Nutritional influences on illness: the influence of vitamins on congestive heart failure.
Perhaps one-third of patients with congestive heart failure (CHF) are thiamine-deficient. (1) In fact, CHF may be part of the presentation of wet beriberi, the classic cardiovascular disease of thiamine deficiency, manifested by peripheral vasodilatation with increased cardiovascular output, myocardial lesions, sodium and water retention, and biventricular myocardial failure. The elderly, the malnourished, and those with AIDS are particularly vulnerable. Repletion of the deficiency produces a rapid improvement. (2)
Moreover, the diuretic furosemide may cause urinary loss of thiamine, leading to impaired cardiac function. (3) When this occurs, thiamine supplementation has been shown to be beneficial under double-blind conditions. (4) Even refractory heart failure can be quickly reversed when it is secondary to a deficiency of thiamine. (5)
Vitamin C Supplementation
CHF is associated with both endothelial dysfunction and increased free radical formation, suggesting that endothelial-derived vasodilators, such as nitric oxide, are inactivated by the radicals. By improving endothelial function, high-dosage ascorbic acid infusions have been shown repeatedly under double-blind conditions to have beneficial effects in CHF.
In CHF patients, the vitamin restores endothelium-mediated, flow-dependent vasodilation. (6), (7) It also prevents hyperoxia-mediated vasoconstriction, (7) a common problem in CHF due to the use of oxygen-enriched gas mixtures for the prevention and treatment of hypoxia. Moreover, low baroreflex sensitivity in CHF is a predictor of sudden death from malignant ventricular arrhythmias, (8) and the vitamin improves baroreflex sensitivity and vagal sinus modulation. (9)
Although nitroglycerin is effective as a coronary artery vasodilator, intolerance to nitrates may develop with regular use. Fortunately, ascorbic acid helps to prevent the development of nitrate intolerance. (10)
Vitamin D Deficiency
In infants, vitamin D deficiency is a known cause of CHF. (11) While proof of causation is lacking for adult CHF, low vitamin D status is known to be associated with CHF severity and may well play a role in its pathogenesis. (12), (13) Low levels of activated (1, 25-dihydroxy) vitamin D along with hyperparathyroidism and osteopenia are common findings in this population; (12) in fact, the majority of CHF patients have 25-hydroxyvitamin D levels in the insufficiency range (< 20 ng/ml; < 50 nmol/l). (14) Moreover, those with more severe CHF have both lower levels of vitamin D metabolites and higher bone turnover. (12)
It is interesting that CHF patients have a history of relatively few outdoor activities. (14) While a sedentary lifestyle could be a secondary effect of the illness, there is also evidence that, compared to healthy controls, indicators of ultraviolet B exposure are already reduced in CHF patients during childhood, adolescence, and early adulthood, (14) suggesting that the vitamin deficiency may have predated the onset of the disorder.
Also, elevated circulating concentrations of proinflammatory cytokines are thought to contribute to the pathogenesis of CHF, while the results of in vitro and human studies suggest that vitamin D suppresses proinflammatory cytokines and increases anti-inflammatory cytokines. (15)
Daily oral intake of 50-100 micrograms vitamin D appears to be the most effective way to improve vitamin D status in this group of patients. (14)
Vitamin E Supplementation
Animal studies have demonstrated that vitamin E administration may reduce the oxidative stress that is often found to be associated with poor ejection fractions and cardiac failure. (16) Vitamin E may even prevent or retard the development of CHF. (17)
In a double-blind study, 20 patients and ten matched healthy controls received 400 mg vitamin E or placebo for four weeks. Vitamin E supplementation significantly reduced the levels of malonyldialdehyde and superoxide anion (suggesting reduced antioxidant stress) and elevated the levels of antioxidant enzymes. (18) A subsequent double-blind trial, however, found that, after 12 weeks, vitamin E at a similar dosage level failed to result in any significant improvements in prognostic or functional indexes of heart failure or in the quality of life of patients with advanced heart failure. (19)
Even more disconcerting is increasing evidence that vitamin E supplementation may be contraindicated in CHF. According to an extension of the double-blind Heart Outcomes Prevention Evaluation (HOPE) trial, published in JAMA, supplementation with 400 IU of vitamin E daily increased the risk of heart failure in a large group of patients at least 55 years old with cardiovascular disease or diabetes mellitus. (20)
Subsequently, these findings have been confirmed and extended in a randomized controlled trial with a large group of postinfarction patients (the GISSI-Prevenzione trial). While, after three and a half years of follow-up, patients who received vitamin E had a non-significant 20% increase in the risk of developing CHF, the treatment was associated with a significant 50% increase in CHF risk in those patients who presented with left ventricular dysfunction (ejection fraction < 50%). (21) Such findings suggest that vitamin E supplementation should be avoided in patients who are prone to developing CHF.
Dr. Werbach cautions that the nutritional treatment of illness should be supervised by physicians or practitioners whose training prepares them to recognize serious illness and to integrate nutritional interventions safely into the treatment plan.
(1.) Hanninen SA. et al. The prevalence of thiamin deficiency in hospitalized patients with congestive heart failure. J Am Coll Cardiol. 2006; 47:354-61.
(2.) Blanc P, Boussuges A. [Cardiac beriberi.] Arch Mal Coeur Vaiss. April 1, 2000; 93(4):371-9 (in French).
(3.) Seligmann H, et al. Thiamine deficiency in patients with congestive heart failure receiving long-term furosemide therapy: a pilot study, Am J Med. 1991; 91(2):151-5.
(4.) Shimon I. et al. Improved left ventricular function after thiamine supplementation in patients with congestive heart failure receiving long-term furosemide therapy. Am J Med 1995; 98:485-90.
(5.) Mendoza CE. Reversal of refractory congestive heart failure after thiamine supplementation: report of a case and review of the literature. J Cardiovasc Pharmacol Therapeut. 2003; 8(4):313-16.
(6.) Hornig B, et al. Vitamin C improves endothelial function of conduit arteries in patients with congestive heart failure. Circulation. 1998; 97:363-8.
(7.) Mak S, et al. Vitamin C prevents hyperoxia-mediated vasoconstriction and impairment of endothelium-dependent vasodilation. Am J Physiol Heart Circ Physiol. 2002; 282:H2414-H2421.
(8.) La Rovere MT, et al. Baroreflex sensitivity and heart rate variability in the identification of patients at risk for life-threatening arrhythmias. Implications for clinical trials. Circulation. 2001; 103:2072-77.
(9.) Piccirillo G, et al. Influence of vitamin C on baroreflex sensitivity in chronic heart failure. Hypertension. 2003: 41:1240-45.
(10.) Watanabe H. et al. Randomized, double-blind, placebo-controlled study of ascorbate on the preventive effect of nitrate tolerance in patients with congestive heart failure. Circulation. 1988:97(9):886-91.
(11.) Brunvand L, et al. Congestive heart failure caused by vitamin D deficiency? Acta Paediatr. 1995; 84:106-8.
(12.) Shane E, et al. Bone mass, vitamin D deficiency, and hyperparathyroidism in congestive heart failure. Am J Med. 1997; 103:197-207.
(13.) Zittermann A. et al. Low vitamin D status: a contributing factor in the pathogenesis of congestive heart failure? J Am Coll Cardiol. 2003; 41(1):105-12.
(14.) Zittermann A, et al. Vitamin D insufficiency in congestive heart failure: why and what to do about it? Heart Fail Rev. March 1, 2006; 11(1):25-33.
(15.) Schleilhoff SS,et al. Vitamin D supplementation improves cytokine profiles in patients with congestive heart failure: a double-blind, randomized, placebo-controlled trolled trial. Am J Clin Nutr. 2006; 83:754-9.
(16.) Li RK, et al. Vitamin E and oxidative stress in the heart of the cardiomyopathic Syrian hamster. Free Radic Biol Med. 1998; 24(2):252-8.
(17.) Dhalla AK, et al. Role of oxidative stress in transition of hypertrophy to heart failure. J Am Coll Cardiol. 1996; 28(2):506-14.
(18.) Ghatak A, et al. Oxy free radical system in heart failure and therapeutic role of oral vitamin E. Int J Cardiol. 1996; 57(2):119-27.
(19.) Keith ME, et al. A controlled clinical trial of vitamin E supplementation in patients with congestive heart failure. Am J Clin Nutr. 2001; 73:219-24.
(20.) The HOPE and HOPE-TOO Trial Investigators. Effects of long-term vitamin E supplementation on cardiovascular events and cancer. A randomized controlled trial. JAMA. 2005; 293(11):1338-47.
(21.) Marchioli R, et al. Vitamin E increases the risk of developing heart failure after myocardial infarction: Results from the GISSI-Prevenzione trial. J Cardiovasc Med (Hagerstown). May 1, 2006; 7(5):347-50.
In his latest book, Dr. Werbach has assembled a unique library of case reports concerning nutritional and herbal treatments for 155 different illnesses. It is available in print or on diskette from Third Line Press Inc., 4751 Viviana Drive, Tarzana, California 91356; 818-996-0076; Fax: 818-774-1575; http://www.third-line.com; e-mail: firstname.lastname@example.org.
by Melvyn R. Werbach, MD
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|Author:||Werbach, Melvyn R.|
|Date:||Jun 1, 2008|
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