Inflammation and heart disease: a holistic perspective

Townsend Letter for Doctors and Patients,  May, 2005  by William Ferril

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The amount of insulin within the body determines the amount of fat-maker message. Hormones, like insulin, carry information to the body cells. Hormone information always concerns how cells direct energy expenditure. Insulin carries information that tells the cells to store energy. Most body energy storage occurs as fat. Cholesterol is one type of body fat. The enzyme in the liver that makes sugar into cholesterol turns up its activity when insulin levels rise. Insulin levels rise following carbohydrate meals or excess mental stress (among several other promoters). Rather than tell doctors and the public about this simple cause and effect relationship, the wonders of the statin drugs bombards media outlets.

Statin drugs work, in part, because they poison this liver enzyme's ability to listen to the insulin message. The trouble with poisons concerns their inevitable side effects and toxicities. One nasty side effect from these medications concerns the depletion of Co enzyme Q10 in the body. The heart needs the lion's share of this important nutrient. Deficiency here causes one type of heart failure.

Another emerging understanding for how statin drugs lower heart disease risk involves their ability to subdue inflammation. Rather than come clean and educate physicians about the most likely mechanism for how this occurs, the statin-selling companies perpetrate the story that it remains largely a mystery. The argument for it being a mystery diminishes once a few critical clues enter into the discussion.

The first clue involves the long-known association between heart disease and the Type A personality types. Type A personality types are classically described as hard driving, over achieving, and always worried about their next deal. Physiologically, these emotions when chronically expressed, lead to a constant stress hormone response. The stress response was designed to survive physical stressors. In order to survive a physical stress, the massive dumping of fuel into the bloodstream makes sense because exercising muscles consume the fuel. Additionally, physical stressors often lead to trauma. This explains why the acute phase reactants predictably elevate with the onset of the stressor. The acute phase reactants prove appropriate with trauma, but deleterious with mental stress. C-reactive protein is only one acute phase reactant. Others include complement, interferon, fibrinogen, ferritin, ceruloplasmin and amyloid. Fibrinogen directly increases the clotting tendencies of blood. Ferritin elevations increase iron absorption into the body tissues.

With mental stress, once iron absorbs into the body, it proves very difficult to remove. This detail may help explain the emerging realization that many heart disease patients have elevated ferritin levels. It further explains a potential reason that chelation therapy maintains its devotees, despite the ongoing criticism. Specifically, EDTA binds and removes iron from the body. This fact may prove the number one benefit for this approach.

Lastly, concerning the acute phase reactants' elevation in the setting of mental stressors, involves its inappropriate effect toward an increase in angiogenesis propensity. The angiogenesis propensity increases when the acute phase reactants elevate. This again makes sense with physical stressors because these traumas associate with the need for new blood vessel formation.

Chronic mental stress promotes two powerful processes that promote the angiogenesis critical to tumor growth: increased insulin needs and the heightened angiogenesis propensity described above. These facts, taken together, provide a likely mechanism for why overweight and stressed individuals suffer increased morbidity and mortality from cancer.

The second clue involves the emerging research results that document that the statin drugs lower C-reactive protein levels. Once one recalls the connection between HMG Co A reductase activity and steroid synthesis rates, a more holistic picture emerges. Anything that subdues the ability of the adrenal glands to make steroids, will also diminish the magnitude of cortisol released for a given stressor. In turn, less cortisol release subdues the acute phase reactants' release. C-reactive protein (CRP) is only one of the acute phase reactants. The normalization of acute phase reactants, in the chronic mentally stressed state, leads to less inflammation for the reasons described above.

These facts initially sound "too good to be true." This old adage once again proves useful because the downside to this scenario provides insight into the advantages of counseling Type A personality owners about the bigger picture of cause and effect relationships.

In order to better appreciate the downside of the statins, one needs to recall the typical body habitus of the Type A personality. The majority of them are large in the waistline, or at the very least, they have increased visceral fat. Currently, a waist measurement above 40 inches is felt to predict these metabolic syndrome types at risk for accelerated aging and blood vessel disease. Over fifty years ago, obese individuals were found to have increased stress steroid metabolites in their urine.