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Information on the latest vitamin D news and research.

Find out more information on deficiency, supplementation, sun exposure, and how vitamin D relates to your health.

Heart failure following heart attack: Can vitamin D help?

Myocardial infarction (MI) is the most common form of acute cardiac injury and a leading cause of death in the Western world. Advances in treatment have led to a decline in mortality during the acute phase. On the other hand, there has been an increase in heart failure in patients surviving an MI due to significant heart damage.

The heart has little regenerative capacity and MI generates repair mechanisms that produce a cardiac scar. The development of heart failure after MI is determined by the size of the injured area, the wound healing response that occurs in the days after the event, and the healing of the scar.

The healing process of the heart after an infraction can be divided into three phases: the inflammatory phase, the proliferative phase, and wound scarring phase. Dying heart cells trigger an inflammatory reaction, signaled by inflammatory cytokines, such as IL-6, IL-8 and C-reactive protein (CRP). The higher the cytokine levels, the more severe the cardiac injury. (Anything that would lower cytokine levels after an MI should lessen chronic heart damage, in theory.)

The proliferative phase is triggered by adhesion molecules, such as VCAM-1 and E-selectin, which begins to form the scar. As with cytokines, anything that would lessen the levels of adhesion molecules should lessen the eventual cardiac scar.

Recently, Dr Yoav Arnson and colleagues of Tel Aviv University decided to see if vitamin D affected the cardiac scaring process.

Arnson Y, Itzhaky D, Mosseri M, Barak V, Tzur B, Agmon-Levin N, Amital H.  Vitamin D Inflammatory Cytokines and Coronary Events: A Comprehensive Review. Clin Rev Allergy Immunol. 2013 Jan 12.

They gave 25 MI patients standard care plus 4,000 IU/day of pure 25(OH)D or calcidiol (which is roughly equivalent to 40,000 IU/day of vitamin D3) for five days, comparing them to 25 MI patients treated with standard care alone. They measured cytokine and adhesion molecule levels before and after treatment.

Levels of the inflammatory cytokine IL-6 decreased by 31 % in the treated patients, compared to a 48.7 % increase in the untreated group (p=.05). Another inflammatory cytokine (IL-8) decreased by 25 % in the vitamin D treated patients, compared to a 76 % increase in the control group (p=.01). CRP concentrations increased by 108% in the treated patients, compared to an average 361% increase for the patients without vitamin D supplementation (p=.03).

The tests of the adhesion molecules, VCAM-1 and E-selectin, also showed a favorable result for vitamin D. For example, in the treated group, VCAM-1 levels decreased 3%, compared to a 23% increase in the control group (p=.03). E-selectin levels showed a favorable trend, decreasing by 8% among the treated patients, compared to a 0.4% decrease in the control group (p=0.15).

The authors concluded,

“Understanding the inflammatory response to ischemic myocardial injury and the role of cytokines after  MI may allow us to promote improved healing and cardiac remodeling after MI. Low levels of 25(OH)D are known to be associated with increased atherosclerosis and higher risk of MI. The results of this study demonstrated that vitamin D can attenuate the inflammatory process following AMI. As vitamin D deficiency is widespread in many populations and is in theory amenable to potential interventions, clarification of its role in myocardial ischemia and infarction may be of great public health relevance.”

While calcidiol or pure 25(OH)D is no longer available in the USA, oral vitamin D3 is rapidly converted to 25(OH)D in the liver, roughly at a rate of 50,000 IU of D3 becoming 5,000 IU of 25(OH)D. Based on this study, I recommend that health care professionals prescribe patients with a heart attacks  pharmacological doses of vitamin D, such as 50,000 to 100,000 IU/day for ten days, beginning immediately after presentation. This is safe and will result in less inflammation and scarring and should result in less heart failure after an MI.

  About: John Cannell, MD

Dr. John Cannell is founder of the Vitamin D Council. He has written many peer-reviewed papers on vitamin D and speaks frequently across the United States on the subject. Dr. Cannell holds an M.D. and has served the medical field as a general practitioner, emergency physician, and psychiatrist.

3 Responses to Heart failure following heart attack: Can vitamin D help?

  1. Rita and Misty says:

    Vitamin D deficiency, anyone???


    “We observed increasing risk of ischemic heart disease, myocardial infarction, and early death with decreasing plasma 25-hydroxyvitamin D levels. These findings were substantiated in meta-analyses.” http://www.ncbi.nlm.nih.gov/pubmed/22936341

    I’ve said it before and I say again and again (BTW, I think I’m getting hoarse..maybe a megaphone would help):

    Because of our indoor lifestyles, Vitamin D deficiency is at epidemic proportions in the United States…actually worldwide. And it is worse among those with darker skin pigmentation, as melanin factors greatly into Vitamin D production.

    The sunlight needs for people with darker skin pigmentation, living at higher latitudes, are immense and are not being met. A lighter pigmented person standing in full sun can produce a day’s bodily requirement of Vitamin D in about 15 minutes. In stark contrast, a person with darker skin pigmentation, standing in the same spot, will need approximately 6 times more sun exposure to produce the same amount of vitamin D. The following link will provide you with a thorough explanation:

    Furthermore, current research indicates that Vitamin D improves the antibacterial, antiviral and anti-parasitic functioning of the immune system, and people with low vitamin D levels in their blood are more likely to die from cancer, heart disease, stroke and many other diseases. According to reports by the United States Center for Disease Control and Prevention, African American suffer greatly from chronic diseases such as cancer, heart disease, fibromyalgia, lupus, and obesity which can be effectively controlled or prevented with vitamin D supplementation.

  2. I’ve seen mentioned, I think here, that there are “at least 20 other compounds besides D3” generated by solar UVb. Anyone know what these compounds do in the body? What they are and what compounds they are derived from?

  3. Rita and Misty says:


    D3 supplementation is good, but sunlight, yes, does confer additional benefits. Two additional benefits of sunlight versus supplementation would be helping your body produce adequate amounts of Serotonin & Melatonin!

    Need more convincing to go get some rays:

    “The sun may be best known for boosting production of vitamin D, but there are many other UVR-mediated effects independent of this pathway.

    Direct immune suppression: Exposure to both UVA and UVB radiation can have direct immunosuppressive effects through upregulation of cytokines (TNF-α and IL-10) and increased activity of T regulatory cells that remove self-reactive T cells. These mechanisms may help prevent autoimmune diseases.

    Alpha melanocyte-stimulating hormone (α-MSH): Upon exposure to sunshine, melanocytes and keratinocytes in the skin release α-MSH, which has been implicated in immunologic tolerance and suppression of contact hypersensitivity. α-MSH also helps limit oxidative DNA damage resulting from UVR and increases gene repair, thus reducing melanoma risk, as reported 15 May 2005 in Cancer Research.

    Calcitonin gene-related peptide (CGRP): Released in response to both UVA and UVB exposure, this potent neuropeptide modulates a number of cytokines and is linked with impaired induction of immunity and the development of immunologic tolerance. According to a report in the September 2007 issue of Photochemistry and Photobiology, mast cells (which mediate hypersensitivity reactions) play a critical role in CGRP-mediated immune suppression. This could help explain sunlight’s efficacy in treating skin disorders such as psoriasis.

    Neuropeptide substance P: Along with CGRP, this neuropeptide is released from sensory nerve fibers in the skin following UVR exposure. This results in increased lymphocyte proliferation and chemotaxis (chemically mediated movement) but may also produce local immune suppression.

    Endorphins: UVR increases blood levels of natural opiates called endorphins. Melanocytes in human skin express a fully functioning endorphin receptor system, according to the June 2003 Journal of Investigative Dermatology, and a study published 24 November 2005 in Molecular and Cellular Endocrinology suggests that the cutaneous pigmentary system is an important stress-response element of the skin.”

    Check out one of my favorite articles on this subject.