Sunday, November 4, 2018

Review of anti-statinists article 2018


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
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.
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.
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
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

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”


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

  1. Walsh JM, Pignone M. Drug treatment of hyperlipidemia in women. J Am Med Assoc. 2004;291:2243–2252

  2. 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

  3. 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

  4. 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







No comments:

Post a Comment

update trials of Alzheimers

 The best part of the day is when I have a bowel movement.   Recently started Miralax. I found MOM too harsh. Pacing helps but I get exhaust...