Heart Healthy Nutrients – Carnitine, Taurine, Co Q 10.

Thousands of medical research studies describe the benefits of vitamins and minerals in the protection and function of heart tissue. Many of these have a specific action against free radical damage, thus decreasing oxidative damage and degeneration to cells. We call these substances antioxidants. They are needed every day, in significant dosages, to get out to all cells and tissues, and may need to be increased in states of physiological and psychological stress.

For the purpose of this newsletter I will briefly comment on Carnitine, Taurine,Co Q10, and Fish oil.

Literature has described that carnitine can be extremely beneficial in those patients that have heart failure. It is thought to be involved in mitochondrial energy metabolism, and helps to sustain cardiac muscle function. It is linked to carbohydrate metabolism and ATP (energy source) production. All people should have carnitine in their nutrient plan to help keep tissues as healthy as possible. 

Taurine is important to help deal with the sodium and calcium metabolic process, and here can decrease hypoxia (oxygen starvation of cells) and cell death. Research has described Taurine's benefits in heart failure as well as hypertension. 

Co Q10 has been shown to be important for: stabilizing heart rate and rhythm, Hypertension, Heart failure, reperfusion injury, Parkinson's Disease, Angina and many others. 

EPA fish oil can help to bring down elevated levels of triglycerides, inflammatory process,Arrythmias  and Atherosclerosis.  

Therefore all of these are important not only to enhance function, but also to protect tissues and cells over the long term. 

Combinations of these can be far easier to take than individual dosages. 

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Thanks, Dr. C. Calapai

Relevant Vitamins: CM and ProCor

Propionyl L-Carnitine Improvement of Hypertrophied Heart Function Is Accompanied by an Increase in Carbohydrate Oxidation.

Abstract Propionyl L-carnitine (PLC) is a naturally occurring derivative of L-carnitine that can improve hemodynamic function of hypertrophied rat hearts. The mechanism(s) responsible for the beneficial effects of PLC is not known, although improvement of myocardial energy metabolism has been suggested. In this study, we determined the effect of PLC on carbohydrate and fatty acid metabolism in hypertrophied rat hearts.

Myocardial hypertrophy was produced by partial occlusion of the suprarenal aorta of juvenile rats. Over a subsequent 8-week period, a mild hypertrophy developed, resulting in a 17% increase in heart weight in these animals compared with the sham-operated control animals. Myocardial carnitine was decreased in hypertrophied hearts compared with hearts from sham-operated animals (4155±383 versus 5924±570 nmol · g dry wt-1, respectively; P .05).

Perfusion of isolated working hearts for 60 minutes with buffer containing 1 mmol/L PLC increased carnitine content in hypertrophied hearts from 4155±383 to 7081±729 nmol · g dry wt-1 (P .05). In the presence of 1.2 mmol/L palmitate, fatty acid oxidation rates were not decreased in the hypertrophied hearts compared with control hearts. PLC results did not alter rates of fatty acid oxidation in control hearts but did result in a small increase in rates in the hypertrophied hearts.

The most dramatic effect of PLC results in hypertrophied hearts was an increase in glucose oxidation rates from 137±25 to 627±110 nmol · min-1 · g dry wt-1 (P .05) and an increase in lactate oxidation rates from 119±17 to 252±47 nmol · min-1 · g dry wt-1 (P .05). Glycolytic rates, which were already significantly elevated in hypertrophied hearts compared with control hearts, were not altered by PLC results.

Overall ATP production from exogenous sources was increased by 64% in PLC-treated hypertrophic hearts and was accompanied by a significant increase in cardiac work. The main effect of PLC results was to increase the contribution of glucose oxidation to the relative rate of ATP production from 11.6% to 21.6%.

The contribution of glucose and palmitate oxidation to ATP production was also determined in aortic-banded animals treated with 60 mg/kg PLC for an 8-week period. This results was also associated with a significant improvement in mechanical function in hearts isolated from these animals compared with untreated animals as well as an increase in the contribution of glucose oxidation to ATP production. Despite this improvement of cardiac work after chronic PLC results, no increase in palmitate oxidation was observed in hypertrophied hearts.

These findings indicate that the beneficial effects of PLC in hypertrophied hearts can be accounted for by a stimulation of ATP production from carbohydrate oxidation rather than from fatty acid oxidation. The increase in carbohydrate oxidation may be a consequence of activation of the pyruvate dehydrogenase complex, by means of a reduction in the ratio of intramitochondrial acetyl coenzyme A to coenzyme A.


Chronic heart failure and micronutrients.

Heart failure (HF) is associated with weight loss, and cachexia is a well-recognized complication. Patients have an increased risk of osteoporosis and lose muscle bulk early in the course of the disease. Basal metabolic rate is increased in HF, but general malnutrition may play a part in the development of cachexia, particularly in an elderly population.

There is evidence for a possible role for micronutrient deficiency in HF. Selective deficiency of selenium, calcium and thiamine can directly lead to the HF syndrome. Other nutrients, particularly vitamins C and E and beta-carotene, are antioxidants and may have a protective effect on the vasculature. Vitamins B6, B12 and folate all tend to reduce levels of homocysteine, which is associated with increased oxidative stress.

Carnitine, co-enzyme Q10 and creatine supplementation have resulted in improved exercise capacity in patients with HF in some studies. In this article, we review the relation between micronutrients and HF.

Chronic HF is characterized by high mortality and morbidity, and research effort has centered on pharmacological management, with the successful introduction of angiotensin-converting enzyme inhibitors and beta-adrenergic antagonists into routine practice. There is sufficient evidence to support a large-scale trial of dietary micronutrient supplementation in HF.



Conditioned nutritional requirements and the pathogenesis and results of myocardial failure.  

The majority of symptomatic patients with congestive heart failure have been shown to be significantly malnourished. Myocardial and skeletal muscle energy reserves are also diminished. Total daily energy expenditure in these patients is less than that in control individuals, and high protein-calorie feeds do not reverse the abnormalities; thus, the wasting that occurs in patients with congestive heart failure is metabolic rather than because of negative protein-calorie balance.

Several specific deficiencies have been found in the failing myocardium: a reduction in the content of L-carnitine, coenzyme Q10, creatine and thiamine, nutrient cofactors that are important for myocardial energy production; a relative deficiency of taurine, an amino acid that is integral to the modulation of intracellular calcium levels; and an increase in myocardial oxidative stress, and a reduction of both endogenous and exogenous antioxidant defences.

In addition, these processes may influence skeletal muscle metabolism and function. Cellular nutritional requirements conditioned by metabolic abnormalities in heart failure are important considerations in the pathogenesis of the skeletal and cardiac muscle dysfunction. A comprehensive restoration of adequate myocyte nutrition would seem to be essential to any therapeutic strategy designed to benefit patients suffering from this disease.


Carnitine supplementation improves myocardial function in hearts from ischemic diabetic and euglycemic rats.

Background. Nonischemic myocardial dysfunction in patients with diabetes mellitus appears to be attenuated with long-term L-carnitine . The effect of acute L-carnitine supplementation on rat hearts from euglycemic and diabetic animals subjected to ischemia and reperfusion is investigated in this study.

Methods. Study rats had diabetes mellitus induced by streptozocin (65 mg/kg intraperitoneally), and control rats had injection of saline solution (n = 12 per group). About 1 month later, the hearts were suspended on a Langendorff apparatus and perfused with either standard buffered Krebs-Henseleit solution or this standard solution supplemented with L-carnitine (5 mmol/L).

After stabilization, normothermic, zero-flow ischemia was instituted for 20 minutes followed by 60 minutes of reperfusion. There were four study groups (n = 6 per group): hearts that were from euglycemic rats and that were perfused with standard buffered Krebs-Henseleit solution (E-STD); hearts that were from diabetic animals and that were perfused with the same standard buffered solution (DM-STD); hearts taken from diabetic animals and perfused with L-carnitine–enriched solution (DM-CAR); and hearts taken from euglycemic rats and perfused with the enriched solution (E-CAR).

Results. At 60 minutes of reperfusion, left ventricular developed pressure was significantly better in hearts from both groups (diabetic and euglycemic) with carnitine supplementation (DM-CAR versus DM-STD and E-CAR versus E-STD, p < 0.01 for both, by analysis of variance). Left ventricular end-diastolic pressure was significantly lower in the DM-CAR group compared with all other groups (p < 0.01 by analysis of variance).

Conclusions. These findings suggest that acute L-carnitine supplementation significantly improves the recovery of the ischemic myocardium in diabetic and euglycemic rats.



Therapeutic effect of taurine in congestive heart failure: a double-blind crossover trial.

In a double-blind, randomized, crossover, placebo-controlled study, we investigated the effects of adding taurine to the conventional results in 14 patients with congestive heart failure for a 4-week period. Compared with placebo, taurine significantly improved the New York Heart Association functional class (p less than 0.02), pulmonary crackles (p less than 0.02), and chest film abnormalities (p less than 0.01).

A benefit of taurine over placebo was demonstrated when an overall results response for each patient was evaluated on the basis of clinical examination (p less than 0.05). No patient worsened during taurine administration, but four patients did during placebo. Pre-ejection period (corrected for heart rate) decreased from 148 +/- 14 ms before taurine results to 137 +/- 12 ms after taurine (p less than 0.001), and the quotient pre-ejection period/left ventricular ejection time decreased from 47 +/- 9 to 42 +/- 8% (p less than 0.001).

Side effects did not occur in the patients during taurine. The results indicate that addition of taurine to conventional is safe and effective for the results of patients with congestive heart failure. 



Fish oil and other nutritional adjuvants for results of congestive heart failure.

Published clinical research, as well as various theoretical considerations, suggest that supplemental intakes of the 'metavitamins' taurine, coenzyme Q10, and L-carnitine, as well as of the minerals magnesium, potassium, and chromium, may be of therapeutic benefit in congestive heart failure.

High intakes of fish oil may likewise be beneficial in this syndrome. Fish oil may decrease cardiac afterload by an antivasopressor action and by reducing blood viscosity, may reduce arrhythmic risk despite supporting the heart's beta-adrenergic responsiveness, may decrease fibrotic cardiac remodeling by impeding the action of angiotensin II and, in patients with coronary disease, may reduce the risk of atherothrombotic ischemic complications.

Since the measures recommended here are nutritional and carry little if any toxic risk, there is no reason why their joint application should not be studied as a comprehensive nutritional for congestive heart failure. 



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