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BLOG: July 2008

Cholesterol kids

Most everyone knows what led to the creation of "cholesterol kids" generation: mainly over-consumption of junk food combined with physical inactivity. The question is, are we going to help these kids, or let greedy pharmaceutical companies, assisted by corrupted or incompetent medical professionals, happily proclaim it is the reality we live in - and use it to fatten more their insatiable pockets by promoting unproven, potentially harmful drug (statin) therapy disguised as solution to the problem?

And, yes, these companies are very capable of making the switch turn their way. According to the recent U.S. Agency for Healthcare Research and Quality report, statin sales between 2000 and 2005 jumped from $7.7 billion to $19.7 billion, with the number of users, at nearly 30 million, almost doubled, and the average yearly cost per individual user increased from $484 to $661. The enormous volume of profit brought in by statin sales provides both, motive and means to try to secure and, if anyhow possible, expand the market.

Children cholesterol problem has recently gotten attention of the American Academy of Pediatricians (AAP). The media states that it is "for the first time" that a large, influential medical organization recommends more aggressive use of statins - type of cholesterol lowering drug - for patients down to age of 8. Not quite. In the March of 2007, the American Heart Association (AHA) recommended, pretty much along the same lines, that the official guidelines should be updated to expand screening for cholesterol from about 25% to 36-45% of children and adolescents, as well as to lower the bar and encourage use of statins for "high-risk" children.

Under the pretext of unraveling epidemic of cardiovascular disease, often beginning to develop in early childhood as a result of obesity accompanied with dyslipidemia (elevated or imbalanced blood lipids, with focus on cholesterol), the AAC Committee on Nutrition, decided that new recommendations (also published in Pediatrics journal) should call for expanded cholesterol screening, beginning after the age of 2, and encourage more aggressive drug - primarily statin - treatment in "high risk" children after the age of 8.

Unlike the previous, now retired 1998 AAP policy, based on the 1992 Guidelines drawn up by the National Cholesterol Education Program (NCEP), stating that drug treatment should be considered in obese children older than 10

if they fail to lose weight after a 6- to 12-month of
dietary/lifestyle-change therapy,

the new policy - while stating that weight management and increased physical activity should be the primary treatment for overweight or obese children that have either high triglyceride or low HDL concentration - doesn't set any specific suggestion with respect to the duration, or even initiation of such treatment.

But it does promote blanket recommendation that "pharmacologic intervention should be considered" for children 8 years and older with LDL concentration of 190 mg/dL or higher in general, with 160 mg/dL or higher for those with a family history of early heart disease, and for children with 130 mg/dL or higher with diabetes mellitus.

Anyone that knows how the U.S. drug market operates realizes that these recommendations give to pharmaceutical companies all they need to start aggressively promoting cholesterol lowering drugs - primarily statins - and, in effect,

start medicating children the way they already medicate adults.

And, be assured, the members of the AAC Committee are very familiar with how the U.S. drug market works. Hence, undoubtedly, they base their new recommendation on the overwhelming evidence of:

exclusively high efficacy of statin drugs in lowering cholesterol in children and resulting reduction of the risk of cardiovascular complications and death much later in their life, combined with

highest margin of safety with respect to short- and long-term adverse effects

Or do they? The AAC Committee paper explaining the guidelines references to a "number of studies" that have shown statins to be "safe and effective" for children, but the actual list contains no more than several short-term small studies, none effectively much longer than 1 year.

In one of the two recent studies cited as more reliable due to the actual measurement of the statin effect on blood vessels (de Jongh et al.), as few as 50 children with familial hypercholesterolemia (inherited disturbance of liver cholesterol production) were followed for 28 weeks. Simvastatin dosage started at 10mg/day, doubling to 20mg and 40mg a day during the first three 8-week periods. Observed effect was the increase in flow-mediated dilation of the brachial artery - used as a surrogate marker for cardiovascular disease - that was three times greater in the statin, compared to placebo group (32% vs. 10% respectively).

Statin group also had lower levels of total cholesterol (30%), triglycerides (17%), and LDL cholesterol (40%), while slightly higher HDL cholesterol (4.5%). These remained nearly unchanged in the placebo group.

In the other cited "measurement" study (Wiegman et al.), one half of 214 children 8-18 years of age, also with familial hypercholesterolemia, have been put on 20-40mg/day of pravastatin and followed for up to 2 years (with the average study duration likely gravitating to 1 year). Measured carotid (neck) artery wall thickness at the end of trial averaged 0.01mm decrease in the statin-treated group, and 0.005mm increase in the placebo group. Statin group also had 24% lower LDL cholesterol, which remained nearly unchanged in the placebo group. No differences between the 2 groups were noted in development, muscle or liver enzymes or endocrine function parameters.

 If accurate, these numbers indicate two things. One is that the youngsters, expectedly, did have the process of arterial plaque formation already initiated. But this doesn't imply statin deficiency; rather deficiency of antioxidants and detox nutrients, preventing oxidative damage to blood vessel lining and cholesterol itself -

the primary cause of plaque formation.

The other one is that with the average inner diameter of carotid arteries in healthy adults of some 3-4mm, the build-up rate would cause its effective inner diameter to shrink, on average, 25-33%

in about 100 years.

Taking it for what it is, the results of these two small studies indicate that statins could have positive effect not only on the cholesterol levels, but also on atherosclerotic blood vessel deterioration in those with familial hypercholesterolemia. What these studies certainly are not, is any type of conclusive evidence of statin treatment being:

(1) outcome (i.e. reduction of heart attacks, strokes and related deaths) efficient,

(2) safe in prolonged use for the general children/adolescent population, and

(3) superior to all other alternatives.

CONTINUES: Children cholesterol and big business