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.
If you have hypertension, make sure you also don't have a specific gene variation that affects the way vitamin D makes changes to your arteries, particularly your aorta. 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. Radio talk shows may recommend 2,000 mg. And some doctors talk about 5,000 mg of vitamin D3 in people with very low vitamin D3 levels on blood tests. But how much vitamin D is absorbed into your cells, not just in your blood?
And how much is safe for people with different genetic variations? How do your genes respond to extra vitamin D3 not coming from food? Are you absorbing your vitamin D3? And is sunlight still inadequate? Are you afraid of skin cancer from exposure to sunlight, even for five minutes at noon?
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?
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?
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?
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?
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.”
What happens 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?
That’s the problem. How do you solve it? Will taking vitamin K2 in the MK-7 form help you if you have this gene variation? 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?
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?
Y could keep asking those experts who are talking about health care with you. That's why it's a good idea to find out how your body, your genes, respond to vitamin D with the right type of test of how much vitamin D is actually in your cells not only in your bloodstream.
Comments