Now they want you to risk your child's future and put him or her on a
medication for life when there is no evidence that medication will be
effective for prevention of heart disease. What about developing
brains? What about the fact that statins have been proven to cause
higher rates of myositis and myopathy in active people?
One in 500 of French Canadian descent and one in 67 Aschkenazy Jews to
name just two groups have familial hypercholesterolemia. So we should
put all those children on an unproven class of drugs...to what end?
Epidemiologist and Cochrane Collaboration member James Wright has said
there is no evidence for use in primary prevention.
We can prove statins lower cholesterol but we have not proven they
affect all cause mortality. We don't know what will happen to children
and youth when they have taken these drugs for 15-20 years. They are
safe the story says. For how long? Effective the story says. To do
what?
Athletes deny their pain to continue their sport. Young sports
enthusiasts will deny their pain perhaps until it's too late to stop
the decline into rhabdomyolysis. Will we be creating a generation of
athlerosclerotic-free wheel chair bound myopaths?
A cholesterol level of 240 is not necessarily a pathology since
approximately half of those who have heart attacks have so-called
normal cholesterol levels. This is medicating on spec. Gambling with
children's lives.
Here is the last sentence of this rearranged press release posing as
news. How despicable that physicians play this deadly game with our
lives and now the lives of our children.
"Dr. Gotto is a consultant for AstraZeneca, Bristol-Myers Squibb Co.,
Kowa, Merck & Co. Inc., Merck-Schering Plough, Novartis, Pfizer Inc.,
and Reliant Pharmaceuticals."
Statins Safe, Effective in Children With Familial Hypercholesterolemia
CME
News Author: Laurie Barclay, MD
CME Author: Charles Vega, MD, FAAFP
Release Date: July 20, 2004; Valid for credit through July 20, 2005
July 20, 2004 — Statins are safe and effective for children with
familial hypercholesterolemia, according to the results of a
double-blind, randomized trial published in the July 21 issue of JAMA.
This disorder is characterized by markedly elevated levels of
low-density lipoprotein cholesterol (LDL-c) beginning at birth.
"Children with familial hypercholesterolemia have endothelial
dysfunction and increased carotid intima-media thickness (IMT), which
herald the premature atherosclerotic disease they develop later in
life," write Albert Wiegman, MD, PhD, from the University of Amsterdam
in the Netherlands, and colleagues. "Although intervention therapy in
the causal pathway of this disorder has been available for more than a
decade, the long-term efficacy and safety of cholesterol-lowering
medication have not been evaluated in children."
Between December 1997 and October 1999, 214 children with familial
hypercholesterolemia, aged 8 to 18 years, were randomized to receive
pravastatin, 20 to 40 mg/day, or placebo for two years. Before
receiving study medication, all children began a fat-restricted diet
and were encouraged to participate in regular physical activity.
In the pravastatin group, mean carotid IMT showed a trend toward
regression compared with baseline (-0.010 ± 0.048 mm; P = .049). In
the placebo group, there was a trend toward progression (+0.005 ±
0.044 mm; P = .28). The mean change in IMT between the two groups was
significant (0.014 ± 0.046 mm; P = .02).
Mean change in LDL-c levels was a 24.1% reduction in the pravastatin
group, and a 0.3% increase in the placebo group (P < .001). Growth,
maturation, hormonal levels, and muscle and liver enzymes were similar
in both groups.
Study limitations were possible confounding by healthy lifestyle and
diet, use of a surrogate marker of future vascular disease rather than
clinical endpoints, and lack of generalizability to children with
other causes of increased atherosclerotic risk.
"We were able to show that statin treatment improved the lipoprotein
profile toward more physiological levels and we observed regression of
carotid IMT. This shows that the increased arterial wall thickness
progression found in children with familial hypercholesterolemia is
reversible," the authors write. "Although this trial in children with
familial hypercholesterolemia has, to our knowledge, the most
extensive follow-up to date, data on even longer-term safety and
efficacy of statin therapy in children are needed."
The Zorg Onderzoek Nederland and Bristol-Myers Squibb Inc. supported
this study.
In an accompanying editorial, Antonio M. Gotto, Jr., MD, DPhil, from
Weill Medical College of Cornell University in New York, NY, suggests
that most children with familial hypercholesterolemia may need drug
therapy. However, Dr. Gotto recognizes that potential risks of therapy
must be considered in young patients.
"In the case of familial hypercholesterolemia, the promise of reducing
future cardiovascular morbidity and mortality, as well as future
demands on acute care and more expensive preventive approaches, would
make aggressive treatment of high-risk young patients a worthwhile
long-term initiative," Dr. Gotto writes. "Appropriate targeting of
lifestyle and drug therapies will optimize primary prevention in this
group at demonstrated risk for early disease."
Dr. Gotto is a consultant for AstraZeneca, Bristol-Myers Squibb Co.,
Kowa, Merck & Co. Inc., Merck-Schering Plough, Novartis, Pfizer Inc.,
and Reliant Pharmaceuticals.
JAMA. 2004;292:331-337, 377-378