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Conditioned nutritional requirements: therapeutic relevance to heart failure.
Herz 2002; 27(2):174-8HERZ

Abstract

BACKGROUND

The advent of disease, genetic predisposition or certain drug therapies may significantly alter the nutritional demands of specific organs. Several specific metabolic deficiencies have been found in the failing myocardium: (1) a reduction in L-carnitine, coenzyme Q10, creatine, and thiamine--nutrient cofactors important for myocardial energy production; (2) a relative deficiency of taurine, an amino acid integral to intracellular calcium homeostasis; (3) increased myocardial oxidative stress and a reduction of antioxidant defenses. Deficiencies of carnitine or taurine alone are well documented to result in dilated cardiomyopathy in animals and humans. Each of these deficiencies is amenable to restoration through dietary supplementation. A variety of nutrients have been investigated as single therapeutic agents in pharmacologic fashion, but there has been no broad-based approach to nutritional supplementation in congestive heart failure to correct this complex of metabolic abnormalities.

METHOD AND RESULTS

We have demonstrated deficiencies in carnitine, taurine and coenzyme Q10 in cardiomyopathic hamster hearts during the late stage of the cardiomyopathy. In another study, we randomized placebo diet against a supplement containing taurine, coenzyme Q10, carnitine, thiamine, creatine, vitamin E, vitamin C, and selenium to cardiomyopathic hamsters during the late stages of the disease. Supplementation for 3 months markedly improved myocyte sarcomeric structure, developed pressure, +dp/dt, and -dp/dt. We also documented carnitine, taurine and coenzyme Q10 in biopsies taken from human failing hearts, the levels correlating with ventricular function. A double-blind, randomized, placebo-controlled trial of a supplement containing these nutrients, given for 30 days, restored myocardial levels and resulted in a significant decrease in left ventricular end-diastolic volume.

CONCLUSION

These experiments suggest that a comprehensive restoration of adequate myocyte nutrition may be important to any therapeutic strategy designed to benefit patients suffering from congestie heart failure. Future studies in this area are of clinical importance.

Authors+Show Affiliations

University of Toronto, Toronto, Canada. michael.sole@uhn.on.caNo affiliation info available

Pub Type(s)

Journal Article
Review

Language

eng

PubMed ID

12025462

Citation

Sole, Michael J., and Kursheed N. Jeejeebhoy. "Conditioned Nutritional Requirements: Therapeutic Relevance to Heart Failure." Herz, vol. 27, no. 2, 2002, pp. 174-8.
Sole MJ, Jeejeebhoy KN. Conditioned nutritional requirements: therapeutic relevance to heart failure. Herz. 2002;27(2):174-8.
Sole, M. J., & Jeejeebhoy, K. N. (2002). Conditioned nutritional requirements: therapeutic relevance to heart failure. Herz, 27(2), pp. 174-8.
Sole MJ, Jeejeebhoy KN. Conditioned Nutritional Requirements: Therapeutic Relevance to Heart Failure. Herz. 2002;27(2):174-8. PubMed PMID: 12025462.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Conditioned nutritional requirements: therapeutic relevance to heart failure. AU - Sole,Michael J, AU - Jeejeebhoy,Kursheed N, PY - 2002/5/25/pubmed PY - 2002/8/29/medline PY - 2002/5/25/entrez SP - 174 EP - 8 JF - Herz JO - Herz VL - 27 IS - 2 N2 - BACKGROUND: The advent of disease, genetic predisposition or certain drug therapies may significantly alter the nutritional demands of specific organs. Several specific metabolic deficiencies have been found in the failing myocardium: (1) a reduction in L-carnitine, coenzyme Q10, creatine, and thiamine--nutrient cofactors important for myocardial energy production; (2) a relative deficiency of taurine, an amino acid integral to intracellular calcium homeostasis; (3) increased myocardial oxidative stress and a reduction of antioxidant defenses. Deficiencies of carnitine or taurine alone are well documented to result in dilated cardiomyopathy in animals and humans. Each of these deficiencies is amenable to restoration through dietary supplementation. A variety of nutrients have been investigated as single therapeutic agents in pharmacologic fashion, but there has been no broad-based approach to nutritional supplementation in congestive heart failure to correct this complex of metabolic abnormalities. METHOD AND RESULTS: We have demonstrated deficiencies in carnitine, taurine and coenzyme Q10 in cardiomyopathic hamster hearts during the late stage of the cardiomyopathy. In another study, we randomized placebo diet against a supplement containing taurine, coenzyme Q10, carnitine, thiamine, creatine, vitamin E, vitamin C, and selenium to cardiomyopathic hamsters during the late stages of the disease. Supplementation for 3 months markedly improved myocyte sarcomeric structure, developed pressure, +dp/dt, and -dp/dt. We also documented carnitine, taurine and coenzyme Q10 in biopsies taken from human failing hearts, the levels correlating with ventricular function. A double-blind, randomized, placebo-controlled trial of a supplement containing these nutrients, given for 30 days, restored myocardial levels and resulted in a significant decrease in left ventricular end-diastolic volume. CONCLUSION: These experiments suggest that a comprehensive restoration of adequate myocyte nutrition may be important to any therapeutic strategy designed to benefit patients suffering from congestie heart failure. Future studies in this area are of clinical importance. SN - 0340-9937 UR - https://www.unboundmedicine.com/medline/citation/12025462/Conditioned_nutritional_requirements:_therapeutic_relevance_to_heart_failure_ L2 - https://medlineplus.gov/heartfailure.html DB - PRIME DP - Unbound Medicine ER -