D3. Sale and intake of vitamin D2 should end, as there is no solid support for its efficacy against non-skeletal diseases, unlike vitamin D3.
Another supporting clinical trial would be good, but we have a great one in Lappe et al. If we ever decide to do another RCT we should use no less than 4000 IU/d of vitamin D3 and 1000-1250 mg/day of calcium. Such a trial may be impossible, though, because members of the placebo group may eventually take supplements on their own, or human subjects protection committees may not allow depriving anyone of vitamin D at these doses in this emerging era of knowledge about their powerful benefits at appropriate, monitored doses in preventing very serious diseases that we have never before been able to effectively prevent, including breast cancer, colorectal cancer, pancreatic cancer, type 1 diabetes, and much of multiple sclerosis and type 2 diabetes. It is an exciting time for using vitamin D at no less than 4000 IU/day with regular serum 25(OH)D monitoring to prevent these fatal diseases. "

http://www.youtube.com/watch?v=brEKx27oHLs

                                                                     

Curcumin/Boswellia shows promise in chronic kidney disease

The July 2013 issue of the Journal of Complementary and Integrative Medicine reports the finding of researchers at Baylor University of a reduction in a marker of inflammation among chronic kidney disease patients given a combination of Curcuma longa (curcumin) and Boswellia serrata.

The study included sixteen individuals receiving standard care for chronic kidney disease who were not undergoing dialysis. Participants were randomized to receive capsules containing curcumin from turmeric extract plus Boswellia serrata, or a placebo for eight weeks. Blood samples collected before and after treatment were analyzed for plasma interleukin-6 (IL-6), tumor-necrosis-factor-alpha (markers of inflammation), and the endogenous antioxidant enzyme glutathione peroxidase, as well as serum C-reactive protein (CRP, another marker of inflammation.)

Participants' blood test results at the beginning of the study revealed increased inflammation and reduced glutathione peroxide levels. At the study's conclusion, those who received curcumin and Boswellia serrata experienced a reduction in interleukin-6 in comparison with pretreatment values, indicating decreased inflammation, while IL-6 values rose among those who received a placebo.

In their discussion of the findings, the authors remark that curcumin and Boswellia serrata have been separately shown to lower interleukin-6 via inhibition of the nuclear factor kappa beta and mitogen activated protein kinase (MAPK) signaling pathways. Although tumor-necrosis factor-alpha was not reduced in the current study, they observe that the ACE inhibiting drugs used by the majority of the patients, which are known to lower tumor-necrosis factor-alpha, could have influenced the results.

"Our findings partially support previous research on the anti-inflammatory effects of curcumin and Boswellia serrata," Jennifer J. Moreillon and colleagues write. "Larger randomized trials are needed to further investigate the role of anti-inflammatory supplements in moderate chronic kidney disease. Particularly, it is of great importance to determine how these compounds decrease inflammation and thus, cardiovascular mortality."

Boswellia improves lipids, liver enzymes and long term glucose control in diabetics

Tuesday, February 18, 2014. The results of a trial reported in an article published on February 4, 2014 in the Journal of Diabetes & Metabolic Disorders reveal a benefit for supplementation with Boswellia serrata among men and women with type 2 diabetes.

"This study was aimed to investigate the antidiabetic, hypolipidemic and hepatoprotective effects of supplementation of Boswellia serrata in type 2 diabetic patients," write Akram Ahangarpour and colleagues. They enrolled 60 type 2 diabetics between 30 and 48 years of age who were divided to receive three 300 milligram (mg) doses of Boswellia serrata daily or no supplementation for six weeks. Blood samples collected before and after the treatment period were analyzed for lipids, triglycerides, liver enzymes, and fructosamine, which assesses long term glucose control. Participants were questioned weekly concerning whether they experienced side effects or drug interactions.

At the end of six weeks, subjects who received Boswellia had a significant increase in high-density lipoprotein (HDL) levels in addition to reductions in total and low-density lipoprotein (LDL) cholesterol, fructosamine and the liver enzymes SGPT and SGOT. No side effects or drug interactions were reported. The authors suggest that Boswellia's antioxidant effect and its ability to lower blood glucose could be responsible for the subjects' reduction in fructosamine, which is a measurement of glycosylated proteins.

The current findings are in agreement with those of other studies which have observed improvements in lipids and liver enzymes in association with Boswellia serrata supplementation. "Daily consumption of 900 mg of Boswellia serrata possibly depicts a safe and effective means to decrease the risk factors associated with type 2 diabetic subjects," the authors conclude.

10 Facts About Fluoride You Need To Know

If fluoride is really the panacea for dental disease that it’s been portrayed as, then why is it that the United States is one of the only developed countries that fluoridates their citizens’ drinking water? Hint: It’s not because the other countries aren’t aware of fluoride’s supposed “miracle” powers for your teeth … it’s because they fully realize that adding a known poison to your population’s water supply is probably not a good idea.

Even in North America, water fluoridation has come under increasing scrutiny; since 2010, more than 75 US and Canadian communities have voted to end water fluoridation, and the issue is heating up as more and more people begin to demand water that does not expose them to this highly toxic industrial waste product.
If you’re new to this issue, and even if you’re not, please take 20 minutes to watch Michael Connett, an attorney with the Fluoride Action Network (FAN), summarize 10 important facts about fluoride that everyone needs to know.

                                                                               

10 Facts About Fluoride You Need To Know

1. Most Developed Countries Do Not Fluoridate Their Water
More people drink fluoridated water in the US alone than in the rest of the world combined. In Western Europe, for instance, 97 percent of the population drinks non-fluoridated water.
2. Fluoridated Countries Do Not Have Less Tooth Decay Than Non-Fluoridated Countries
According to the World Health Organization (WHO), there is no discernible difference in tooth decay between developed countries that fluoridate their water and those that do not. The decline in tooth decay the US has experienced over the last 60 years, which is often attributed to fluoridated water, has likewise occurred in all developed countries (most of which donot fluoridate their water).
3. Fluoride Affects Many Tissues in Your Body Besides Your Teeth
Many assume that consuming fluoride is only an issue that involves your dental health. But according to a 500-page scientific review, fluoride is an endocrine disruptor that can affect your bones, brain, thyroid gland, pineal gland and even your blood sugar levels.2
There have been over 34 human studies and 100 animal studies linking fluoride to brain damage,3 including lower IQ in children, and studies have shown that fluoride toxicity can lead to a wide variety of health problems, including:

• Increased lead absorption
• Disrupts synthesis of collagen
• Hyperactivity and/or lethargy
• Muscle disorders
• Thyroid disease
• Arthritis
• Dementia
• Bone fractures
• Lowered thyroid function
• Bone cancer (osteosarcoma)
• Inactivates 62 enzymes and inhibits more than 100
• Inhibits formation of antibodies
• Genetic damage and cell death
• Increased tumor and cancer rate
• Disrupts immune system
• Damages sperm and increases infertility

4. Fluoridation is Not a “Natural” Process
Fluoride is naturally occurring in some areas, leading to high levels in certain water supplies “naturally.” Fluoridation advocates often use this to support its safety, however naturally occurring substances are not automatically safe (think of arsenic, for instance).
Further, the fluoride added to most water supplies is not the naturally occurring variety but rather fluorosilicic acid, which is captured in air pollution control devices of the phosphate fertilizer industry. As FAN reported:
“This captured fluoride acid is the most contaminated chemical added to public water supplies, and may impose additional risks to those presented by natural fluorides. These risks include a possible cancer hazard from the acid’s elevated arsenic content, and a possible neurotoxic hazard from the acid’s ability–under some conditions–to increase the erosion of lead from old pipes.”
5. 40% of American Teenagers Show Visible Signs of Fluoride Overexposure
About 40 percent of American teens have dental fluorosis, a condition that refers to changes in the appearance of tooth enamel that are caused by long-term ingestion of fluoride during the time teeth are forming. In some areas, fluorosis rates are as high as 70-80 percent, with some children suffering from advanced forms.
It’s likely this is a sign that children are receiving large amounts of fluoride from multiple sources, including not only drinking water but also fluoride toothpaste, processed beverages/foods, fluoride pesticides, tea, non-stick pans and some fluorinated drugs. So not only do we need to address the issue of water fluoridation, but how this exposure is magnified by other sources of fluoride that are now common.
It’s also important to realize that dental fluorosis is NOT “just cosmetic.” It can also be an indication that the rest of your body, such as your bones and internal organs, including your brain, have been overexposed to fluoride as well. In other words, if fluoride is having a visually detrimental effect on the surface of your teeth, you can be virtually guaranteed that it’s also damaging other parts of your body, such as your bones.
6. For Infants, Fluoridated Water Provides No Benefits, Only Risks
Infants who consume formula made with fluoridated tap water may consume up to 1,200 micrograms of fluoride, or about 100 times more than the recommended amounts. Such “spikes” of fluoride exposure during infancy provide no known advantage to teeth, but they do have plenty of known harmful effects.
Babies given fluoridated water in their formula are not only more likely to develop dental fluorosis, but may also have reduced IQ scores. In fact, a Harvard University meta-analysis funded by the National Institutes of Health (NIH) concluded that children who live in areas with highly fluoridated water have “significantly lower” IQ scores than those who live in low fluoride areas.5 A number of prominent dental researchers now advise that parents should not add fluoridated water to baby formula.
7. Fluoride Supplements Have Never Been Approved by the FDA
The fluoride supplements sometimes prescribed to those who are not drinking fluoridated water have not been approved by the US Food and Drug Administration (FDA) for the prevention of tooth decay. In fact, the fluoride supplements that the FDA has reviewed have been rejected.
“So with fluoridation, we are adding to the water a prescription-strength dose of a drug that has never been approved by the FDA,” FAN noted.
8. Fluoride is the Only Medicine Added to Public Water
Fluoride is added to drinking water to prevent a disease (tooth decay), and as such becomes a medicine by FDA definition. While proponents claim this is no different than adding vitamin D to milk, fluoride is not an essential nutrient. Many European nations have rejected fluoride for the very reason that delivering medication via the water supply would be inappropriate. Water fluoridation is a form of mass medication that denies you the right to informed consent.
9. Swallowing Fluoride Provides Little Benefit to Teeth
It is now widely recognized that fluoride’s only justifiable benefit comes from topical contact with teeth, which even the US Centers for Disease Control and Prevention (CDC) has acknowledged. Adding it to water and pills, which areswallowed, offers little, if any, benefit to your teeth.
10. Disadvantaged Communities are the Most Disadvantaged by Fluoride
Fluoride toxicity is exacerbated by conditions that occur much more frequently in low-income areas. This includes:

• Nutrient deficiencies
• Infant formula consumption
• Kidney disease
• Diabetes

African American and Mexican American children have significantly higher rates of dental fluorosis, and many low-income urban communities also have severe oral health crises, despite decades of water fluoridation. FAN continues:
“The simple fact is that poor populations need dental care, not fluoridation chemicals in their water. The millions of dollars spent each year promoting fluoridation would be better spent advocating for policies that provide real dental care: like allowing dental therapists to provide affordable care to populations with little access to dentists. In short, fluoridation provides good PR for dental trade associations, but bad medicine for those it’s supposedly meant to serve.”
This article was brought to you by Dr. Mercola. Founder of the world’s #1 natural health site.

Fish oil supplements and high fat, low carb diet prevent dementia in new studies

One of the most dreaded diseases of our modern age isn't heart disease or even cancer. Instead, it's Alzheimer's disease and dementia. Now new research is indicating that by consuming fish oil, you can protect yourself from these conditions, revealed Fox News on Jan. 23.
Conducted at the University of South Dakota, the latest study revealed that individuals with higher blood levels of omega-3 fatty acids may have larger brain volumes in old age. Omega-3 fatty acids are found in fish oil and cold water fish, and the study is highly significant because a reduction in brain volume is linked to dementia and Alzheimer’s.
The research determined that women in the study who had higher levels of omega-3s had larger total brain volumes eight years later. Also important: MRIs revealed that higher levels of omega-3s were associated with increased volume in a specific brain region – the hippocampus.
“The hippocampus is known to be related to the progression of dementia,” said lead author Dr. Bill Harris, professor of medicine at Sanford School of Medicine at the University of South Dakota.
“As it shrinks, dementia becomes more of a problem. So we did find that people with higher omega-3s had higher volumes in the hippocampus – located right in the middle of the head, right at the top of the brain stem.”
What you should know to benefit from the study: Omega-3s consist of three types of fats:

• ALA, found in plant oils such as flax seed and canola
• EPA and DHA, found in marine oils

Although Harris said you can increase your intake of fish or take fish oil supplements, he emphasizes that the benefits are greatest if you enhance your diet with supplements made from EPA and DHA.
“[With ALA], in order for it to become effective, it has to be converted in the body after you eat it to these fish oil omega-3s,” Harris said. “That conversion process is very inefficient in most people, so you don’t really raise your omega-3 index by eating plant-based omega-3s.”
Read the labels carefully. Examples of brands with EPA and DHA include Jarrow Formulas EPA-DHA Balance Odorless and Life Extension Mega EPA/DHA (click for details).
But what about other aspects of your diet? Are there certain foods, in addition to fish, to eat more of - and, conversely, foods to avoid? Neurologist Dr. David Perlmutter says that the answer is yes, referring to studies showing that a high fat, low carb diet can protect your brain from dementia and Alzheimer's disease while boosting weight loss.
He recently talked with Medscape to explore the science behind his best-selling book: "Grain Brain: The Surprising Truth about Wheat, Carbs, and Sugar--Your Brain's Silent Killers" (click for details).
Dr. Perlmutter says that a high fat diet that eliminates grains and sugar as well as reducing other carbohydrates can prevent or dramatically reduce your risk of dementia. He cited recent studies that support his views.
"A study published in August 2013 in the New England Journal of Medicine (NEJM)[2] was very supportive, indicating that even subtle elevations of fasting blood sugar translates to dramatically increased risk for dementia," noted Dr. Perlmutter.
Referring to that study, he cited the conclusion: "Our results suggest that higher glucose levels may be a risk factor for dementia, even among persons without diabetes."
But there's a difference between associations and causality, pointed out Medscape. Dr. Perlmutter says he recognizes that truth, but believes that the evidence shows "a lower-carbohydrate diet is the right choice for the heart and the immune system. There's no downside to it."
When questioned as to the type of diet or intervention that he recommends to protect or slow the onset of dementia, Dr. Perlmutter doesn't hesitate: A high fat, low carb diet, he contends, is the winner.
"The data show that individuals with lower blood sugar levels have a lower risk for dementia. Therefore, we've got to keep blood sugar low. We do so by using the time-honored dietary intervention of a lower-carbohydrate, higher-fat diet," he declares. Learn more about "Grain Brain: The Surprising Truth about Wheat, Carbs, and Sugar--Your Brain's Silent Killers" by clicking here.

                                                                  

In 2013 I wrote a book with the title ''Natural methods of treating cancer''. In this book I suggest that we can cure cancer with an alkaline, low glycemic load/index diet, with high doses of intravenous vitamin C, with high doses of vitamins and antioxidants and with cannabis.
Yesterday I saw an article of BBC News that confirms one of my theories.
 High doses of intravenous vitamin C can be a safe and effective treatment of cancer, as BBC News in 9 February reported. Let's see the article:

Vitamin C keeps cancer at bay, US research suggests

By Helen Briggs BBC News  

High-dose vitamin C can boost the cancer-killing effect of chemotherapy in the lab and mice, research suggests.

Given by injection, it could potentially be a safe, effective and low-cost treatment for ovarian and other cancers, say US scientists.
Reporting in Science Translational Medicine, they call for large-scale government clinical trials.
Pharmaceutical companies are unlikely to run trials, as vitamins cannot be patented.
Vitamin C has long been used as an alternative therapy for cancer.
In the 1970s, chemist Linus Pauling reported that vitamin C given intravenously was effective in treating cancer.

However, clinical trials of vitamin C given by mouth failed to replicate the effect, and research was abandoned.

It is now known that the human body quickly excretes vitamin C when it is taken by mouth.
However, scientists at the University of Kansas say that when given by injection vitamin C is absorbed into the body, and can kill cancer cells without harming normal ones.
The researchers injected vitamin C into human ovarian cancer cells in the lab, into mice, and into patients with advanced ovarian cancer.
They found ovarian cancer cells were sensitive to vitamin C treatment, but normal cells were unharmed.
The treatment worked in tandem with standard chemotherapy drugs to slow tumour growth in mouse studies. Meanwhile, a small group of patients reported fewer side-effects when given vitamin C alongside chemotherapy.
No patent potential Co-researcher Dr Jeanne Drisko said there was growing interest in the use of vitamin C by oncologists.
"Patients are looking for safe and low-cost choices in their management of cancer," she told BBC News. "Intravenous vitamin C has that potential based on our basic science research and early clinical data."
One potential hurdle is that pharmaceutical companies are unlikely to fund trials of intravenous vitamin C because there is no ability to patent natural products.
"Because vitamin C has no patent potential, its development will not be supported by pharmaceutical companies," said lead researcher Qi Chen.
"We believe that the time has arrived for research agencies to vigorously support thoughtful and meticulous clinical trials with intravenous vitamin C."
Dr Kat Arney, science communications manager for Cancer Research UK, said there was a long history of research into vitamin C for treating cancer.
"It's difficult to tell with such a small trial - just 22 patients - whether high-dose vitamin C injections had any effect on survival, but it's interesting that it seemed to reduce the side-effects of chemotherapy," she said.
"Any potential treatment for cancer needs to be thoroughly evaluated in large clinical trials to make sure it's safe and effective, so further studies are needed before we know for sure what benefits high dose vitamin C may have for patients."

http://www.bbc.co.uk/news/health-26038460

Iodine, tocotrienols, berries, and lipoic acid to protect against radiation exposure

The unfolding events relating to Japan’s damaged nuclear reactors is raising the concern in the U.S. of a worst-case scenario of a meltdown with a consequent cloud of radioactive particles following the jet stream over to the U.S. The prevailing jet stream winds would impact Los Angeles to Alaska, and would include Hawaii. Radioactive pollution would reach the U.S. within 36 hours. It would then travel the typical jet stream across the U.S that you see on your daily weather programs. While we all hope this does not happen, and various experts may debate the severity of public health issues involved if it should, it never hurts to have a better understanding of the subject. What would you do if such a cloud was headed your way?
Japanese health authorities are passing out iodine tablets to those in the vicinity of these reactors, as it is common knowledge that the thyroid gland is a weak spot when it comes to radiation exposure. By flooding the body with iodine, the iodine is taken up by the thyroid which then blocks radiation uptake into the thyroid. This reduces the risk for future thyroid cancer (which is already an epidemic cancer in the U.S. in part likely due to excess CT scans).
Such iodine saturation should occur 24 hours prior to exposure and be maintained during the duration of excess exposure. This solution is not without risks, especially when potassium iodide is used. That is because excess iodine can clog thyroid function, inducing either hypo or hyper thyroid. However, that risk is trivial compared to acute radiation exposure – thus iodine makes sense. I like water-soluble iodine that in my experience is much less problematic when higher doses are used. Liquids can be applied directly over the neck region or taken orally, and reapplied as desired based on concerns.
Protecting the thyroid with iodine seems to be about all that public health officials are willing to recommend to the public. However, there are other important steps every person should consider. Radiation interaction within your body generates massive amounts of damaging free radicals, in turn potentially inducing DNA damage that may lead to future cancer – often manifesting a decade or two later. This means it is a good idea to maximize your overall antioxidant defenses. Ideally, this system would be bolstered in advance to provide maximum defense. Unfortunately, the antioxidant defense systems of a majority of Americans are in shoddy condition.
Many nutrients contain antioxidants and many of these behave in your vital antioxidant network to protect your DNA from damage. In your diet, these nutrients come from fruits, vegetables, whey protein, and whole grains. Additionally, almost any nutrient supplement with antioxidant properties, such as vitamin C, will help bolster your antioxidant team. I would suggest to everyone a broad-base of antioxidant support as the minimum. Indeed, a cocktail of antioxidants¹ (selenium, vitamin C, N-acetyl cysteine, alpha lipoic acid, alpha-tocopherol succinate, and co-enzyme Q10) started 24 hours after a lethal level of radiation exposure has been show to be highly protective.
I would like to highlight three specific nutrients that have science showing they can protect your body against radiation damage:  tocotrienols, berries, and lipoic acid.
Tocotrienols are a unique form of vitamin E that offers protection that regular vitamin E does not. In a recent animal experiment carried out by the U.S. Armed Forces Radiobiology Research Institute it was shown that gamma tocotrienol³² can protect against whole body radiation exposure.
Excessive radiation exposure damages DNA, especially DNA relating to the system in our bone marrow that produces all the red and white blood cells that are vital for survival. Therefore, radiation exposure has adverse consequences on circulatory health and immune system competence, disturbing energy balance and increasing the risk for cancer. Of particular importance are the haematopoietic stem cells (HSCs) that constantly rejuvenate blood and can become any of the white or red blood cells, as well as the haematopoietic progenator cells (HPCs) that transform into specific blood cells. Both HSCs and HPCs are the life force of blood cell rejuvenation and essential to your good health.
In this armed forces experiment, mice were exposed to non-lethal amounts of whole body radiation; there was a control group and a group fed gamma tocotrienol. Stem cell colonies (HSCs) were 80 - 86% maintained in the gamma tocotrienol treated mice, while they were 50% reduced in controls. Similarly, progenator cells (HPCs) had recovered completely within 7 days in the gamma tocotrienol treated mice, while they remained at 30% for weeks in the controls. A detailed analysis of the bone marrow showed that gamma tocotrienol maintained the regenerative integrity of bone marrow cells. The authors concluded that gamma tocotrienol “protected hematopoietic tissue by preserving the HSCs and HPCs and by preventing persistent DNA damage.”
Another recent animal study shows that gamma tocotrienol³² can offset the adverse effects of radiation exposure, including the reduction of peroxynitrite, the most damaging free radical. This is important because as free radicals begin forming, their reactions can cascade into producing large amounts of the most damaging of all free radicals, peroxynitrite. Short-circuiting peroxynitrite formation in response to radiation exposure is of immense importance to protecting DNA.
Lipoic acid is a very small and versatile fat- and water-soluble antioxidant. Animal studies show that it helps maintain the antioxidant defense system⁴ in multiple body tissues upon radiation exposure, especially protecting the brain, liver, spleen, kidney, and testes.
The health status of some 6,000 workers from Latvia⁵ who went to clean-up the Chernobyl Nuclear Power Plant has been followed for several decades. These workers suffered higher-than-normal rates of problems in their nervous, digestive, respiratory, cardiovascular, endocrine (especially thyroid) and immunological systems.
A study conducted on some of these workers 10 years after the fact showed that 600 mg of lipoic acid⁶ for two months was able to normalize many, but not all, of their lab abnormalities. Too bad they didn’t have protection prior to and during exposure. Pretreatment with lipoic acid⁷ has been shown to significantly reduce radiation exposure damage to the brain.
Recent animal research conducted by the United States Department of Agriculture showed that blueberry and strawberry extracts⁸ helped prevent brain damage from radiation exposure. Interestingly, the polyphenols of each fruit protected different areas of the brain – supporting a variety of dietary berry intake and/or supplements with multiple berries.
Having an adequate antioxidant defense system for more optimal health is common sense. During times of increased stress your needs for antioxidants rise – and this relates to any type of stress. Radiation exposure is simply one more type of stress – a rather nasty type. The demands in your life or existing health concerns may already be testing your antioxidant reserves. Bolstering your antioxidant defense system to compensate for a potential challenge is also common sense.

 Byron J. Richards,
Board Certified Clinical Nutritionist


http://www.wellnessresources.com/health/articles/iodine_tocotrienols_berries_and_lipoic_acid_to_protect_against_radiation_ex/

Referenced Studies:

1. ^ Antioxidants Protect Against Lethal Level of Radiation Exposure  Radiat Res.  Brown SL, Kolozsvary A, Liu J, Jenrow KA, Ryu S, Kim JH.
2. ^ Gamma Tocotrienol and Radiation Exposure  Radiat Res.  Kulkarni S, Ghosh SP, Satyamitra M, Mog S, Hieber K, Romanyukha L, Gambles K, Toles R, Kao TC, Hauer-Jensen M, Kumar KS.
3. ^ Gamma Tocotrienol and Radiation Damage  Int J Radiat Oncol Biol Phys.  Berbee M, Fu Q, Boerma M, Pathak R, Zhou D, Kumar KS, Hauer-Jensen M.
4. ^ Lipoic Acid Protects Against Radiation Exposure  Cell Biol Toxicol.  Manda K, Ueno M, Moritake T, Anzai K.
5. ^ Long-Term Consequences of Radiation Exposure  Inflammopharmacology.  Eglite ME, Zvagule TJ, Rainsford KD, Reste JD, Curbakova EV, Kurjane NN.
6. ^ Lipoic Acid Helps Radiation Exposed Workers  Lik Sprava.   Zueva NA, Metelitsa LA, Kovalenko AN, Efimov AS.
7. ^ Lipoic Acid Potects Brain from Radiation Damage  Behav Brain Res.  Manda K, Ueno M, Anzai K.
8. ^ Blueberries and Strawberries Protect the Brain from Radiation Damage  Neurobiol Aging.   Shukitt-Hale B, Carey AN, Jenkins D, Rabin BM, Joseph JA. 

Brown SL, Kolozsvary A, Liu J, Jenrow KA, Ryu S, Kim JH. Antioxidant diet supplementation starting 24 hours after exposure reduces radiation lethality. Radiat Res.  2011 April  173(4):462-8.
Henry Ford Hospital, Department of Radiation Oncology, Detroit, Michigan 48202, USA

Study Abstract:

Antioxidants mitigate radiation-induced lethality when started soon after radiation exposure, a delivery time that may not be practical due to difficulties in distribution and because the oral administration of such agents may require a delay beyond the prodromal stage of the radiation syndrome. We report the unexpected finding that antioxidant supplementation starting 24 h after total-body irradiation resulted in better survival than antioxidant supplementation started soon after the irradiation. The antioxidant dietary supplement was l-selenomethionine, sodium ascorbate, N-acetyl cysteine, alpha-lipoic acid, alpha-tocopherol succinate, and co-enzyme Q10. Total-body irradiation with 8 Gy in the absence of antioxidant supplementation was lethal by day 16. When antioxidant supplementation was started soon after irradiation, four of 14 mice survived. In contrast, 14 of 18 mice receiving antioxidant supplementation starting 24 h after irradiation were alive and well 30 days later. The numbers of spleen colonies and blood cells were higher in mice receiving antioxidant supplementation starting 24 h after irradiation than in mice receiving radiation alone. A diet supplemented with antioxidants administered starting 24 h after total-body irradiation improved bone marrow cell survival and mitigated lethality, with a radiation protection factor of approximately 1.18.

 Kulkarni S, Ghosh SP, Satyamitra M, Mog S, Hieber K, Romanyukha L, Gambles K, Toles R, Kao TC, Hauer-Jensen M, Kumar KS. Gamma-tocotrienol protects hematopoietic stem and progenitor cells in mice after total-body irradiation. Radiat Res.  2010 June  173(6):738-47.
Armed Forces Radiobiology Research Institute, Uniformed Services University of the Health Sciences, Bethesda, Maryland 20889, USA.

Study Abstract:

We analyzed the radioprotective effects of gamma-tocotrienol (GT3) on hematopoietic stem cells (HSCs) and progenitor cells (HPCs) in sublethally irradiated mice. Flow cytometry analysis indicated that radiation depleted HPCs (c-Kit(+), Lin(-)) to 40% at days 2 and 4 after total-body irradiation (TBI) in all treatment groups. The HPC numbers in GT3-treated mice recovered almost completely (90%) at day 7 but remained depleted in vehicle-treated mice (30%) even at day 13 after TBI. An in vitro colony-forming assay on sorted HSCs (Lin(-), Sca1(+), c-Kit(+)) indicated that TBI reduced the number of colonies to 40% and 50% at day 17 and 60, respectively, in vehicle-treated groups compared to unirradiated controls (naïve). GT3-treated irradiated mice maintained higher numbers of colonies (86% and 80% compared to naïve mice), thereby preserving the self-renewable capacity of HSCs. Histopathology of sternal bone marrow indicated more regenerative microfoci for myeloid cells and megakaryocytes and higher overall cellularity in GT3-treated mice compared to vehicle controls at days 7 and 13 after TBI. GT3 treatment also reduced the frequency of micronucleated erythrocytes significantly in irradiated mice. Our results demonstrate that GT3 protected hematopoietic tissue by preserving the HSCs and HPCs and by preventing persistent DNA damage.

Berbee M, Fu Q, Boerma M, Pathak R, Zhou D, Kumar KS, Hauer-Jensen M. Reduction of Radiation-Induced Vascular Nitrosative Stress by the Vitamin E Analog γ-Tocotrienol: Evidence of a Role for Tetrahydrobiopterin. Int J Radiat Oncol Biol Phys.  2010 October
Berbee M, Fu Q, Boerma M, Pathak R, Zhou D, Kumar KS, Hauer-Jensen M.

Study Abstract:

PURPOSE: The vitamin E analog γ-tocotrienol (GT3) is a powerful radioprotector. GT3 reduces postradiation vascular peroxynitrite production, an effect dependent on inhibition of hydroxy-methylglutaryl-coenzyme A reductase. Hydroxy-methylglutaryl-coenzyme A reductase inhibitors mediate their pleiotropic effects via endothelial nitric oxide synthase that requires the cofactor tetrahydrobiopterin (BH4). This study investigated the effects of radiation on BH4 bioavailability and of GT3 on BH4 metabolism.
METHODS AND MATERIALS: Mice were exposed to 8.5 Gy of total body irradiation (TBI). Lung BH4 and total biopterin concentrations were measured 0, 3.5, 7, 14, and 21 days after TBI by use of differential oxidation followed by high-performance liquid chromatography. The effect of exogenous GT3 and BH4 treatment on postradiation vascular oxidative stress and bone marrow colony-forming units were assessed in vivo. The effect of GT3 on endothelial cell apoptosis and endothelial expression of guanosine triphosphate (GTP) cyclohydrolase 1 (GTPCH), GTPCH feedback regulatory protein (GFRP), GFRP transcription, GFRP protein levels, and GFRP-GTPCH protein binding was determined in vitro.
RESULTS: Compared with baseline levels, lung BH4 concentrations decreased by 24% at 3.5 days after TBI, an effect that was reversed by GT3. At 14 and 21 days after TBI, compensatory increases in BH4 (58% and 80%, respectively) were observed. Relative to vehicle-treated controls, both GT3 and BH4 supplementation reduced postirradiation vascular peroxynitrite production at 3.5 days (by 66% and 33%, respectively), and BH4 resulted in a 68% increase in bone marrow colony-forming units. GT3 ameliorated endothelial cell apoptosis and reduced endothelial GFRP protein levels and GFRP-GTPCH binding by decreasing transcription of the GFRP gene.
CONCLUSIONS: BH4 bioavailability is reduced in the early postradiation phase. Exogenous administration of BH4 reduces postirradiation vascular oxidative stress. GT3 potently reduces the expression of GFRP, one of the key regulatory proteins in the BH4 pathway, and may thus exert some of its beneficial effects on postradiation free radical production partly by counteracting the decrease in BH4.

 Manda K, Ueno M, Moritake T, Anzai K. alpha-Lipoic acid attenuates x-irradiation-induced oxidative stress in mice. Cell Biol Toxicol.  2007 March  23(2):129-37.
National Institute of Radiological Sciences, Chiba, Japan.

Study Abstract:

The development of nontoxic but effective radioprotectors is needed because of the increasing risk of human exposure to ionizing radiation. We have reported that alpha-lipoic acid confers considerable radio-protective effect in mouse tissues when given prior to x-irradiation. In the present study, alpha-lipoic acid supplementation prior to x-irradiation with 4 and 6 Gy significantly inhibited the radiation-induced decline in total antioxidant capacity (TAC) of plasma. Radiation-induced decline in non-protein sulfhydryl content (NPSH) of different tissues, namely, brain, liver, spleen, kidney, and testis, was also ameliorated significantly at both 4 and 6 Gy doses. Maximal augmentation of radiation-induced protein carbonyl content was observed in spleen followed by brain, kidney, testis, and liver. Maximal protection in terms of carbonyl content was observed in spleen (116%) at 6 Gy dose, and minimal protection was found in liver (22.94%) at 4 Gy dose. Maximal increase in MDA (malondialdehyde) content was observed in brain, followed by testis, spleen, kidney, and liver. Protection by alpha-lipoic acid pretreatment in terms of MDA content was maximal in brain (51.67%) and minimal in spleen. The findings support the idea that alpha-lipoic acid is a free-radical scavenger and a potent antioxidant.

Eglite ME, Zvagule TJ, Rainsford KD, Reste JD, Curbakova EV, Kurjane NN. Clinical aspects of the health disturbances in Chernobyl Nuclear Power Plant accident clean-up workers (liquidators) from Latvia. Inflammopharmacology.  2009 June
Institute of Occupational Safety and Environmental Health, Riga Stradins University, 16 Dzirciema Street, Riga, 1069, Latvia,

Study Abstract:

The health status of some 6,000 workers from Latvia who went to clean-up the Chernobyl Nuclear Power Plant (CNPP) site following the explosion on 26 April 1986 has been analyzed. The data on these workers have been recorded in the Latvian State Register of Occupational disease patients and people exposed to ionizing radiation due to Chernobyl NPP accident (Latvian State Register) that was established in 1994. From these data, estimates have been made of external ionizing radiation to which these workers were exposed together with observations on the impact of exposure to heavy metals (especially lead and zinc) and radioactive isotopes released during the reactor ‘meltdown’. These factors along with psycho-emotional and social-economic stresses account for a marked excess of mortality and morbidity in the group of CNPP accident clean-up workers compared with that of the non-exposed normal Latvian population adjusted for age and sex. The number of diseases or conditions in the CNPP accident clean-up workers has progressively risen from an average of 1.3 in 1986 to 10.9 in 2007. This exceeds for the Latvian population when adjusted for age and sex. The most serious conditions affect the nervous, digestive, respiratory, cardiovascular, endocrine (especially thyroid) and immunological systems. While the morbidity associated with diseases of the respiratory and digestive systems has decreased in recent years that in the other systems is increasing. In recent years, there has been an increased occurrence of cancers affecting the thyroid, prostate and stomach. Clinical and laboratory investigations suggest that surviving CNPP accident clean-up workers exhibit signs of immuno-inflammatory reactions causing premature aging with evidence of autoimmune diseases and immunological deficiencies or abnormalities. It is suggested that the CNPP accident clean-up workers may have a specific syndrome, the ‘Chernobyl post-radiation neurosomatic polypathy’, due to sustained oxidant stress injury, as a result of exposure to radiation and lead.

Zueva NA, Metelitsa LA, Kovalenko AN, Efimov AS. Immunomodulating effect of berlithione in clean-up workers of the Chernobyl nuclear plant accident. Lik Sprava.   2002 January  :24-6.

Study Abstract:

Effects of the antioxidant berlithione (alpha-lipoic acid) on indices for the immune system, such as complement titer, C3-component of the complement, reaction of the autorosette formation were studied together with those on parameters characterizing cell-bound and humoral immunity. 11-12 years following the Chernobyl accident, nine liquidators of its aftermaths were examined, aged 51.8 +/- 7.2 years, body mass (BM) 27.3 +/- 4.2 kg/m2, radiation dose 73.2 +/- 35.3 rem, who took part in the elimination of the effects of the accident for no more than 3 months in 1986—at the beginning of 1987. All examinees were prescribed the drug berlithione (alpha-lipoic acid), 600 mg per day over two months. A two-month treatment with berlithione, 600 mg/day, resulted in normal levels of indices for unspecific defence; among these were phagocytic activity of neutrophiles, content of the complement, its C3-component, and reaction of autorosette formation in the accident effects liquidators, but no impact was found on cell-mediated and humoral immunity

Manda K, Ueno M, Anzai K. Memory impairment, oxidative damage and apoptosis induced by space radiation: ameliorative potential of alpha-lipoic acid. Behav Brain Res.  2008 March  5;187(2):387-95.
National Institute of Radiological Science, Chiba, Japan.

Study Abstract:

Exposure to high-energy particle radiation (HZE) may cause oxidative stress and cognitive impairment in the same manner that seen in aged mice. This phenomenon has raised the concerns about the safety of an extended manned mission into deep space where a significant portion of the radiation burden would come from HZE particle radiation. The present study aimed at investigating the role of alpha-lipoic acid against space radiation-induced oxidative stress and antioxidant status in cerebellum and its correlation with cognitive dysfunction. We observed spontaneous motor activities and spatial memory task of mice using pyroelectric infrared sensor and programmed video tracking system, respectively. Whole body irradiation of mice with high-LET (56)Fe beams (500 MeV/nucleon, 1.5 Gy) substantially impaired the reference memory at 30 day post-irradiation; however, no significant effect was observed on motor activities of mice. Acute intraperitoneal treatment of mice with alpha-lipoic acid prior to irradiation significantly attenuated such memory dysfunction. Radiation-induced apoptotic damage in cerebellum was examined using a neuronal-specific terminal deoxynucleotidyl transferase-mediated nick end-labeling method (NeuroTACS). Radiation-induced apoptotic and necrotic cell death of granule cells and Purkinje cells were inhibited significantly by alpha-lipoic acid pretreatment. Alpha-lipoic acid pretreatment exerted a very high magnitude of protection against radiation-induced augmentation of DNA damage (comet tail movement and serum 8-OHdG), lipid proxidation products (MDA+HAE) and protein carbonyls in mice cerebellum. Further, radiation-induced decline of non-protein sulfhydryl (NP-SH) contents of cerebellum and plasma ferric reducing power (FRAP) was also inhibited by alpha-lipoic acid pre-treatment. Results clearly indicate that alpha-lipoic acid is a potent neuroprotective antioxidant. Moreover, present finding also support the idea suggesting the cerebellar involvement in cognition.

Shukitt-Hale B, Carey AN, Jenkins D, Rabin BM, Joseph JA. Beneficial effects of fruit extracts on neuronal function and behavior in a rodent model of accelerated aging. Neurobiol Aging.   2007 August  28(8):1187-94.
USDA-ARS, Human Nutrition Research Center on Aging at Tufts University, Boston, MA 02111, United States.

Study Abstract:

Exposing young rats to particles of high-energy and charge (HZE particles) enhances indices of oxidative stress and inflammation and disrupts the functioning of the dopaminergic system and behaviors mediated by this system in a manner similar to that seen in aged animals. Previous research has shown that diets supplemented with 2% blueberry or strawberry extracts have the ability to retard and even reverse age-related deficits in behavior and signal transduction in rats, perhaps due to their antioxidant and anti-inflammatory properties. This study evaluated the efficacy of these diets on irradiation-induced deficits in these parameters by maintaining rats on these diets or a control diet for 8 weeks prior to being exposed to whole-body irradiation with 1.5 Gy of 1 GeV/n high-energy (56)Fe particles. Irradiation impaired performance in the Morris water maze and measures of dopamine release 1 month following radiation; these deficits were protected by the antioxidant diets. The strawberry diet offered better protection against spatial deficits in the maze because strawberry-fed animals were better able to retain place information (a hippocampally mediated behavior) compared to controls. The blueberry diet, on the other hand, seemed to improve reversal learning, a behavior more dependent on intact striatal function. These data suggest that (56)Fe particle irradiation causes deficits in behavior and signaling in rats which were ameliorated by an antioxidant diet and that the polyphenols in these fruits might be acting in different brain regions.

Vitamin D stops plaque build up in arteries

Scientists have now proven that a lack of vitamin D¹ helps damaged cholesterol (oxidized cholesterol) form plaque and that adequate vitamin D stops damaged cholesterol from forming plaque.  This should make it painfully clear that the “public health” advice of the American Cancer Society to use sun block and stay out of the sun has directly contributed to heart disease in a major way in America. 
The research was conducted on type II diabetics who are known to have double the risk for heart disease.  It was found that they do not process cholesterol efficiently, and a lack of vitamin D was determined to be the main reason for this problem.  In low vitamin D patients, their macrophages readily absorbed damaged cholesterol, turned into foam cells, and initiated the process of plaque formation. 
The researchers also showed that when human macrophages are placed in a vitamin D adequate environment their uptake of cholesterol is suppressed.  Of course, having adequate antioxidants on board helps prevent cholesterol from being damaged in the first place, which is why the tocotrienol form of vitamin E is so protective to your cardiovascular system.

Oh J, Weng S, Felton SK, Bhandare S, Riek A, Butler B, Proctor BM, Petty M, Chen Z, Schechtman KB, Bernal-Mizrach L, Bernal-Mizrachi C. 1,25 (OH) vitamin D inhibits foam cell formation and suppresses macrophage cholesterol uptake in patients with type 2 diabetes mellitus. Circulation  2009 August
Geriatrics and Division of Nutritional Science, Department of Medicine, and Division of Biostatistics, Washington University, St Louis, Mo.

Study Abstract:

Background— Cardiovascular disease is the leading cause of death among those with diabetes mellitus. Vitamin D deficiency is associated with an increased risk of cardiovascular disease in this population. To determine the mechanism by which vitamin D deficiency mediates accelerated cardiovascular disease in patients with diabetes mellitus, we investigated the effects of active vitamin D on macrophage cholesterol deposition.
Methods and Results— We obtained macrophages from 76 obese, diabetic, hypertensive patients with vitamin D deficiency (25-hydroxyvitamin D <80 nmol/L; group A) and 4 control groups: obese, diabetic, hypertensive patients with normal vitamin D (group B; n=15); obese, nondiabetic, hypertensive patients with vitamin D deficiency (group C; n=25); and nonobese, nondiabetic, nonhypertensive patients with vitamin D deficiency (group D; n=10) or sufficiency (group E; n=10). Macrophages from the same patients in all groups were cultured in vitamin D—deficient or 1,25-dihydroxyvitamin D3 [1,25(OH)2D3] –supplemented media and exposed to modified low-density lipoprotein cholesterol. 1,25(OH)2D3 suppressed foam cell formation by reducing acetylated or oxidized low-density lipoprotein cholesterol uptake in diabetic subjects only. Conversely, deletion of the vitamin D receptor in macrophages from diabetic patients accelerated foam cell formation induced by modified LDL. 1,25(OH)2D3 downregulation of c-Jun N-terminal kinase activation reduced peroxisome proliferated–activated receptor- expression, suppressed CD36 expression, and prevented oxidized low-density lipoprotein–derived cholesterol uptake. In addition, 1,25(OH)2D3 suppression of macrophage endoplasmic reticulum stress improved insulin signaling, downregulated SR-A1 expression, and prevented oxidized and acetylated low-density lipoprotein–derived cholesterol uptake.
Conclusion— These results identify reduced vitamin D receptor signaling as a potential mechanism underlying increased foam cell formation and accelerated cardiovascular disease in diabetic subjects.
From press release:
Low levels of vitamin D are known to nearly double the risk of cardiovascular disease in patients with diabetes, and researchers at Washington University School of Medicine in St. Louis now think they know why.
They have found that diabetics deficient in vitamin D can’t process cholesterol normally, so it builds up in their blood vessels, increasing the risk of heart attack and stroke. The new research has identified a mechanism linking low vitamin D levels to heart disease risk and may lead to ways to fix the problem, simply by increasing levels of vitamin D.
“Vitamin D inhibits the uptake of cholesterol by cells called macrophages,” says principal investigator Carlos Bernal-Mizrachi, M.D., a Washington University endocrinologist at Barnes-Jewish Hospital. “When people are deficient in vitamin D, the macrophage cells eat more cholesterol, and they can’t get rid of it. The macrophages get clogged with cholesterol and become what scientists call foam cells, which are one of the earliest markers of atherosclerosis.”
Macrophages are dispatched by the immune system in response to inflammation and often are activated by diseases such as diabetes. Bernal-Mizrachi and his colleagues believe that in diabetic patients with inadequate vitamin D, macrophages become loaded with cholesterol and eventually stiffen blood vessels and block blood flow.
Bernal-Mizrachi, an assistant professor of medicine and of cell biology and physiology, studied macrophage cells taken from people with and without diabetes and with and without vitamin D deficiency. His team, led by research assistants Jisu Oh and Sherry Weng, M.D., exposed the cells to cholesterol and to high or low vitamin D levels. When vitamin D levels were low in the culture dish, macrophages from diabetic patients were much more likely to become foam cells.
In the Aug. 25 issue of the journal Circulation, which currently is available online, the team reports that vitamin D regulates signaling pathways linked both to uptake and to clearance of cholesterol in macrophages.
“Cholesterol is transported through the blood attached to lipoproteins such as LDL, the ‘bad’ cholesterol,” Bernal-Mizrachi explains. “As it is stimulated by oxygen radicals in the vessel wall, LDL becomes oxidated, and macrophages eat it uncontrollably. LDL cholesterol then clogs the macrophages, and that’s how atherosclerosis begins.”
That process becomes accelerated when a person is deficient in vitamin D. And people with type 2 diabetes are very likely to have this deficiency. Worldwide, approximately one billion people have insufficient vitamin D levels, and in women with type 2 diabetes, the likelihood of low vitamin D is about a third higher than in women of the same age who don’t have diabetes.
The skin manufactures vitamin D in response to ultraviolet light exposure. But in much of the United States, people don’t make enough vitamin D during the winter — when the sun’s rays are weaker and more time is spent indoors.
The good news is when human macrophages are placed in an environment with plenty of vitamin D, their uptake of cholesterol is suppressed, and they don’t become foam cells. Bernal-Mizrachi believes it may be possible to slow or reverse the development of atherosclerosis in patients with diabetes by helping them regain adequate vitamin D levels.
“There is debate about whether any amount of sun exposure is safe, so oral vitamin D supplements may work best,” he says, “but perhaps if people were exposed to sunlight only for a few minutes at a time, that may be an option, too.”
He has launched a new study of diabetics who are both deficient in vitamin D and have high blood pressure. He wants to learn whether replacing vitamin D will lower blood pressure and improve blood flow. For this study, Bernal-Mizrachi is recruiting patients with type 2 diabetes ages 30 to 80 who are not taking insulin to control their blood sugar. Study volunteers also must have high blood pressure.

Tocotrienols protect against mercury toxicity

Tocotrienols have now demonstrated superior anti-oxidant function that protects against exposure from methylmercury.  Exposure to methylmercury is primarily from pollution (coal burning releases 48 tons a year into the atmosphere) and fatty fish.  Methylmercury is a potent neurotoxin.
The new study shows that tocotrienols offer significant nerve-cell protection¹ from methylmercury exposure, a benefit that is far superior to plain vitamin E.  Earlier studies have shown that tocotrienols are an excellent brain antioxidant as well as a great cardiovascular support nutrient.

Shichiri M, Takanezawa Y, Uchida K, Tamai H, Arai H. Protection of cerebellar granule cells by tocopherols and tocotrienols against methylmercury toxicity. Brain Res.  2007 November  1182:106-15.
Department of Health Chemistry, Graduate School of Pharmaceutical Sciences, The University of Tokyo, 7-3-1, Hongo, Bunkyo-ku, Tokyo 113-0033, Japan.

Study Abstract:

Excessive free radical formation has been implicated as one of the causative factors in neurotoxic damage associated with variety of metals, including methylmercury (MeHg). Although the mechanisms associated with MeHg-dependent neurotoxicity remains are unclear, it is known that MeHg leads to neurotoxicity in cerebellar granule cells (CGCs). In vitro exposure of murine CGC primary cultures to MeHg resulted in time- and concentration-dependent cell death. The present study was designed to assess the effect of fat-soluble antioxidant tocopherols and tocotrienols (unsaturated vitamin E) on MeHg-induced neurotoxicity using cultured CGCs. Significant protection from MeHg-induced neuronal cell death was observed with both tocopherols and tocotrienols. Moreover, we observed that tocotrienols are multi-fold more potent than tocopherols in protecting CGCs against MeHg neurotoxicity. At micromolar concentration, tocotrienols, but not tocopherols, showed complete protection by an antioxidant mechanism. Similarly, tocopherols and tocotrienols showed a protective effect on CGCs migration against MeHg-toxicity. These results suggested that oxidative events may contribute to MeHg toxicity in isolated cerebellar granule neurons, and that tocotrienols are potent supplements for pharmacological protection of the developing brain exposed to MeHg.

Bone loss linked to hardening arteries

Postmenopausal women have another good reason to do everything they can to help maintain healthy bone density – the failure to do so is now linked to an increase in plaque in the carotid artery¹.  This relationship existed independent of a woman’s LDL cholesterol levels.  The researchers found that if a woman’s lumbar spine had lost bone density then plaque accumulation in arteries was consistent with the amount of bone loss.
This means that bone loss is now an independent risk factor for heart disease.  When estrogen levels drop at menopause bones take an “inflammatory hit.”  Consequent bone loss for the next five years depends on the extent of inflammatory damage, which depends on the underlying health of the individual.  Women who enter menopause in a fatigued, stressed, or worn down condition – especially if there are other health problems, are invariably at risk for the most bone loss during this time. 
Factors involved with bone inflammation are also cardiovascular stressful, leading to cardiovascular wear and tear.  This new study indicates that these processes directly contribute to hardening of the arteries and heart disease, regardless of how well other heart-related risk factors are managed.  It means that to be healthy after menopause a woman must have adequate bone nutrition, manage stress, stay fit, and nip any health problems in the bud.

 Byron J. Richards,
Board Certified Clinical Nutritionist 

http://www.wellnessresources.com/health/articles/bone_loss_linked_to_hardening_arteries/

 Sumino H, Ichikawa S, Kasama S, Takahashi T, Sakamoto H, Kumakura H, Takayama Y, Kanda T, Murakami M, Kurabayashi M. Relationship between carotid atherosclerosis and lumbar spine bone mineral density in postmenopausal women. Hypertens Res.  2008 June  31(6):1191-7.
Department of Nursing, Faculty of Nursing, Takasaki University of Health and Welfare, Takasaki, Japan.

Study Abstract:

Osteoporosis and increased carotid intima-media thickness (IMT) have been associated with atherosclerosis. We investigated the correlation between carotid IMT and lumbar spine bone mineral density (BMD) in postmenopausal women. We studied the carotid IMT in 175 postmenopausal women, including 43 women (control) with normal spinal BMD, 73 women with osteopenia, and 59 women with osteoporosis. Carotid IMT was assessed by ultrasonography. BMD at the lumbar spine (lumbar 2 to 4 vertebrae) was measured by dual-energy X-ray absorptiometry. Age, years since menopause, and carotid IMT were significantly greater in the osteoporosis group than in the control (all p<0.01) and osteopenia groups (all p<0.01). Estradiol was significantly lower in the osteoporosis group than in the control group (p<0.05). BMD was significantly lower in the osteoporosis group than in the osteopenia or control group (both p<0.01) and in the osteopenia group than in the control group (p<0.01). After adjusting for age, years since menopause, and estradiol, women with osteoporosis had significantly greater carotid IMT than controls (p<0.05). The univariate linear regression analysis revealed that carotid IMT was significantly positively correlated with age, years since menopause, and low-density lipoprotein (LDL) cholesterol (all p<0.05) and was significantly negatively correlated with estradiol and BMD (all p<0.05), but showed no significant association with other clinical variables. In multivariate regression analysis, the carotid IMT was significantly positively correlated with LDL cholesterol (p<0.01) and negatively correlated with BMD (p<0.01), but not with other variables. Carotid atherosclerosis might be associated with lumbar spine bone mass in postmenopausal women, suggesting that postmenopausal women with osteoporosis may have more advanced carotid atherosclerosis than those with a normal bone mass.

Gamma tocotrienol in the war on cancer

A flurry of recent studies demonstrates that gamma tocotrienol, a unique form of vitamin E, offers protection at the molecular level from a number of different types of cancer.
Breast Cancer¹ – A study showed that gamma tocotrienol, at levels of dietary supplement intake, reduced the spreading of breast cancer cells by 58%.
Prostate Cancer² – A study showed that gamma tocotrienol was able to kill prostate cancer cells by modulating gene signals, including reduction of the key pro-inflammatory gene signal, NF-kappaB .  Additionally, it was found to modulate other genes that inhibited the ability of the prostate cancer cells to spread, meaning that in addition to killing prostate cancer cells it was able to reduce their invasiveness.
Stomach Cancer³ – A study showed that gamma tocotrienol induced cell death and prevented cell metastasis of stomach cancer cells.  The authors concluded, “These findings suggest a potential mechanism of gamma-tocotrienol-mediated antitumor metastasis activity and indicate the role of vitamin E as potential chemopreventative agents against gastric cancer.” 
Colon Cancer – A study showed that gamma tocotrienol could knock out colon cancer cells.  Once again, part of the mechanism of action was a potent reduction of the inflammatory gene signal NF-kappaB .
Malignant Melanoma⁵ – Skin cancer is a major concern for many.  A new study shows that gamma tocotrienol can kill melanoma cells, primarily by reducing NF-kappaB and related gene signals.  It also reduced gene signals associated with invasiveness.  And it also helped chemo drugs work better, consistent with earlier findings of synergistic benefit.
While no person should consider any one vitamin a treatment or prevention of cancer, this data clearly shows that gamma tocotrienol is a powerful tool working in your favor.

 Byron J. Richards,
Board Certified Clinical Nutritionist 

 http://www.wellnessresources.com/health/articles/gamma_tocotrienol_in_the_war_on_cancer/

 Referenced Studies:

1. ^ Gamma Tocotrienol, Resveratraol, and Breast Cancer  Int J Oncol.  Hsieh TC, Wu JM.
2. ^ Gamma Tocotrienol and Prostate Cancer  Br J Cancer.   Yap WN, Chang PN, Han HY, Lee DT, Ling MT, Wong YC, Yap YL.
3. ^ Gamma Tocotrienol and Gastric Cancer  J Nutr Biochem.   Liu HK, Wang Q, Li Y, Sun WG, Liu JR, Yang YM, Xu WL, Sun XR, Chen BQ.
4. ^ Gamma Tocotrienol and Colon Cancer  Nutrition.  Xu WL, Liu JR, Liu HK, Qi GY, Sun XR, Sun WG, Chen BQ.
5. ^ Gamma Tocotrienol and Malignant Melanoma  Nutr Cancer.  Chang PN, Yap WN, Lee DT, Ling MT, Wong YC, Yap YL. 

Hsieh TC, Wu JM. Suppression of cell proliferation and gene expression by combinatorial synergy of EGCG, resveratrol and gamma-tocotrienol in estrogen receptor-positive MCF-7 breast cancer cells. Int J Oncol.  2009 October  33(4):851-9.
Department of Biochemistry and Molecular Biology, New York Medical College, Valhalla, NY 10595, USA.

Study Abstract:

Numerous dietary phytochemicals have shown anti-breast carcinogenic activities when tested in vitro; however, in most cases, the demonstrated efficacy of individual phytochemicals requires doses not readily achievable in vivo. Therefore, whether diets might exert translational promises and benefits in clinical settings and prevention of breast cancer remain unclear. Since cancer cells are endowed with complex, redundant, converging and diverging pathways spanning both the genetic and metabolic networks that are not merely replicates of those in normal cells, it is of interest to test whether a multicomponent approach involving lower, physiologically relevant doses of natural dietary agents may be developed as a chemopreventive strategy for breast cancer. Herein, we investigated, using the estrogen receptor-positive MCF-7 breast cancer cells as a model, whether the combination of epigallocatechin gallate (EGCG), resveratrol and gamma-tocotrienol at suboptimal doses elicits synergism in suppressing cell proliferation, modulating gene expression, and increasing antioxidant activity, as compared to each of the three phytochemicals added alone. The results showed that there was a approximately 33, 50 and 58% inhibition of cell proliferation by > or =50 microM EGCG, > or =25 microM resveratrol and > or =10 microM gamma-tocotrienol, respectively, added as a single agent. When a suboptimal dose (10 microM) of each phytochemical was used, a significant additive effect in suppression of cell proliferation was observed with the combination of resveratrol and gamma-tocotrienol whereas the three phytochemicals added together did not produce more pronounced inhibition of cell proliferation. A significant additive effect in reducing cyclin D1 and bcl-2 expression was found when gamma-tocotrienol was added with either EGCG or resveratrol. Functional synergism among the three phytochemicals was only observed in the induction of quinone reductase NQO1. These results suggest that diet-based protection against breast cancer may partly derive from synergy amongst dietary phytochemicals directed against specific molecular targets in responsive breast cancer cells, and provide support for the feasibility of the development of a diet-based combinatorial approach in the prevention and treatment of breast cancer.

 Yap WN, Chang PN, Han HY, Lee DT, Ling MT, Wong YC, Yap YL. Gamma-tocotrienol suppresses prostate cancer cell proliferation and invasion through multiple-signalling pathways. Br J Cancer.   2008 December  99(11):1832-41.
Davos Life Science Pte. Ltd., Cancer Research Laboratory, 11 Biopolis way, #07-03, The Helios 138667, Singapore.

Study Abstract:

Tocotrienol-rich fraction (TRF) has demonstrated antiproliferative effect on prostate cancer (PCa) cells. To elucidate this anticancer property in PCa cells, this study aimed, first, to identify the most potent isomer for eliminating PCa cells; and second, to decipher the molecular pathway responsible for its activity. Results showed that the inhibitory effect of gamma-tocotrienol was most potent, which resulted in induction of apoptosis as evidenced by activation of pro-caspases and the presence of sub-G(1) cell population. Examination of the pro-survival genes revealed that the gamma-tocotrienol-induced cell death was associated with suppression of NF-kappaB, EGF-R and Id family proteins (Id1 and Id3). Meanwhile, gamma-tocotrienol treatment also resulted in the induction of JNK-signalling pathway and inhibition of JNK activity by a specific inhibitor (SP600125) was able to partially block the effect of gamma-tocotrienol. Interestingly, gamma-tocotrienol treatment led to suppression of mesenchymal markers and the restoration of E-cadherin and gamma-catenin expression, which was associated with suppression of cell invasion capability. Furthermore, a synergistic effect was observed when cells were co-treated with gamma-tocotrienol and Docetaxel. Our results suggested that the antiproliferative effect of gamma-tocotrienol act through multiple-signalling pathways, and demonstrated for the first time the anti-invasion and chemosensitisation effect of gamma-tocotrienol against PCa cells.

Liu HK, Wang Q, Li Y, Sun WG, Liu JR, Yang YM, Xu WL, Sun XR, Chen BQ. Inhibitory effects of gamma-tocotrienol on invasion and metastasis of human gastric adenocarcinoma SGC-7901 cells. J Nutr Biochem.   2009 February
Department of Nutrition and Food Hygiene, Public Health School, Harbin Medical University, NanGang District, Harbin, Heilongjiang Province 150086, People's Republic of China.

Study Abstract:

Natural vitamin E is a mixture of two classes of compounds, tocopherols and tocotrienols. Recent research has revealed that tocotrienols, especially gamma-tocotrienol, exhibit not only the same antioxidant ability as tocopherols, but also remarkable anticancer capacity in cancer cell lines. In this study, the invasion and metastatic capacities of gastric adenocarcinoma SGC-7901 cells and the correlation with antimetastasis mechanisms induced by gamma-tocotrienol were explored. The results showed the inhibitory effects of gamma-tocotrienol at doses of 15, 30, 45 and 60 mumol/L for 48 h on cell migration and cell matrigel invasion; activities of matrix metalloproteinase (MMPs) increased in SGC-7901 cells when compared to the control group (P<.05 or P<.01). An increasing trend in the chemotactic responses to fibronectin (FN) in SGC-7901 cells was found in the gamma-tocotrienol treatments. SGC-7901 cell attachment decreased in the gamma-tocotrienol-treated groups in comparison with the control group (P<.01). The mRNA expressions of MMP-2 and MMP-9 showed that gamma-tocotrienol significantly reduced the matrigel invasion capability through down-regulation of the mRNA expressions of MMP-2 and MMP-9 (P<.01), and up-regulation of tissue inhibitor of metalloproteinase-1 (TIMP-1) and TIMP-2 in SGC-7901 cells by treatment with gamma-tocotrienol for 48 h (P<.05). gamma-Tocotrienol also significantly increased the mRNA expression of nm23-H1 in SGC-7901 cells (P<.01). These findings suggest a potential mechanism of gamma-tocotrienol-mediated antitumor metastasis activity and indicate the role of vitamin E as potential chemopreventative agents against gastric cancer.

 Xu WL, Liu JR, Liu HK, Qi GY, Sun XR, Sun WG, Chen BQ. Inhibition of proliferation and induction of apoptosis by gamma-tocotrienol in human colon carcinoma HT-29 cells. Nutrition.  2009 May  25(5):555-66.
Department of Nutrition and Food Hygiene, Public Health School, Harbin Medical University, Harbin, People's Republic of China.

Study Abstract:

OBJECTIVE: gamma-Tocotrienol is a major component of the tocotrienol-rich fraction of palm oil, but there is limited evidence that it has antitumor activity. In particular, the effects of gamma-tocotrienol on human colon carcinoma cells have not been reported. To investigate the chemopreventive effects of gamma-tocotrienol on colon cancer, we examined its capacity to inhibit proliferation and induce apoptosis in HT-29 cells and explored the mechanism underlying these effects.
METHODS: We cultured HT-29 cells in the presence of gamma-tocotrienol. The effect of gamma-tocotrienol on cell proliferation was investigated by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay, mitotic index, and colony formation. The cell-cycle distribution was investigated by flow cytometry. We measured apoptosis by nuclear staining, transmission electron microscopy, and DNA fragmentation. Apoptosis-related proteins and the nuclear factor-kappaB p65 protein were determined by western blotting and immunofluorescence.
RESULTS: gamma-Tocotrienol inhibited cell growth and arrested HT-29 cells in G(0)/G(1) phase. The 50% inhibitory concentration was 31.7 micromol/L (48 h). gamma-Tocotrienol-induced apoptosis in HT-29 cells was accompanied by downregulation of Bcl-2, upregulation of Bax, and activation of caspase-3. Furthermore, we found that gamma-tocotrienol reduced the expression level of total nuclear factor-kappaB p65 protein and inhibited its nuclear translocation.
CONCLUSION: The results indicated that gamma-tocotrienol inhibits cell proliferation and induces apoptosis in HT-29 cells in a time- and dose-dependent manner, and that this process is accompanied by cell-cycle arrest at G(0)/G(1), an increased Bax/Bcl-2 ratio, and activation of caspase-3. Our data also indicated that nuclear factor-kappaB p65 protein may be involved in these effects.

Chang PN, Yap WN, Lee DT, Ling MT, Wong YC, Yap YL. Evidence of gamma-tocotrienol as an apoptosis-inducing, invasion-suppressing, and chemotherapy drug-sensitizing agent in human melanoma cells. Nutr Cancer.  2009 June  61(3):357-66.
Davos Life Science Pte. Ltd., Cancer Research Laboratory, 138667, Singapore

Study Abstract:

To date, the most effective cure for metastatic melanoma remains the surgical resection of the primary tumor. Recently, tocotrienol-rich-fraction has shown antiproliferative effect on cancer cells. To elucidate this anticancer property in malignant melanoma, this study aimed, first, to identify the most potent isomer for eliminating melanoma cells and second to decipher the molecular pathway responsible for its activity. Results showed that the inhibitory effect of gamma-tocotrienol was most potent, which resulted in induction of apoptosis as evidenced by activation of procaspases and the accumulation of sub-G1 cell population. Examination of the prosurvival genes revealed that the gamma-tocotrienol-induced cell death was associated with suppression of NF-kappaB, EGF-R, and Id family proteins. Meanwhile, gamma-tocotrienol treatment also resulted in induction of JNK signaling pathway, and inhibition of JNK activity by selective inhibitor was able to partially block the effect of gamma-tocotrienol. Interestingly, gamma-tocotrienol treatment led to suppression of mesenchymal markers and the restoration of E-cadherin and gamma-catenin expression, which was associated with suppression of cell invasion capability. Furthermore, synergistic effect was observed when cells were cotreated with gamma-tocotrienol and chemotherapy drugs. Together, our results demonstrated for the first time the anti-invasion and chemonsensitization effect of gamma-tocotrienol against human malignant melanoma cells.

Gamma tocotrienol assists bone strength

A new study shows that vitamin E, and in particular the form known as gamma tocotrienol¹, helps build stronger bones with better biomechanical strength.
The authors concluded, “Vitamin E supplementation, especially with the gamma isomer, improves bone structure, which contributed to stronger bone. Therefore, vitamin E has the potential to be used as an anabolic agent to treat osteoporosis or as bone supplements for young adults to prevent osteoporosis in later years.”
This new study goes along with three earlier studies lending support to the tocotrienol form of vitamin E as a superior bone support nutrient.  The earlier studies showed that tocotrienols reduce inflammation in bone² that leads to bone loss, can offset the harmful effects of steroid use³ on bones, and assist in the process of normal bone calcification⁴.
While tocotrienols are often used for cardiovascular and brain health, here we see that they are yet another wonderful nutrient for bone health.

 Referenced Studies:

1. ^ Gamma Tocotrienol Helpful for Bone Building   J Bone Miner Metab.  Shuid AN, Mehat Z, Mohamed N, Muhammad N, Soelaiman IN.
2. ^ Tocotrienols Help Stop Bone Loss  Clin Exp Pharmacol Physiol.  Ahmad NS, Khalid BA, Luke DA, Ima Nirwana S.
3. ^ Tocotrienols Prevent Bone Loss and Weight Gain During Steroid Treatment  J Med Food.  Ima-Nirwana S, Suhaniza S.
4. ^ Tocotrienols Help Bone Calcification  Asia Pac J Clin Nutr.  Norazlina M, Ima-Nirwana S, Abul Gapor MT, Abdul Kadir Khalid B. 

 Shuid AN, Mehat Z, Mohamed N, Muhammad N, Soelaiman IN. Vitamin E exhibits bone anabolic actions in normal male rats. J Bone Miner Metab.  2009 September
Department of Pharmacology, Faculty of Medicine UKM, Universiti Kebangsaan Malaysia, Jln Raja Muda Abdul Aziz, 50300, Kuala Lumpur, Malaysia.

Study Abstract:

Recently, vitamin E has been found to promote the bone structure of nicotine-treated rats well above their baseline values, thus suggesting that vitamin E may have some anabolic action. A bone anabolic agent acts by improving the bone structure leading to stronger bone. To assess the possible anabolic action vitamin E on bone, we supplemented alpha-tocopherol (ATF) or gamma-tocotrienol (GTT) at 60 mg/kg or vehicle [normal control (NC) group] for 4 months to normal male rats and measured their bone structure and biomechanical properties. Histomorphometric analysis revealed that vitamin E-supplemented rats have better trabecular volume, thickness, number, and separation than rats receiving vehicle only. For the first time we reported that GTT improves all the parameters of bone biomechanical strength, while ATF only improved some of the parameters compared to the NC group. Vitamin E supplementation, especially with the gamma isomer, improves bone structure, which contributed to stronger bone. Therefore, vitamin E has the potential to be used as an anabolic agent to treat osteoporosis or as bone supplements for young adults to prevent osteoporosis in later years

Ahmad NS, Khalid BA, Luke DA, Ima Nirwana S. Tocotrienol offers better protection than tocopherol from free radical-induced damage of rat bone. Clin Exp Pharmacol Physiol.  2005 September  32(9):761-70.
Department of Pharmacology, Faculty of Medicine, Universiti Kebangsaan Malaysia, Jalan Raja Muda Abdul Aziz, Kuala Lumpur, Malaysia.

Study Abstract:

1. Free radicals generated by ferric nitrilotriacetate (FeNTA) can activate osteoclastic activity and this is associated with elevation of the bone resorbing cytokines interleukin (IL)-1 and IL-6. In the present study, we investigated the effects of 2 mg/kg FeNTA (2 mg iron/kg) on the levels of serum IL-1 and IL-6 with or without supplementation with a palm oil tocotrienol mixture or alpha-tocopherol acetate in Wistar rats.
2. The FeNTA was found to elevate levels of IL-1 and IL-6. Only the palm oil tocotrienol mixture at doses of 60 and 100 mg/kg was able to prevent FeNTA-induced increases in IL-1 (P < 0.01). Both the palm oil tocotrienol mixture and alpha-tocopherol acetate, at doses of 30, 60 and 100 mg/kg, were able to reduce FeNTA-induced increases in IL-6 (P < 0.05). Therefore, the palm oil tocotrienol mixture was better than pure alpha-tocopherol acetate in protecting bone against FeNTA (free radical)-induced elevation of bone-resorbing cytokines.
3. Supplementation with the palm oil tocotrienol mixture or alpha-tocopherol acetate at 100 mg/kg restored the reduction in serum osteocalcin levels due to ageing, as seen in the saline (control) group (P < 0.05). All doses of the palm oil tocotrienol mixture decreased urine deoxypyridinoline cross-link (DPD) significantly compared with the control group, whereas a trend for decreased urine DPD was only seen for doses of 60 mg/kg onwards of alpha-tocopherol acetate (P < 0.05).
4. Bone histomorphometric analyses have shown that FeNTA injections significantly lowered mean osteoblast number (P < 0.001) and the bone formation rate (P < 0.001), but raised osteoclast number (P < 0.05) and the ratio of eroded surface/bone surface (P < 0.001) compared with the saline (control) group. Supplementation with 100 mg/kg palm oil tocotrienol mixture was able to prevent all these FeNTA-induced changes, but a similar dose of alpha-tocopherol acetate was found to be effective only for mean osteoclast number. Injections of FeNTA were also shown to reduce trabecular bone volume (P < 0.001) and trabecular thickness (P < 0.05), whereas only supplementation with 100 mg/kg palm oil tocotrienol mixture was able to prevent these FeNTA-induced changes.

Ima-Nirwana S, Suhaniza S. Effects of tocopherols and tocotrienols on body composition and bone calcium content in adrenalectomized rats replaced with dexamethasone. J Med Food.  2004 April  7(1):45-51.
Department of Pharmacology, Faculty of Medicine, Universiti Kebangsaan Malaysia, Kuala Lumpur, Malaysia. 

Study Abstract:

Long-term glucocorticoid treatment is associated with severe side effects, such as obesity and osteoporosis. A palm oil-derived vitamin E mixture had been shown previously to be protective against osteoporosis in rats given 120 microg/kg dexamethasone daily for 12 weeks. In this study we determined the effects of two isomers of vitamin E (i.e., palm oil-derived gamma-tocotrienol and the commercially available alpha-tocopherol, 60 mg/kg of body weight/day) on body composition and bone calcium content in adrenalectomized rats replaced with two doses of dexamethasone, 120 microg/kg and 240 microg/kg daily. Treatment period was 8 weeks. gamma-Tocotrienol (60 mg/kg of body weight/day) was found to reduce body fat mass and increase the fourth lumbar vertebra bone calcium content in these rats, while alpha-tocopherol (60 mg/kg of body weight/day) was ineffective. Therefore, in conclusion, palm oil-derived gamma-tocotrienol has the potential to be utilized as a prophylactic agent in prevention of the side effects of long-term glucocorticoid use.

Norazlina M, Ima-Nirwana S, Abul Gapor MT, Abdul Kadir Khalid B. Tocotrienols are needed for normal bone calcification in growing female rats. Asia Pac J Clin Nutr.  2002 November  11(3):194-9.
Department of Pharmacology, Faculty of Medicine, Universiti Kebangsaan Malaysia, Kuala Lumpur.

Study Abstract:

In this study the effects of vitamin E deficiency and supplementation on bone calcification were determined using 4-month-old female Sprague-Dawley rats. The rats weighed between 180 and 200 g. The study was divided in three parts. In experiment I the rats were given normal rat chow (RC, control group), a vitamin E deficient (VED) diet or a 50% vitamin E deficient (50%VED) diet. In experiment 2 the rats were given VED supplemented with 30 mg/kg palm vitamin E (PVE30), 60 mg/kg palm vitamin E (PVE60) or 30 mg/kg pure alpha-tocopherol (ATF). In experiment 3 the rats were fed RC and given the same supplements as in experiment 2. The treatment lasted 8 months. Vitamin E derived from palm oil contained a mixture of ATF and tocotrienols. Rats on the VED and 50%VED diets had lower bone calcium content in the left femur compared to the RC group (91.6 +/- 13.3 mg and 118.3 +/- 26.0 mg cf 165.7 +/- 15.2 mg; P < 0.05) and L5 vertebra (28.3 +/- 4.0 mg and 39.5 +/- 6.2 mg compared with 51.4 +/- 5.8 mg; P < 0.05). Supplementing the VED group with PVE60 improved bone calcification in the left femur (133.6 +/- 5.0 mg compared with 91.6 +/- 13.3 mg; P < 0.05) and L5 vertebra (41.3 +/- 3.3 mg compared with 28.3 +/- 4.0 mg; P < 0.05) while supplementation with PVE30 improved bone calcium content in the L5 vertebra (35.6 +/- 3.1 mg compared with 28.3 +/- 4.0 mg; P < 0.05). However, supplementation with ATF did not change the lumbar and femoral bone calcium content compared to the VED group. Supplementing the RC group with PVE30, PVE60 or ATF did not cause any significant changes in bone calcium content. In conclusion, vitamin E deficiency impaired bone calcification. Supplementation with the higher dose of palm vitamin E improved bone calcium content, but supplementation with pure ATF alone did not. This effect may be attributed to the tocotrienol content of palm vitamin E. Therefore, tocotrienols play an important role in bone calcification.