My comments in purple.
"Conclusion
Our conclusion is that the statements from the supporters of the cholesterol campaign
and the drug companies are invalid, compromised by
and the drug companies are invalid, compromised by
1-misleading statistics,
Using relative reduction of risk vs. absolute reduction in risk
is not such an important difference when using RRR for trials of 5,000 people
and then extrapolating to a population of 100,000,000.
is not such an important difference when using RRR for trials of 5,000 people
and then extrapolating to a population of 100,000,000.
2-excluding unsuccessful trials,
This of course is the point.
The present author is using trials that prove his point,
and he ignores trails that don’t prove his point.
I doubt I have the time or knowledge to check if
his trails are the same RCT double blind large numbers
with positive primary outcome that the statins academics are using.
In short I suspect Uffe’s trails are poor trials.
Please use nonHDLc data.
The present author is using trials that prove his point,
and he ignores trails that don’t prove his point.
I doubt I have the time or knowledge to check if
his trails are the same RCT double blind large numbers
with positive primary outcome that the statins academics are using.
In short I suspect Uffe’s trails are poor trials.
Please use nonHDLc data.
3- minimizing the side effects of cholesterol-lowering, and
Pharma has minimized the amount of muscle related pain.
I know this from clinical experience.
However if low dose triple therapy can be used instead
there will be a significant drop in nonLDLc with less side effects
I know this from clinical experience.
However if low dose triple therapy can be used instead
there will be a significant drop in nonLDLc with less side effects
4-ignoring contradictory observations from independent investigators."
Again I am dissatisfied that Uffe does not discuss 1-nonHDLc or
2-remnants or
3-LDLp or apoB.
My review in 2015 of Uffe Ravnkov on statins link
In fairness here is a more detailed rebuttal to Statins.
Why statins have failed to reduce mortality
in just about anybody
Eddie Vos, MEng
Colin P. Rose, MD, PhD
Pierre Biron, MD
127 Courser Road, Sutton, QC, Canada J0E 2K0
Department of Medicine, McGill University, Montreal, QC, Canada H3H 1V6
Department of Pharmacology (Retired), Faculty of Medicine
Universite de Montreal, Montreal, QC, Canada H3C 3J7
published online 11 February 2013.
1-"It is unfortunate that in their Counterpoint Sniderman et al
digress from the issue of mortality."
My comment:
This issue of mortality is the first item Sniderman addresses:
“Moreover, the investigators from the Heart Protection Study (HPS)
demonstrated that all-cause mortality was 14% lower
as the result of a 17% reduction in cardiovascular mortality in the
10,269 patients treated with simvastatin compared with the 10,267
who were allocated to the placebo arm.3”
demonstrated that all-cause mortality was 14% lower
as the result of a 17% reduction in cardiovascular mortality in the
10,269 patients treated with simvastatin compared with the 10,267
who were allocated to the placebo arm.3”
2-"To reiterate, all trials in which investigators used a placebo in women failed,
as stated in the Counterpoint from a reference by Walsh and Pignone1:
“For all trials reporting total mortality,
lipid lowering did not appear to have a beneficial effect for women with or without previous cardiovascular disease
over the 2.8 to 6-year study period in the available trials.”
The relative risks were 1.00 and 0.97, respectively.
Here, too, numerically the most “benefit” was in fewer revascularizations performed,
but this in the secondary prevention group only
[number needed to treat (one year) = ∼140].
That’s it.
Adding another 40,000 on-statin women patient-years to the trial database
cannot change this fact of mortality benefit failure.
Indeed, the article by Brown et al2 referred to in the Counterpoint
showed impressive images of arteries opening
(arguably by delipidation of lesions),
but there was only one death in this study (n = 146)
in which the patient used either
1- lovastatin,
2-30 grams of bile acid sequestrant per day, or
3- a mega-dose of high-density lipoprotein–increasing vitamin B3,
niacin,
arguably the only promoter rather than inhibitor of biochemistry
in cholesterol-affecting studies.
Unfortunately, in this type of study(Brown) one cannot tell
whether an artery has stronger fibrous caps
because cholesterol itself has no known role in the synthesis
of the relevant arterial and cardiac proteins, structural collagen,
and architectural elastin.
If any symptom relief was obtained, as
it well may have,
this could lead to a few less elective revascularizations performed
during such 30-month study length.
However, all this distracts from other potentially life-saving causal avenues
of research.
It also distracts from the
failure of our six-decades-old “war” on cholesterol to have saved lives.
Clinicians should remain mindful that without yearly numbers needed to treat,
nonfatal relative risks and surrogate measures do not represent
life extensions in what is still our most fatal type of disease—
cardiovascular disease—
and that the easiest to count and often-hidden end point
is all-cause mortality in patient groups, witness:
The Cholesterol Treatment Trialists’ Collaboration.
We maintain that statins
have not been demonstrated to be life-extending drugs
except, possibly and for a brief window of time (years),
in younger, high-risk men.
We could say it no better than paraphrasing the cited
mortality is a rather insensitive and unhelpful end point in statin trials
Back to Article Outline
References
Walsh JM, Pignone M. Drug treatment of hyperlipidemia in women. J Am Med Assoc. 2004;291:2243–2252
Brown BG, Albers JJ, Fisher LD, Schaefer SM, Lin J-T. Regression of coronary artery disease as a result of intensive lipid-lowering therapy in men with high levels apolipoprotein B. N Engl J Med. 1990;323:1289–1298
Heart Protection Study Collaborative Group. MRC/BHF Heart Protection Study of cholesterol lowering with simvastatin in 20 536 high-risk individuals: a randomised placebo-controlled trial. Lancet. 2002;360:7–22
Cholesterol Treatment Trialists' (CTT) Collaboration. Efficacy and safety of cholesterol-lowering treatment: prospective meta-analysis of data from 90 056 participants in 14 randomised trials of statins. Lancet. 2005;366:1267–1278
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