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Scrutinizing the role of vitamins in healthy living

What happens when you take calcium with vitamin D? And do you need a specific dose of magnesium with your fat-soluble vitamins such as K, A, D, E? That's a question consumers often ask when they go into a health food store if their own health care team or primary care physician doesn't know the answer without first having to look it up or even having the time with a heavy patient load each day.

Scrutinizing the role of vitamins in healthy living.
Anne Hart, photography.

Why aren't scientists ever mentioning what happens when you take magnesium supplements? For example, 360 mg for women and 420 mg for men of magnesium, such as magnesium citrate, if the brand you select has a low enough level of mercury or lead to meet California's minimum requirements for supplements. How about getting your minerals from foods?

What doctors in the latest study also may be saying that is if your physician tells you to take calcium and vitamin D you shouldn't stop taking them, but instead to discuss your worries with your doctor. That may be because the study needs continuing research to find out what's really happening.

Unfortunately for this study, no one is mentioning the benefits of taking magnesium in small amounts and getting your calcium from a balanced diet of foods. See the latest article or abstract on the study, "Calcium supplements with or without vitamin D and risk of cardiovascular events: reanalysis of the Women's Health Initiative limited access dataset and meta-analysis", by Mark J Bolland, Andrew Grey, Alison Avenell, Greg D Gamble, Ian R Reid. The study appears in BMJ 2011; 342:d2040 doi: 10.1136/bmj.d2040.

Can vitamin D alone be tied to heart disease if you have a particular variant of genes?

Can vitamin D in excess possibly be tied to heart disease if you have specific types of genes? Why are so many Sacramento consumers rushing to wolf down higher and higher doses of vitamin D3 supplements without knowing whether they are deficient?

And why is there so much about vitamin D in the media these days? There are blood tests to determine whether you need extra vitamin D. And if you do, how do you know whether you have the genetic variant that processes vitamin D differently than most people?

Are there some people who shouldn't be taking supplements containing vitamin D and just get what they need of the vitamin from healthy foods? According to a December 3, 2009 article in HealthDay Daily News, "Vitamin D May Be Tied to Heart Disease Via Genes," if you have a specific gene variant that reduces vitamin D activation in the body and high blood pressure, according to a new study, you were found to be twice as likely as those without the variant to have congestive heart failure as well as the high blood pressure, the study found.

Also see the Dec 3, 2009 UPI article: Heart failure linked to vitamin D gene, (U.S. researchers linked congestive heart failure to a gene variant affecting vitamin D activation.) What does this study mean for consumers of vitamin supplements?

The purpose of the study is to hopefully identify people at increased risk for heart disease, according to Robert U. Simpson, an assistant professor of pharmacology at the University of Michigan Medical School and his research colleagues, as reported by HealthDay Daily News.

The University of Michigan Medical School researchers analyzed the genetic profiles of 617 people. One-third had hypertension, one-third had hypertension and congestive heart failure, and the remaining third served as healthy controls.

Scientists found that a variant in the CYP27B1 gene was associated with congestive heart failure in people with hypertension. The study is in the November 2009 issue of the journal, Pharmacogenomics.

Previous research showed that mutations that inactivate the gene reduce the conversion of vitamin D into an active hormone. "This study is the first indication of a genetic link between vitamin D action and heart disease," Simpson noted in a news release from the University of Michigan.

"If subsequent studies confirm this finding and demonstrate a mechanism, this means that, in the future, we may be able to screen earlier for those most vulnerable and slow the progress of the disease," he added.

Vitamin D supplements and genetic variations

When consumers examine this study, the main question arises as to whether someone with the gene mutation should or should not take supplements of vitamin D. For example, would the vitamin D from vitamin pills quicken the path towards congestive heart failure in a person with high blood pressure and the gene mutation, or would extra vitamin D be beneficial and slow down the decline?

Does the gene variant that inactivates the gene prevent vitamin D from dietary sources from being converted into an active hormone? Or is more vitamin D needed? Does the gene mutation cause vitamin D to calcify the aorta or not? What should persons with the gene mutation and high blood pressure eat--more or less vitamin D either in supplements or dietary means? That's the question consumers would like to know when they read the study. The natural form of vitamin D is vitamin D3.

What are the risks of taking vitamin D supplements? Do you have that specific gene mutation?

Do you have the gene mutation? Did anyone in your family have it? Could you find out whether you've inherited that specific gene mutation? What are some of the risks of taking too much vitaminD? Where can you go to find out whether you have the gene mutation, assuming you also have high blood pressure and a family history of hypertension and congestive heart failure. Those are health questions consumers would like to have answered.

Researchers at Johns Hopkins are reporting what is believed to be the first conclusive evidence in men that the long-term ill effects of vitamin D deficiency are amplified by lower levels of the key sex hormone estrogen, but not testosterone, according to a Nov.17th, 2009 news article, "Effects Of Vitamin D Deficiency Amplified By Shortage Of Estrogen."

In a recent national study of men presented on Nov. 15 at the American Heart Association's (AHA) annual Scientific Sessions in Orlando, FL, researchers reported that the new findings build on previous studies showing that deficiencies in vitamin D and low levels of estrogen, found naturally in differing amounts in men and women, were independent risk factors for hardened, narrowed arteries and weakened bones.

What does vitamin D actually do? It plays an important role in calcium balance so you get normal bone strength. The major function of vitamin D is to improve the efficiency of calcium absorption from the small intestine, according to Dr. Ray Sahelian's newsletter and nutrition information sites. Can taking too much vitamin D calcify your aorta? What are the risks? And do you have to inherit a specific gene variation for vitamin D to calify your coronary arteries? What does the research show?

What happens to the way your body handles, absorbs, or builds up vitamin D after menopause when the estrogen level plummets? And were you born with or without the gene variation that takes the vitamin D3 you eat along with the calcium and calcifies your arteries with it instead of putting it into your bones where it belongs? How do you find a genetics/DNA test to tell you whether you have inherited that genetic mutation or variation?

Epidemiological data show low levels of vitamin D lead to a higher incidence of breast cancer, colon cancer, prostate cancer, ovarian cancer, as well as multiple myeloma, according to Dr.Sahelian's site. Patients with Crohn's disease are known to have low levels. Vitamin D supplementation may even improve mood during the winter months, according to Dr. Sahelian. But you'd be better off taking less than more until you know how much you'll really need of vitamin D.

Scientists repeatedly warn vitamin consumers of the danger regarding excessive intake. Vitamin D taken in high amounts can cause excessive calcification of bone, calcification of soft tissue, kidney stones, headaches, weakness, nausea, and vomiting.

There answer right now is that no one knows exactly the long-term effects of high dose daily use of vitamin D. Find out whether or not you need to supplement at all. Research is ongoing. In the meantime, are you taking a teaspoon full of cod liver oil that already has 400 units of vitamin D in it along with some vitamin A? Look at the label and see whether it tell you the vitamin content of the oil. How do you compare the different answers given by your various heath care professionals?

When you take all those vitamin D3 supplements that are recommended in so many articles in the media, how do you know whether your body will use it to protect your organs against bone loss or use it to send calcium deposits into your organs, heart valves, and arteries?

Find out from your doctor whether or not your blood test tell you that you may or may not need to supplement. Does your diet have plenty of vitamin D? Do you get enough sun exposure?

Most people may benefit from taking 400 units a day either as part of a multivitamin product and a balanced diet. A few people without much sun exposure and a poorer diet, or if you live in latitudes where there's not much sun, might benefit from 600-800 units of vitamin D3.

The only questions scientists have is that over a long term, we don't know what the risks are. You're doctor should talk with you if you have chronic medical conditions whether you need up to 1,000 units daily. But the question is for how long without posing a risk of calcifying your arteries from too high a dose for too long a time of taking supplements of vitamin D.

When you do take a supplement, be sure it's natural vitamin D3, not synthetic vitamin D2. The conclusion is the final word is not yet in on the danger of calcifying your brain and arteries with too much vitamin D supplementation.

Why take the risk when you can keep your supplementation, if any, to a dose related to what your body needs. You can find out what vitamin deficiencies you have by taking a test to see what's actually absorbed into your cells and what's just floating in your bloodstream.

What needs to be evaluated right now is whether other genes that control calcium homeostasis are involved in the pathogenesis of this disorder. In plain language, how many gene variations control the way calcium and vitamin D3 are processed in your own body? And how can you find out? Are there genetic tests that show you how your body handles vitamin D3?

The media is full of articles saying that the 400 mg of vitamin D3 is too little to protect you against cardiovascular problems, that you probably need 1,000 mg. But what happens if you have a genetic variation or mutation that communicates to your body in a different way, where when you take vitamin D3 and calcium in supplements or at high food intakes, that the calcium doesn’t go into your bones, but into the arteries and valves around your heart?

Will vitamin K2 in the MK-7 form protect you from calcification if you have this genetic variation? And where can you find out if it will? All these answers require scientific studies, namely, research.

Another article at BioMed Experts, Osteoporosis and calcification of the aorta, Bone and Mineral, 1992;19(2):185-94,1992: Frye M A; Melton L J; Bryant S C; Fitzpatrick L A; Wahner H W; Schwartz R S; Riggs B L, notes, “Aortic calcification was not associated with any measures of calcium metabolism, after adjusting for age, except for a slight negative association between linear aortic calcifications and 25(OH) vitamin D levels (P < 0.05).”

Another abstract of a 2003 article, "Influence of sex and estrogen on vitamin D-induced arterial calcification in rats" notes, "It is known that the process of arteriosclerosis is affected by sex and estrogen. The present study was thus undertaken to examine the effects of these factors on arterial calcification, a form of arteriosclerosis, using a rat model of vitamin D toxicity.

The article concludes with, “These results suggest that sex and estrogen can modify the process of arterial calcification. The mechanisms remain to be determined, although the effects were independent of serum calcium level.”

Will taking vitamin K2 in the MK-7 form help you if you have this gene variation whereby taking too much vitamin D starts to calcify your aorta? Or not? Only science can tell you for sure, and the science needs to be tailored to your individual genes. Is science ready yet? Have they developed a test? Or does science still not know yet how many genes need to be tested to see how your body handles vitamin D3 and calcium?

You hear all the talk about increasing your daily natural vitamin D3 intake from 400 mg to at least 1,000 mg to prevent arterial calcification, bone loss, and certain diseases. The media says so many diseases could be due to too low vitamin D3 intake. But what happens if you have a certain gene variation that instead causes vitamin D3 to calcify your aortic valves?

There is some early research that high amounts of vitamin D, such as 2,000 iu, taken daily for many months or years may lead to calcification of arteries, according to Dr. Ray Sahelian's newsletter. How do you know what to take?

Until more studies are published we prefer to be cautious and have people only take one or two vitamin D 400 iu a day. Some doctors are recommending daily dosages of 1000 units or higher. Research in medical journals report that many people in this country are not getting enough of this vitamin. But what is the right dosage for supplementation so you don't calcify the arteries in your brain or heart?

If you have a gene variation, does vitamin D cause calcification of your aorta? See the article at the CAT. Inst. site. Another article in the Journal of Vascular Research, Aortic Calcification Produced by Vitamin D3 plus Nicotine, notes that “Calcification of the elastic arteries of the young rat by treatment with vitamin D and nicotine (VDN) has been proposed as an animal model of arterial calcification associated with age and age-related vascular pathology in man.

The calcium-binding protein, S-100, which is found in human atherosclerotic lesions was associated with medial calcification of the aorta in VDN rats, especially in cases of severe calcification.” The abstract’s conclusion is that, “In conclusion, the mechanisms and consequences of aortic calcification in VDN show several similarities with calcification occurring in human athero- and arteriosclerosis.”

See the conclusion of the article in the MD Consult Preview, The vitamin D receptor genotype predisposes to the development of calcific aortic valve stenosis. - Ortlepp JR - Heart - 01-JUN-2001; 85(6): 635-8 (MEDLINE is the source for the citation and abstract of this record) that notes, “There is a significant association of vitamin D receptor polymorphism with calcific aortic valve stenosis. The B allele of the vitamin D receptor is more common in patients with calcific aortic valve stenosis. It now needs to be evaluated whether other genes that control calcium homeostasis are involved in the pathogenesis of this disorder.”

See the article, at: Oxford Journals, Cardiovascular Research, titled, Uraemic hyperparathyroidism causes a reversible inflammatory process of aortic valve calcification in rats. Uraemic hyperparathyroidism causes a reversible inflammatory process of aortic valve calcification in rats Renal failure is associated with aortic valve calcification (AVC). Our aim was to develop an animal model for exploring the pathophysiology and reversibility of AVC, utilizing rats with diet-induced kidney disease.

See the publication, Heart, and Education in Heart, a peer review journal for health professionals in all areas of cardiology. The article, Cardiovascular medicine, “The vitamin D receptor genotype predisposes to the development of calcific aortic valve stenosis”, J R Ortlepp, R Hoffmann, F Ohme, J Lauscher, F Bleckmann, P Hanrath, tests the hypothesis that vitamin D receptor polymorphism is associated with calcific aortic valve stenosis.

The conclusion noted, “There is a significant association of vitamin D receptor polymorphism with calcific aortic valve stenosis. The B allele of the vitamin D receptor is more common in patients with calcific aortic valve stenosis. It now needs to be evaluated whether other genes that control calcium homeostasis are involved in the pathogenesis of this disorder.”

What this means is if you have a genetic variation, a polymorphism on your vitamin D receptor, it’s association with calcification of your aortic valve. How do you know whether you have this particular gene variation that makes your body react a certain way to vitamin D3 by developing calcium deposits in your aortic valve?

What should you do? Keep asking whether the test is ready yet. And keep searching to find out whether science has found all the genes necessary to tell you how your body handles vitamin D3 supplements versus natural food intake, calcium, magnesium, and fish oils containing vitamin D3. Until you know, eat whole foods, get enough sunshine or other natural light, and keep researching.

Find out whether you have the B allele of the vitamin D receptor. Science knows those with it, at least in rats and some human patients, it is more common to see calcification of the aortic valve. But because it is more common, how does that tell us whether the gene variation is a risk? Or how many genes or alleles are involved? That's why you have to keep asking those experts that are talking about health care with you.

Also, on the subject of food cravings, according to the article, “Combat Your Food Cravings,” in the June 2009 issue of Natural Solutions magazine, page 79, if you crave sweets, what your body really needs are trace amounts of chromium, carbon, phosphorus, sulfur, and tryptophan. You can get all of these in small amounts from the following foods: To get enough chromium, eat broccoli, grapes, cheese, dried beans, and chicken. Think about this. But do you agree with this information you read in popular consumer magazines on health not meant for your doctor to read, but for the general consumer?

How can you find out whether this idea has been validated in credible medical journals?

Where can you turn to for nutrition information after reading interviews in magazines? The only problem with articles where health professionals are interviewed is where can you go to validate all these statements in scientific studies or journals if references aren't listed in a sidebar? Where can you find the resources without having to subscribe to the medical journals? Start with the public library or some of the online nutrition sites that have references.

Check out the study, "Effects Of Vitamin D Deficiency Amplified By Shortage Of Estrogen." November 17, 2009. Researchers at Johns Hopkins are reporting what is believed to be the first conclusive evidence in men that the long-term ill effects of vitamin D deficiency are amplified by lower levels of the key sex hormone estrogen, but not testosterone [read article].

Vitamin D link and possible help for Parkinson's disease study

Higher vitamin D levels are associated with better cognition and mood in Parkinson's Disease (PD) patients, say new findings published in the Journal of Parkinson's Disease. Amsterdam, NL, 16 January 2014 – A new study exploring vitamin D levels in patients with Parkinson's disease (PD) opens up the possibility of a new avenue of early intervention that may delay or prevent the onset of cognitive impairment and depression. The findings are published in the Journal of Parkinson's Disease (IOS Press.)

In the latest study, investigators conducted a cross-sectional analysis of 286 patients with Parkinson's disease and found that higher plasma vitamin D levels were associated with lower symptom severity, better cognition, and less depression in the entire group, but the relationships were even stronger in those who were not demented. Also see the abstract of another study, "Vitamin D, omega-3 may help clear amyloid plaques found in Alzheimer's."

Or see, "Does Vitamin D Reduce the Risk of Dementia?" Studies in the past focused on the link between dementia risk reduction and vitamin D. Check out, "Why Vitamin D in Alzheimer's Disease? The Hypothesis." Now a new study focuses on the link between vitamin D and Parkinson's disease risk and possible symptoms reduction.

Vitamin D receptors and its final converting enzyme have been found in human brain tissue, including the hippocampus, which plays a significant role in memory and learning. Non-motor symptoms, such as worsening depression, anxiety, and sleep disturbances, can appear prior to the onset of motor symptoms.

Nursing home placement and shortened life expectancy

"About 30% of persons with PD suffer from cognitive impairment and dementia, and dementia is associated with nursing home placement and shortened life expectancy," says Amie L. Peterson, MD, of the Oregon Health and Sciences University, according to a January 16, 2014 news release, Higher vitamin D levels associated with better cognition and mood in PD patients . "We know mild cognitive impairment may predict the future development of dementia. Intervening in the development of dementia has the potential to improve morbidity and mortality in persons with Parkinsons's disease (PD)."

In this analysis, which was an add-on study to an ongoing longitudinal study of neuropsychiatric function in people with Parkinsons's disease (PD), patients were given a battery of tests measuring global cognitive function, verbal memory, semantic verbal fluency, executive function, and depression. On the same day, serum 25-hydroxyvitamin D levels were measured. Of the 286 subjects, 61 were considered to be demented by a consensus panel based on the Diagnostic and Statistical Manual of the American Psychiatric Association (4th edition) and 225 were not demented.

For the entire group, significant negative associations were found between vitamin D levels and disease severity, as measured both by the Hoehn and Yahr Scale and the United Parkinson's Disease Rating Scale motor section

Mean vitamin D3 levels were higher in those who were not demented, although the differences did not reach statistical significance. Investigators found that for the entire group, higher levels of serum vitamin D3 were associated with greater fluency for naming vegetables and animals and immediate and delayed recall on a verbal learning test.

When the group was divided into those who were demented or not, significant findings with vitamin D were found for fluency and verbal learning only for those who were not demented. "The fact that the relationship between vitamin D concentration and cognitive performance seemed more robust in the non-demented subset suggests that earlier intervention before dementia is present may be more effective," says Dr. Peterson.

Earlier intervention before dementia is present

A significant negative association was also found for vitamin D levels and depression, as measured by the Geriatric Depression Scale, for both the entire group and those who were not demented. No significant relationship was found for those who were demented.

The authors point out that a cross-sectional study cannot determine causation: for instance, does low vitamin D affect cognitive performance, or are persons with more advanced PD and worse cognition less ambulatory, get less sun exposure, and subsequently have lower vitamin D? The study also did not consider if patients were taking vitamin D supplements.

Vitamin D's role in health has been a subject of considerable scrutiny in recent years

Low levels increase the risk of type 2 diabetes mellitus, multiple sclerosis, hypertension, cancer, and infections. Vitamin D receptors and its final converting enzyme have been found in human brain tissue, including the hippocampus, which plays a significant role in memory and learning.

Parkinson's Disease is the second most common neurodegenerative disorder in the United States, affecting approximately one million Americans and five million people worldwide. Its prevalence is projected to double by 2030. The most obvious symptoms are movement-related, such as involuntary shaking and muscle stiffness. Non-motor symptoms, such as worsening depression, anxiety, and sleep disturbances, can appear prior to the onset of motor symptoms.

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