Gulf War Syndrome, chronic fatigue, migraine headache, mercury toxicity, diastolic dysfunction (DD), statin cardiomyopathy, and likely many other conditions, share a common and overlooked denominator – mitochondrial damage, deterioration, and dysfunction leading to impaired production of adenosine triphosphate (ATP) and an increase in oxidative burden. Multiple studies have demonstrated a strong epidemiological relationship between mitochondrial degeneration and pathology, yet mitochondrial status receives little or no attention in clinical practice. For example, in migraine sufferers, a reduction in mitochondrial phosphorylation potential in intervals between headaches has been reported. Stubborn Gulf War symptoms have been linked to mitochondrial damage. In heart failure patients, abnormally low ATP has been measured in the mitochondria of biopsied myocytes. In DD, the primary etiology is insufficient ATP due to depletion of vital energy substrates.
This presentation describes an effective metabolic cardiology approach that emphasizes select nutraceuticals to support cellular energy substrates crucial for restoring and rebuilding deficient ATP levels. The preservation of mitochondrial function and subsequent energy production require paramount attention in order to slow down accelerated aging, illness and human suffering. The strategy has significant therapeutic value in reducing cardiometabolic risk for the clinician, within and beyond cardiology.
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