Vitamin D is a group of fat-soluble secosteroids (member of a subclass of steroids) able to facilitate intestinal absorption of calcium and magnesium.
In humans, the important compounds are Vitamin D2 and D3. Vitamin D3 is the most popular known also as cholecalciferol, and is available in diet and supplements.
The major source of synthesis of Vitamin D3 is the skin, and it is synthesised from cholesterol. This reaction needs sunlight exposure (UVB) to take place. Vitamin D can be considered closer to a hormone than a vitamin. It needs to be converted to its active form by an enzyme, therefore, since it can be synthetized in an adequate amount, provided sufficient exposure to sunlight, it is not an essential dietary factor, technically it is not a “real” vitamin. One of its most important roles, is to maintain skeletal calcium balance by promoting calcium absorption. Vitamins coupled with calcium is one of the most popular supplement therapies given to women undergoing menopause, to prevent bone loss that comes with it. Saying this, there is still not enough scientific evidence to assess that it prevents osteoporosis. So usually, all women undergoing menopause therefore have a risk of developing osteoporosis, are given Vitamin D supplements (and often calcium with it). But is Vitamin D acting only in this frame?
Increasing evidence demonstrates that Vitamin D deficiency is linked to increased CardioVascular Disease (CVD) risk.
Several studies show a close connection between hypovitaminosis D and the genesis of rheumatic, autoimmune, neoplastic, and cardiovascular diseases. With reference especially to cardiovascular aspects, multiple heart diseases such as hypertension, myocardial ischemia, and heart failures may arise from deficiency in Vitamin D considered then as an important causative factor. However, the role of Vitamin D remains to be established more precisely; only a few studies and with small numbers, have tested the effects of its supplementation in patients with chronic heart failure diseases, and reported results are unclear and of difficult interpretation. It is important to implement studies in this field in order to assess the real benefits induced by vitamin D supplementation in cardiovascular patients and, in particular, in patients with heart failure (therefore at late stages of CVD). Should the research confirm actual clinical improvement after treatment with Vitamin D, such a supplementation may represent a new low-cost therapeutic approach to improving quality of life, not only for menopausal women but also for patients with likelihood of developing CVD.
The issue now, arises because Vitamin D is often given together with calcium supplements (being the election therapy for bone loss) but calcium supplements are being demonstrated to increase risk of CVD (see previous article on this topic).
Therefore, the two supplements taken together might produce an opposite effect.
In summary, despite intriguing evidence from animal studies and patients’ observational studies that low vitamin D is associated with increased risk of CVD (even if supplemented together with calcium), there is insufficient evidence at this time to prove a real causal relationship and to demonstrate that vitamin D supplements are effective in significantly reducing cardiovascular risk. Although calcium supplementation is the gold standard used for maintaining bone health, there is more than one evidence that it may increase CVD risk. Due to the seemingly conflicting effects of low vitamin D and high calcium levels on CVD, further research is needed now more than ever to examine the effect of combined Calcium/Vitamin D supplementation on specific cardiovascular outcomes, especially because most women undergoing menopause are given this therapy. Until the results of ongoing large-scale Randomized ClinicalTrial (RCTs) are fully available, it is important for clinicians and patients to be aware of the differing vitamin D guidelines to give the best advice possible for their patients and calculate the potential risks or benefits before prescribing any kind supplementation.
Guest Post by Dr. Ornella Capillari
Eur Heart J. 2017 Aug 1;38(29):2279-2286. doi: 10.1093/eurheartj/ehx235.
Effect of vitamin D on all-cause mortality in heart failure (EVITA): a 3-year randomized clinical trial with 4000IU vitamin D daily. Zittermann A, Ernst JB, Prokop S, Fuchs U, Dreier J, Kuhn J, Knabbe C, Birschmann I, Schulz U, Berthold HK, Pilz S, Gouni-Berthold I, Gummert JF, Dittrich M, Börgermann J.
Curr Heart Fail Rep. 2017 Oct;14(5):410-420. doi: 10.1007/s11897-017-0355-7.
Vitamin D and Heart Failure. Brinkley DM, Ali OM, Zalawadiya SK, Wang TJ.
BMC Cardiovasc Disord. 2017 Oct 30;17(1):274. doi: 10.1186/s12872-017-0707-y.
Vitamin D3 repletion versus placebo as adjunctive treatment of heart failure patient quality of life and hormonal indices: a randomized, double-blind, placebo-controlled trial. Moretti HD, Colucci VJ, Berry BD.
Curr Atheroscler Rep. 2017 Jan;19(1):5. doi: 10.1007/s11883-017-0637-2.
Vitamin D, Calcium, and Cardiovascular Disease: A”D”vantageous or “D”etrimental? An Era of Uncertainty. Chin K, Appel LJ, Michos ED.