Here in the UK we’ve had a distinct downturn in temperatures of late, and this is something that will make us more reluctant to venture out. And even if we do, we’re likely to be very well wrapped up and protected from the elements. The net results is that at this time of year we can run a bit short on sunlight, which may impact not only on our mood but also the vitamin D levels in our bodies. There is some evidence that vitamin D deficiency might be a factor in seasonal affective disorder, and mounting evidence links lower levels of this nutrient with heightened risk of chronic disease including cancer and cardiovascular disease. For more on this, have a look at the previous blog post here.
One of the studies cited in this particular blog post found that lower vitamin D levels are associated with an increased risk of cardiovascular disease [1]. This study found that compared to vitamin D levels of 15 ng/ml or more, levels of 10-<15 ng/ml and <10 ng/ml were associated with a 53 and 80 per cent increased risk of cardiovascular disease respectively.
This week saw the publication of a study which delved deeper into the relationship between vitamin levels and cardiovascular disease risk [2].
This paper’s authors details some of the potential mechanisms by which vitamin D deficiency might enhance cardiovascular disease risk. Vitamin D deficiency predisposes, for instance, to high blood pressure, diabetes, metabolic syndrome (which can precede diabetes) and inflammation. All of these states are considered to be risk factors for cardiovascular disease. The authors also write about how vitamin D deficiency which can lead to overactivity of the parathyroid glands, which in turn appears to have a number of effects in the body that might increase cardiovascular disease risk.
They also cite several studies (including the Wang reference below) that have found lower levels of vitamin D to be associated with an elevated risk of cardiovascular events or death from cardiovascular disease.
What the authors acknowledge is the fact that we don’t have evidence in the way of intervention studies that show that increasing vitamin D levels, say through supplementation, reduced cardiovascular disease risk. However, there is such a good amount of epidemiological evidence linking higher vitamin D levels with improved health outcomes (including a reduced risk of not just cardiovascular disease, but cancer too) that ensuring adequate vitamin D levels looks like a good bet for those interested in optimising their health.
The authors of this study also question the recommended daily amounts of vitamin D in the USA. These currently stand at 200, 400 and 600 IU for individuals aged <50 years, 50-70 years and older than 70 years respectively. However, they quote research [3] which suggests that 1000-2000 IU is what is required to satisfy most individual’s needs for vitamin D.
Some of this can be achieved through appropriate sun exposure. The authors state: The most potent sources of vitamin D are sunlight (about 3,000 IU vitamin D3 per 5 to 10 min of mid-day, midyear exposure of arms and legs for a light-skinned Caucasian). The authors also offer supplements as an alternative at a dose of 50,000 IU every 2 weeks, or 1000-2000 IU per day. The article also contains a list of some of the richer food sources of vitamin D, which I have reproduced below (food followed by the IU of vitamin D it contains in each serving).
Cod liver oil, 1 tablespoon 1,360
Wild-caught salmon, 3 oz 600″1,000
Farmed salmon, 3 oz 100″250
Mackerel, cooked, 3 oz 345
Tuna fish, canned in oil, 3 oz 200
Sardines (with bones), canned in oil, drained, 1 oz 250
Vitamin D fortified milk 1 cup 98
In individuals who have proven vitamin D deficiency (25(OH)D levels of less than 20 ng/ml), the authors recommend starting by loading individuals with 50,000 IU of vitamin D per week for 8 weeks.
References:
1. Wang TJ, et al. Vitamin D deficiency and risk of cardiovascular disease. Circulation 2008;117(4):503-11
2. Lee JH, et al. Vitamin D Deficiency: An Important, Common, and Easily Treatable Cardiovascular Risk Factor? J Am Coll Cardiol, 2008; 52:1949-1956
3. Bischoff-Ferrari HA, et al. Estimation of optimal serum concentrations of 25-hydroxyvitamin D for multiple health outcomes Am J Clin Nutr 2006;84:18-28.
Even on a sunny day like today you will not be able to make any vitamin D via the skin….from roughly September till March the angle of the sun’s rays in the UK is not right for making vitamin D.
You can get your level of serum D checked from the 25(OH)D blood test. I currently take 2,000 ius D3 per day and my 25(OH)D level is 155 nmol/L or 62 ng/mL which is a good level.
Anne
According to the blog of cardiologist Wm Davis, vitamin D in tablet form doesn’t raise your blood level but in gel caps it does.
What is a safe dose for breast-feeding mums?
Not only are animal fats a good source of Vitamin D, there appear to be several strands of thought that consider dietary grains will adversely affect the metabolims of Vitamin D. And I have seen a reference, which no doubt others here have seen too, to a paper which reported that coeliac children with Vitamin D deficiency no longer had a deficiency on a gluten free diet.
Interesting that wild salmon has so much more Vitamin D than farmed salmon. This must have implications for those of us eating grain fed animals. Winter born lambs are fed grains and summer lambs are finished off wth them (grains being fattening!).
So it’s worth thinking about where your food source obtained its own food source from.
Synthetic Vit D2 analog is added to milk in the US, and it isn’t the same Vit D3 molecular structure that the body makes in response to sunlight, so it must be converted first (but how efficiently does that occur?).
The Vitamin D Council recommends 1000iU Vit D3 per every 25 pounds of body weight in the winter. The test results in our family indicate this is probably a good recommendation: those either getting a lot of daily summer sun or taking 1000iU per body weight in the fall/winter/spring seasons when more time is spent indoors show optimal 25 (OH) D levels, and those taking lower Vit D amounts or not getting much summer sun have tested much lower (though not deficient). And we are in “sunny” So Cal where it is too often assumed that Vit D production isn’t a problem.
Which kind of vitamin D does this refer to? D2 (ergocacliferol) and D3 (cholecalciferol) which is the 25(OH)vitD or is it the vitamin D hormone which these are converted to, 1,25dihydroxyvitD (caclitriol)? Which kind is measured for these tests?
When will docs make the connection? Statin drugs lower your levels of Vitamin D drastically along with many other nasty side effects that docs refuse to attribute to the statin drug. Almost all heart patients are prescribed Statins. Now we find Vitamin D deficiency leads to heart disease. Statin drugs are currently the most profitable drug, worldwide, for Big Pharma. See any connection? While Big Pharma thrives, many have repeat heart attacks.
My own solution after heart surgery was to get off statins, take CoQ10, Carnitine, 1000mg day of D3, Omega 3 fish oils and do all the other common sense things like eat carefully and exercise. Adding some non-constipating iron was the icing on the cake. It isn’t hard, I feel great, but while taking statins I was lethargic, had severe leg cramps, insommnia, brain fog, became depressed and felt another heart attack was inevitable. Thanks, Dr. Briffa, for alerting us to the importance of proper supplies of Vit D3. Would love to learn more about importance of all fat soluable vitamins to our health.
Matty, do you have to watch you don’t get too much iron? Isn’t excess iron implicated in heart issues for men (not women as we have a monthly bleed)?
Vitamin D benefits are voided by Vitamin A
retinyl overdoses present in many multi-vitamin and Cod Liver Oil daily doses.
How little retinyl is still an overdose? 5000 IU daily
BACKGROUND http://en.wikipedia.org/wiki/Vitamin_A documents:
Vitamin A, a bi-polar molecule formed with bi-polar bonds between carbon and hydrogen, is linked to a family of similarly shaped molecules, the retinoids, which complete the remainder of the vitamin sequence. Its important part is the retinyl group, which can be found in several forms. In foods of animal origin, the major form of vitamin A is an ester, primarily retinyl palmitate, which is converted to an alcohol (retinol) in the small intestine. Vitamin A can also exist as an aldehyde (retinal), or as an acid (retinoic acid). Precursors to the vitamin (provitamins) are present in foods of plant origin as some of the members of the carotenoid family of compounds.
EXTRACTS from http://www.vitamindcouncil.org NEWSLETTERS by John Cannell, MD
November 11, 2008:
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Today, sixteen well-known experts, including professors Walter Willett and Ed Giovannucci of Harvard, Dr. John Hathcock of the Council for Responsible Nutrition, and Professor Reinhold Vieth of the University of Toronto, published an unprecedented warning about the ingestion of cod liver oil and resultant vitamin A toxicity.
Cod Liver Oil, Vitamin A Toxicity, Frequent Respiratory Infections, and the Vitamin D Deficiency Epidemic
…. http://www.annals.com/toc/auto_abstract.php?id=15313
In addition to warning about the consumption of cod liver oil, the above experts recommended healthy children take 1,000 IU/day of vitamin D for every 25 pounds of body weight. In some cases this is more than ten times current recommendations for children by the government and professional organizations.
Finally, the group recommended that “children with chronic illness such as autism, diabetes, and/or frequent infections” may need to take even more vitamin D, “doses adequate to maintain their 25-hydroxy vitamin D in the mid normal of the reference range (65 ng/ml) – and should be so supplemented year around.” Less than one percent of American children currently have such levels.
December, 2008
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The crux of the problem is that a form of vitamin A, retinoic acid, weakly activates the vitamin D response element on the gene and perhaps blocks vitamin D’s more robust activation. The first paper below is free to download. As the authors say, “there is a profound inhibition of vitamin D-activated . . . gene expression by retinoic acid.”
MacDonald PN, et al. Retinoid X receptors stimulate and 9-cis retinoic acid inhibits 1,25-dihydroxyvitamin D3-activated expression of the rat osteocalcin gene. Mol Cell Biol. 1993 Sep;13(9):5907-17.
… http://www.ncbi.nlm.nih.gov/pubmed/8395017?ordinalpos=3&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DefaultReportPanel.Pubmed_RVDocSum
Thompson PD, et al. Heterodimeric DNA binding by the vitamin D receptor and retinoid X receptors is enhanced by 1,25-dihydroxyvitamin D3 and inhibited by 9-cis-retinoic acid. Evidence for allosteric receptor interactions. J Biol Chem. 1998 Apr 3;273(14):8483-91.
… http://www.ncbi.nlm.nih.gov/pubmed/9525962?ordinalpos=6&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DefaultReportPanel.Pubmed_RVDocSum
Vitamin A production is tightly controlled in the body, the source (substrate) being carotenoids from vegetables in your intestine. The body uses these carotenoid substrates to make exactly the right amount of retinol for your body. That is, it is a closed, tightly regulated, system, one designed to perfection by God and Nature. When you take vitamin A as retinol, such as in cod liver oil, you intervene in this closed system and bypass the controls.
…
Although activated vitamin D and vitamin A signal through common cofactors, they compete for each other’s function. Retinoic acid antagonizes the action of vitamin D and its active metabolite. In humans, even the vitamin A in a single serving of liver impairs vitamin D’s rapid intestinal calcium response. In a dietary intake study, Oh et al found that a high retinol intake completely thwarted vitamin D’s otherwise protective effect on distal colorectal adenoma, and they found a clear relationship between vitamin D and vitamin A intakes, as the women in the highest quintile of vitamin D intake also ingested around 10,000 IU/d of retinol.
Rohde CM, Deluca HF. All-trans retinoic acid antagonizes the action of calciferol and its active metabolite, 1,25-dihydroxycholecalciferol, in rats. J Nutr. 2005;135(7):1647-1652.
… http://www.ncbi.nlm.nih.gov/pubmed/15987844?ordinalpos=1&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum
Johansson S, Melhus H. Vitamin A antagonizes calcium response to vitamin D in man. J Bone Miner Res. 2001;16(10):1899-1905.
… http://www.ncbi.nlm.nih.gov/pubmed/11585356?ordinalpos=1&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DefaultReportPanel.Pubmed_RVDocSum
Oh K, Willett WC, Wu K, Fuchs CS, Giovannucci EL. Calcium and vitamin D intakes in relation to risk of distal colorectal adenoma in women. Am J Epidemiol. 2007;165(10):1178-1186.
… http://www.ncbi.nlm.nih.gov/pubmed/17379616?ordinalpos=1&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DefaultReportPanel.Pubmed_RVDocSum
Furthermore, the consumption of preformed retinol , even in amounts consumed by many Americans in both multivitamins and cod liver oil , may cause bone toxicity in individuals with inadequate vitamin D status. Women in the highest quintile of total vitamin A intake have a 1.5-times elevated risk of hip fracture.
Feskanich D, Singh V, Willett WC, Colditz GA. Vitamin A intake and hip fractures among postmenopausal women. JAMA 2002;287:47-54.
… http://www.ncbi.nlm.nih.gov/pubmed/11754708?ordinalpos=4&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DefaultReportPanel.Pubmed_RVDocSum
Indeed, a recent Cochrane Review found that vitamin A supplements increased total mortality rate by 16%, perhaps through antagonism of vitamin D.
Bjelakovic G, et al. Antioxidant supplements for prevention of mortality in healthy participants and patients with various diseases. Cochrane Database Syst Rev 2008 Apr 16;(2):CD007176.
… http://www.ncbi.nlm.nih.gov/pubmed/18425980?ordinalpos=1&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DefaultReportPanel.Pubmed_RVDocSum
=== End of Newsletter Extracts ===
Nutrition is a symphony, not a solo performance. Thus when looking a a nutrient like Vitamin D, one also needs to look at what other co-nutrients are necessary in the processes the principal nutrient is used. 2 examples:
Example 1: Digestion – Vitamins A, D, E, & K are all fat soluble. When ingested without fat, the vitamins may be poorly absorbed. A gel cap may provide the oil needed for absorption via the digestive tract, but so do other digestible food oils.
Example 2: The process of building and maintaining bone uses {vitamin A, vitamin B12, high vitamin D, vitamin K (and preferentially vitamin K2 mkx where x is 7, 8, and/or 9) , calcium, magnesium, silicon, and boron }.
On the subject of co-nutrients, a strong inverse relationship exists with K2 intake and severe aortic calcification, CHD, and risk of death from the same. Reference Johanna M. Geleijnse’s “Dietary Intake of Menaquinone Is Associated with a Reduced Risk of Coronary Heart Disease: The Rotterdam Study.” J. Nutr. 134: 3100—3105, 2004. http://jn.nutrition.org/cgi/reprint/134/11/3100 (free) The study found the top 1/3 energy-adjusted K2 intake was > 32.7 ?g/day, reducing CDH death risk by 57% versus those taking < 21.6 mcg. K1 intake had no effect. Intake of K2 was mainly MK-4 from eggs and meat, and MK-8 and MK-9 from cheese, especially curds and low fat cheese [potentially at 90 mcg per 120 g cheese]. [MK-4 in blood plasma half life is 1-2 hours.]
MK-7 as found in the Japanese food natto (fermented soy beans) and available as an over the counter supplement, has a half life in the circulation of 3 days, is preferentially used by the body over MK-4, and is believed to have a beneficial effect superior to MK-4, and similar to MK-8 and MK-9.
This is all very confusing, John. What do you make of Doug’s warnings about the dangers od cod liver oil?
http://www.westonaprice.org/basicnutrition/clarifications.html