Inflammation and Heart Disease A Holistic Perspective: The Case Against Statin By William Ferril, MD

August 11, 2009 at 11:58 pm | Posted in Uncategorized | 1 Comment

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 stain 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 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 effects 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 coritsol release subdues the 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 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.

Uniting these two facts together, it becomes easier to understand one of the metabolic syndrome individual’s driving pathological forces: Exaggerated stress steroid release rate for a given stressor.  Another way to look at this is, in the setting of chronic mental stress, those prehistorically-equipped survival machines selected for down through the ages have become the metabolic syndrome victims from chronic sedentary-type stressors.  What was once a survival benefit derived from mounting a strong fuel release and acute phase reactant release (both secondary to a strong cortisol release) in the setting of physical stress, has now become a curse, promoting excessive body fat accumulation and blood vessel inflammation.

Excessive cortisol release violently activates protein dismantling into more sugar (gluconeogenesis).  Protein content within denotes the metabolically active constituent of body tissue.  Defense of body protein content proves fundamental to healthful longevity.  Healthy people have sufficient growth hormone release that protects their protein from excessive catabolism during these times.  However, middle-aged individuals who chronically experience stress but have sedentary lifestyles, begin to suffer various amounts of glandular decline.

One mechanism for glandular decline involves the inappropriate elevation of blood sugar caused by mental stress in the sedentary state.  Elevated blood sugar suppresses growth hormone release.  Less growth hormone release leads to less defense of body protein ability.  This fact ties in the observation about syndrome X patients evidencing sarcopenia.  It also elucidates the likely association between this Syndrome, and its underlying a variant presentation of Cushing’s disease pathology (see testing below).

With mental stress, the increased blood fuel has nowhere to go.  Hence, for these reasons, increased insulin amounts eventually release to normalize the blood sugar.  Again, this same metabolic derangement operates within the classical Cushing’s disease patient.  Unfortunately, very few physicians appreciate the sequential release of first cortisol (catabolic) followed by increased need for insulin to correct the inappropriate rise in blood sugar.  It is the increased insulin that makes the typical Cushing’s disease patient fat.  It is the increased cortisol that causes excessive catabolism of their body protein and chronic surges in their blood sugar levels.

Unfortunately, insulin releases into the portal vein and heads straight for the liver.  HMG Co A reductase turns on with increasing insulin and off with increasing glucagons.  What was once protein, a few minutes before, now is floating within the bloodstream as sugar.  A few minutes later the protein turned into sugar is changed into cholesterol and fat.  Because the liver (also fat cells) cells have 200,000 pure insulin-type receptors per cell, insulin excess profoundly influences the cholesterol profile.

A cognizance of this anatomical reality helps one to see that the liver functions as an insulin trap and only excessive amounts of insulin secretion can spill past the liver and out into the general circulation.  Healthy people need less insulin because their livers secrete sufficient IGF-1 that largely negates the need for insulin between meals, while fasting or when exercising.  Circulating IGF-1 levels directly depend on sufficient growth hormone release.  Realize, only sufficient growth hormone release defends body protein between meals, while exercising or when fasting.  All other counter-regulatory hormones (cortisol, epinephrine and glucagon) make protein dismantling for fuel creating fair game.

The old name for IFG-1 clarifies its crucial role in sugar metabolism, the nonsuppressible insulin-like activity of the bloodstream.  Many physicians remain unaware of this fact and it seems rather odd to this author that it fails to receive even cursory mention while reviewing Syndrome X pathology.  The healthiest people possess the highest IGF-1 levels.  A falling IGF-1 leads to increased insulin need (insulin resistance).

The very survival of the statin drug-selling rosy picture depends on eviscerating certain scientific consequences that result from a diminished glandular ability.  When healthy, the adrenal glands make both catabolic and anabolic message content.  A higher anabolic message content leads to a faster repair rate.  The lower the antioxidants, the more repairs need to occur.  Here lies the additional risk of chronically consuming statin drugs in place of healing lifestyles:  They contribute to the lack of repair from ongoing wear and tear that the blood vessels encounter.  Disrepair causes inflammatory damage despite their benefit from inducing decreased cholesterol and acute phase reactants levels.

HMG Co A reductase occurs within the adrenals and gonads.  Any drug or toxin that inhibits the steroid manufacture ability within the adrenals or gonads, will also decrease the repair rate that logically follows from diminished anabolic message content.  Here lies another downside that remains ignored until one begins to examine the interrelatedness of steroid synthesis rates and HMG Co A reductase activity.

In one way or another, blood vessel disease results from the repair rate not keeping up with the injury rate.  Statin drugs may in fact lower the injury rate by diminishing the acute phase reactants’ caused inflammation and cortisol-related blood sugar spikes.  The lessened blood sugar spikes lead to decreased insulin need despite a sedentary and stress-filled lifestyle.  A subdued stress response means that less acute phase reactants release, as well.  However, what is not being said concerns their probable negative influence on the repair rate of blood vessels and muscle tissue.  The repair rate of muscles and blood vessels depend on androgen levels, like all other DNA-containing body cells.  Since science has already documented subdued acute phase reactants with statin usage, it remains quite likely that other steroids’ synthesis rates decrease, as well.

The likely consequence of diminished testosterone, which results from statin drug usage, may help further elucidate the ongoing suspicion about their contribution to heart failure.  Many in the holistic community attribute this tendency to the diminished Coenzyme Q10 levels that logically follow.  However, maybe a fall off in testosterone in some chronic statin users, contributes to their pump failure as well.

Following serial 24-hour urine measurements for steroids would provide a logical next step for testing the severity of diminished anabolic message content.  It will also further elucidate the before and after profiles of the stress steroid metabolites of Syndrome X patients.  Recall, that over 50 years ago, obese patients were documented to have elevations in their 24-hour urine test for stress steroid metabolites.  If each doctor in the holistic community began collecting baseline 24-hour urine specimens for steroids, and followed them serially, a new level of understanding would emerge about the association of a heightened stress response, increased insulin need, and elevated acute phase reactants in the development of blood vessel disease.  At the very least, real hormone replacement therapy could be instituted to address these steroid defects before they weaken the statin drug user.  Ideally, these types of tests could be used to help better motivate the type A personality – derived Syndrome X individual take a more active role in which hormones secrete.

Most cited references on statin’s effect on testosterone levels.

1.      Does statin therapy influence steroid hormone synthesis? Bohm M, Herrman W, Wassmann S, Laufs U, Nickenig G. Z Kardiol. 2004 Jan; 93(1) 43-8.

2.      Hormonal changes with cholesterol reduction: a double-blind pilot study. Ormiston T, Wolkowitz OM, Reus VI Johnson R, Manfredi F. J Clin Pharm Ther. 2004 Feb; 29(1): 71-3.

3.      Atorvastatin treatment does not affect gonadal and adrenal hormones in type 2 diabetes patients with mild to moderate hypercholesterolemia. Santini SA, Carrozza C, Lulli P, Zuppi C, CarloTonolo G, Musumeci S. J Atheroscler Thromb. 2003; 10(3): 160-4.

4.      Does simvastatin affect mood and steroid hormone levels in hypercholesterolemic men? A randomized double-blind trial. Hyyppa MT, Kronholm E, Virtanen A, Leino A, Jula A. Psychoneuroendocrinology. 2003 Feb; 28(2): 181-94.

5.      Cholesterol-lowering medication, cholesterol level, and reproductive hormones in women: the Women’s Ischemia Syndrome Evaluation (WISE). Bairey Merz CN, Olson MB, Johnson BD, Bittner V, Hodgson TK Berga SL, Braunstein GD, Pepine CJ, Reis SE, Sopko G, Kelsey SF; Women’s Ischemia Syndrome Evaluation. Am J Med. 2002 Dec 15; 113(9): 723-7.

Effects of high-dose simvastatin on adrenal and gonadal steroido-genesis in men with hypercholesterolemia. Dobs AS, Schrott H, Davidson MH, Bays H, Stein EA, Kush D, Wu M, Mitchel Y, Illingworth RD. Metabolism. 2000 Sep; 49(9):

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