You Gotta Have Heart

healthy-heart-smIf you attended high school most days, you might have learned that atoms are made of protons, electrons and neutrons, having charges that are positive, negative or neutral, in that order. If the charges get out of balance, the atom is either negatively or positively charged. The switch between one type of charge and the other allows electrons to move from one atom to the next. It’s this flow of electrons that we call electricity and is the energy that controls everything about the body. This is the source of the signals that allow us to grab the doorknob or turn the ignition switch, or even to think about what to have for dinner. Instead of flowing along a continuous wire, as happens in the house, these signals jump from one cell to the next—and they do it fast.

The potassium inside a cell and the sodium outside have a lot to do with our electrical capacity. At rest, a cell has more negatively charged potassium inside than positively charged sodium. As the negatives and positives are attracted to each other, they cross the barrier between them—the cell membrane—through a gate, and create electricity in order to initiate a movement, thought or biological function. This impulse triggers the gate on the neighboring cell, then on the next one, the next one. This is how the sinoatrial (SA) node of the heart (its pacemaker) tells it to contract and how your eye tells your brain what you just saw. One of the interesting, though admittedly still painful, facets of life happens when you hit a finger with a hammer. The pain message travels through a sensory nerve to the brain in a fraction of a second, and then the brain associates the assault with discomfort before it tells you to move your finger away from the site of injury. Even though you realize what just happened, it takes a brief moment before the throbbing starts. All this is based on electrical activity. This might happen at 250 miles an hour, much slower than the 180,000 miles per second speed of electricity along a wire.

Our cells—more than 60 trillion—work hard every day to multiply themselves, digest nutrients, remove wastes and make energy from something called ATP. Inside each cell are little power plants called mitochondria, the number depending on the job of the cell. An eyelid will not have as many mitochondria as a bicep. ATP is made inside a mitochondrion, where Co-Enzyme Q 10 directs the function of the electron transport chain by collecting and transferring electrons along the chain. In its reduced form, where it gains an electron, CoQ10 acts as an antioxidant, effectively recycling vitamin E and possibly having an anti-atherogenic effect (Turunen, 2002).

Although often ignored by conventional medicine, it is important to note that CoQ10 shares a metabolic pathway with cholesterol and that stores diminish with age, whether by decreased synthesis or by increased requirements, or even by the elevated lipid peroxidation that accompanies aging. If we regulate cholesterol with a statin drug, we also regulate the manufacture of CoQ10; hence the need for supplementation to maintain the electrical grid. In the first double-blinded study ever that examined CoQ10 in cardiac interventions, it was discovered that enzyme supplementation in heart failure patients reduced hospital admissions and death by improving cardiac function through enhancement of the respiratory chain at doses of 100 mg three times a day (Mortensen, 2013).

Allopathic medicine rarely looks into the micronutrient deficiencies that either foretell or cause impaired function of the heart’s electrical circuits. Its therapeutic options are confined to treating symptoms. Cellular—or membrane—medicine recognizes the important components of the energy formation cycle. Patients who suffered congestive heart myopathies had shown remarkable responses to CoQ10 therapy when assiduously administered in a faithful regimen (Langsjoen, 1985). If such was the case decades ago, why has there been so little publicity?  New York Heart Association (NYHA) class IV heart failure defines almost complete cardiac insufficiency. Patients who were expected to die within two years under conventional therapy did not because it was recognized that CoQ10 is indispensable in mitochondrial bioenergetics (Langsjoen, 1988).

Absorption of supplemental CoQ10 on an empty stomach is poor, with more than sixty percent excreted in feces. It improves when taken with foods having a considerable lipid profile. In the presence of bile detergents lipids are broken into very small particles, thus increasing their surface area and subsequent susceptibility to the lipase enzymes that digest fats. Now, especially in the company of phosphatidylcholine, these particles are absorbed by intestinal mucosa and passed into the bloodstream. It takes about three weeks of faithful supplementation to attain maximum serum concentrations.

As with most integrative modalities, ongoing studies are welcome, but suffer lack of funding because they interfere with the profits garnered by pharmaceuticals. The number of eligible heart transplant patients surpasses the available number of donors. On the bright side, CoQ10 has a beneficial effect on these persons by virtue of providing a pharmacological bridge that offers an improvement in functional status and quality of life (Berman, 2004), including ejection fraction (Fotino, 2013).

For a long time, medicine has sought a means to return flexibility to the cardiovascular system that has succumbed to the ravages of time and insult, such as smoking, excessive sugar intake, and diets that promote advanced glycation endproducts. Patients suffering NYHA class III CHF who received supplemental CoQ10 at 100 mg tid, experienced improvement in left ventricular contractility and ejection fraction after only four weeks (Belardinelli, 2005), indicating the plausibility of such a protocol.

Studies may be clouded by anticipated outcomes, the bias of which may be directedby expectations of funding bodies. In too may instances, Eurasian investigatorsfind more successes than North Americans. The bottom line appears that low CoQ10concentrations are predictive of adverse CHF events, leaving one to understandthe rationale for intervention with the supplement. Endogenous manufacture ofCoQ10 requires sufficient vitamin B6 for biosynthesis. Most of us consume lessthan 10 mg of CoQ10 a day from dietary sources, leaving plenty of room for supplementation,even if we lack a pathology. The last thing we need is a power failure.

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*These statements have not been evaluated by the FDA.
These products are not intended to treat, diagnose, cure, or prevent any disease.

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