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A study published in the American Journal of Cardiology examined the use of ubiquinol and/or D-ribose among participants with heart failure with preserved ejection fraction (HFpEF). Once referred to as diastolic heart failure, HFpEF represents at least half of all cases of heart failure (soon to be the predominant phenotype), with several well-established risk factors, including coronary artery disease and atrial fibrillation. HFpEF is considered a clinical syndrome, in which patients have a normal left ventricle ejection fraction (≥ 50%) despite signs and symptoms of heart failure. This is accompanied by elevated natriuretic peptide levels, and evidence of diastolic dysfunction or relevant structural heart disease, such as an increase in left atrial size.
Although its pathophysiology is not fully understood, HFpEF does have non-cardiac comorbidities, including metabolic syndrome, insulin resistance, and obesity. Additionally, endothelial dysfunction appears to be a primary hallmark of this condition, along with metabolic inflammation (meta-inflammation). There are currently no effective pharmacological therapies for HFpEF, with treatment primarily aimed at mitigating risk factors such as hypertension, reducing hospitalizations with sodium-glucose cotransporter 2 (SGLT2) inhibitors, and minimizing symptoms, such as reducing peripheral edema with diuretics. This is not without consequence; although diuretics are a mainstay of heart failure therapy, they have been associated with increased hospitalization and worsening exercise tolerance among patients with HFpEF, highlighting the need for more effective treatments.
Underlying mitochondrial dysfunction is thought to play a role in HFpEF pathophysiology, characterized chiefly by metabolic inflexibility. This dysfunction includes decreased ATP synthesis, reduced oxidative phosphorylation, decreased activity of the electron transport chain, as well as an excess of free fatty acids that overwhelms mitochondrial fatty acid oxidation capacity. Thus, interventions that enhance mitochondrial function have the potential to benefit patients with HFpEF.
In this recent double-blind clinical trial, 216 patients were randomized to one of four groups; 600mg ubiquinol per day and placebo, d-ribose powder (15g/day) and placebo, both nutrients, or double placebo. There were 7 outcomes monitored in this study, including the Kansas City Cardiomyopathy Questionnaire (KCCQ) clinical summary score, B-type natriuretic peptides, etc. After a 12-week period, ubiquinol and/or d-ribose supplementation significantly improved the KCCQ clinical summary score, the level of vigor, and the left ventricle ejection fraction, with favorable reductions in B-type natriuretic peptides and the lactate/adenosine triphosphate ratio, indicating a shift away from glycolysis, and supporting the use of these nutrients among patient with HFpEF.
This is not the first trial to suggest possible benefits from these nutrients. CoQ10, for example, has been shown to have an inverse correlation with B-type natriuretic peptide levels, as well as the severity of heart failure symptoms, and to be an independent predictor of survival. Supplementation with CoQ10 (along with selenium) was shown to significantly reduce cardiovascular mortality among patients with heart failure, with an effect that persisted for 12 years, following a 4-year period of supplementation. Meta-analyses of CoQ10 use have shown both a lower mortality and higher exercise capacity compared to placebo among participants with heart failure, as well as improved endothelial function. CoQ10 has also been shown to improve cardiovascular risk factors such as blood pressure and hypertriglyceridemia in meta-analyses of multiple randomized controlled trials.
D-ribose is naturally produced via the pentose phosphate pathway and may provide an alternative source of ATP production outside of the electron transport chain. Although there have been fewer clinical trials with D-ribose, existing trials are encouraging, including improvements to the quality of life and diastolic function among participants with HFpEF in small trials.
Several amino acids may also be useful for patients with HFpEF, including L-arginine, L-citrulline, and L-carnitine. L-arginine is the precursor for nitric oxide, and L-citrulline is metabolized to L-arginine, effectively increasing blood levels of L-arginine, both of which may help to improve endothelial dysfunction. In a small study of participants with HFpEF, an improvement in pulmonary artery pressure and right ventricular ejection fraction was observed after 2 months of supplementation with either L-arginine or L-citrulline (no placebo group). A small pilot study found that L-carnitine supplementation maintained muscle strength, prevented fat accumulation, and improved gait speed compared to placebo over a 12-month period, among participants with carnitine deficiency and HFpEF. While frailty and muscle loss are important consequences of heart failure, it is unclear if this benefit would be observed in patients without a documented carnitine deficiency. Endothelial function may also be supported by nitrate-rich beetroot juice. In a small clinical trial, participants with HFpEF receiving beetroot juice had improved exercise capacity as well as exercise vasodilatory and cardiac output reserves and mitochondrial function, compared to placebo.
Good clinical trial data is lacking for other nutrients that have established roles in heart failure, but not specifically HFpEF. For example, hypomagnesemia is a well-known consequence of diuretic therapy, and is an independent risk factor for cardiovascular disease. An analysis of over 450 patients with HFpEF found that lower serum magnesium was predictive of a higher risk for heart failure events, suggesting supplementation may be indicated for patients with lower levels, though no clinical trials have been conducted.
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