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Thursday, January 26, 2012
Cholesterol, statins and death
The reality is that there is no mortality benefit from lowering cholersterol with statin drugs: Both lines on the mortality chart below are superimposed meaning the number of deaths in the statin drug group was identical to the number of deaths in the placebo group. See Chart below:
Translation: Cholesterol lowering with statin drugs does not reduce total mortality in women, PERIOD. It doesn’t reduce mortality in women without heart disease, called primary prevention. It doesn’t reduce mortality in women with heart disease, called secondary prevention.
Not only are statin drugs a failure for women, they also should never be prescribed to the elderly. Mortality in the elderly goes up as cholesterol goes down. Read this Letter to the Editor by Eddie Vos.
http://www.drdach.com/Cholesterol_Women_Dr_Dach.html
Any reduction in coronary disease by statin treatment could easily be outweighed by harm related to drug toxicity when such methods of risk assessment are used.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2014585/?tool=pubmed
The failure of statins to decrease all-cause mortality is possibly best illustrated by atorvastatin: while both the ASCOT7 and TNT8 trials found that atorvastatin therapy decreased the risk of cardiovascular events, in the ASCOT trial (placebo v. 10 mg atorvastatin daily) the all-cause mortality curves effectively touched at mean study end (3.3 years) and in the TNT trial (10 v. 80 mg of atorvastatin daily) there were 26 fewer deaths from coronary artery disease in patients taking the higher dose offset by 31 more noncardiovascular deaths at median study end (4.9 years). Incidentally, the ASCOT trial failed to find a cardiac benefit of statin therapy in women and patients with diabetes.
http://www.cmaj.ca/content/173/10/1207.2.full
This cardiovascular benefit is not reflected in 2 measures of overall health impact, total mortality and total serious adverse events. Therefore, statins have not been shown to provide an overall health benefit in primary prevention trials.
http://www.ti.ubc.ca/pages/letter48.htm
Regarding women, two 2004 analysis [4,5] found
no reduction in deaths from statin over placebo. In
actual patient outcomes, the 6 year 1/4 billion dollar
(approximate simvastatin retail cost) J-LIT
study in 41,801 hypercholesterolemic Japanese
(2/3rds women; mean baseline cholesterol 7 mmol/
L) found mortality in the 2 lowest on-statin cholesterol
categories 2e3 times higher than in patients remaining
near 6.4 mmol/L [6]; its authors cautioned
about ‘hyperresponders’ to statin (Fig. 1). The 4S
study ended with 3 more dead women on statin vs.
placebo [7]; another ‘successful’ study, HPS, found
no significant mortality benefit in women [8].
Interestingly, statins had a close call with their
first mega-trial, EXCEL, ending with almost significantly
more deaths on lovastatin than placebo and
where, at 11 months, the drug’s maker simply
discontinued the placebo group [12]; lovastatin’s
final mega-trial AFCAPS/TexCAPS also ended with
fewer deaths on placebo.
Unless one believes in the sanctity of only 2
studies, pharma-run 4S with unusual mortality
curves and HPS with a rare on-drug run-in phase
and yet unpublished 4 main group mortality
curves, I would argue there are zero mortality
benefit studies for any of the 8 statins that are or
were. Is there a Giordano Bruno or Galileo in the
house, or a female Joan of Arc to change the
paradigm?
As new paradigm and in line with the name of
this Journal, I’d propose long-term protein degradation
by homocysteinylation and glycosylation,
different topics where space restrictions do not
allow me to go but where decades of research has
shown consistent promise. Once arterial structural
decline is present, in order to prevent
sudden deaths, omega-3’s [1] and magnesium supplementation
are avenues deserving urgent
attention.
http://www.health-heart.org/malpractice.pdf
Is it calcium?
It was cardiologist Dr. Stephen Seely who in wrote, in his treatise entitled "Is calcium excess in western diet a major cause of arterial disease? published in the International Journal of Cardiology in 1991, that excess calcium intake is a major cause of atherosclerosis in Western countries.
He contended that young adults need only 300—400 mg of calcium daily, and older adults need even less. In countries where the daily calcium intake is 200—400 mg, arterial diseases are non-existent and blood pressure does not increase with age.
Dr. Seely said, in countries where the daily calcium intake is 800 milligrams (USA, New Zealand, Scandinavian countries, Ireland), arterial disease is the leading cause of mortality. Dr. Seely pointed out that cholesterol only represents 3% of arterial plaque, while calcium makes up 50%. [International Journal Cardiology 1991 Nov; 33 (2):191—8]
Dr. Stephen Seely recommended the best remedy for this problem would be prevention, by reducing calcium consumption only to the level needed by the body. "This could be achieved only by drastic cuts in consumption of milk. Failing that, we could utilize nature's own calcium antagonist, IP6 phytate (rice bran extract)," he said. The author argues that currently available calcium antagonist drugs are less desirable. IP6 phytate is available as a dietary supplement, extracted from rice bran by Tsuno Foods & Rice Co. in Wakayama, Japan, and sold under various brand names (Source Naturals, Jarrow Formulas, Purity Products). (For instruction on how to conduct a rice bran cleanse, search under this term at www.knowledgeofhealth.com )
http://www.lewrockwell.com/sardi/sardi69.html
http://knowledgeofhealth.com/the-man-who-cured-heart-disease-with-a-natural-molecule-20-years-before-cholesterol-drugs/
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