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Anyone?

Looking to defend my refusal to resume statins ... I am gonna stall with exercise, but am preparing a defense anyhow!
 

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Just got done seeing my doc. Did countless amount of blood work, including the NMR LipoProtein test, particule size. My LDL is still small and dense. He has another patient with the same problem, statins have not helped him at all in this regard. He said statins generally do nothing for the size of the LDL particules. SNL has been on a statin for years, exercises like he trying out for the olympics, and eats relatively low carb, his CHL is the same as mine and I do not take a statin. He is DT2 with the same garbage CHL as me.

I am doing the Linus Pauling Protocol to see if that changes anything.
 
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Nothing you can take with you, but my neighbor has been on statins for ever. He was put on them after his first heart attack, since then he has had 12 stents and a third heart attack which resulted in a quadruple by-pass, his CHL was magnificent after years of statins and niacin. A lot of good they did.
 

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Elsevier

Try this out for size, they say it is significant. I might consider significant if would take it from small and dense to all of it large and fluffy, but sadly its not the case.


Summary
Background and aim
Elevation of plasma cholesterol and/or triglycerides, and the prevalence of small dense low density lipoproteins (LDL) particles remarkably increase the risk in patients with familial combined hyperlipidemia (FCHL). There are, at present, inconsistent data on the effects of different treatments on size and density of LDL particles in FCHL patients.

Methods and results
A multicenter, randomized, double-blind, double-dummy, parallel group study was designed to evaluate the effect of 3 months' treatment with atorvastatin (10mg/day) or pravastatin (20mg/day) on the lipid/lipoprotein profile and LDL size in a total of 86 FCHL patients. Both statins significantly lowered plasma total and LDL cholesterol, with a significantly higher hypocholesterolemic effect observed with atorvastatin (−26.8±11.1% and −35.9±11.1%, respectively) compared to pravastatin (−17.6±11.1% and −24.5±10.2%). The percent decrease in plasma triglycerides was highly variable, but more pronounced with atorvastatin (−19.8±29.2%) than with pravastatin (−5.3±48.6%). Opposite changes in LDL size were seen with the 2 treatments, with increased mean LDL particle diameter with atorvastatin, and decreased diameter with pravastatin, and significant between treatment difference in terms of percent modification vs baseline (+0.5±1.6% with atorvastatin vs −0.3±1.8% with pravastatin).


http://www.sinoas.com/journal/UploadFiles/200706/20070626172205280.pdf

This one is worded funny at the end trying to show it has benefits but all its showing is it lowers CHL.

Abstract
Lipoprotein subclass analyses may facilitate coronary heart disease (CHD) risk stratification and provide insight into the
cardioprotective benefits of statins (3-hydroxymethylglutaryl-coenzyme A reductase inhibitors). This study evaluated the influence
of pravastatin on lipoprotein subclass profiles to determine whether subjects with predominantly large LDL (LDL size 20.5 nm)
or small LDL (LDL size 20.5 nm) at baseline differ in responsiveness to drug treatment. Frozen plasma specimens were
analyzed from a subset of participants in the Pravastatin Limitation of Atherosclerosis in the Coronaries (PLAC-I) trial at
baseline and after treatment for 6 months with pravastatin (n=154) or placebo (n=138). Lipids were measured by standard
chemical methods and lipoprotein subclasses by nuclear magnetic resonance (NMR) spectroscopy. Pravastatin-induced changes in
lipid levels were similar in subjects with large or small LDL at baseline. Levels of the most abundant LDL subclass were
preferentially lowered by pravastatin, resulting in an increase in average LDL size for those with a predominance of small LDL.

High-risk CHD subjects with small LDL particles gain at least as much pharmacological benefit from pravastatin as those with
large LDL, as evidenced by reductions in the numbers of total and small LDL particles, and increases in average LDL and HDL
particle size. © 2002 Elsevier Science Ireland Ltd. All rights reserved.

Keywords: Lipoprotein subclasses; Small LDL; HMG-CoA reductase inhibitors; CH

What its saying here is, it will lower LDL mostly small and dense, but if your body does not wants to make any Large and fluffy your S.O.L.
 
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It took a while but my MD finely admitted that of the people that take statins only a small number actually have a decrease in LDL and of those people only 5% actually see a reduction in hart disease.
 

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Not sure if this one was posted above but Lipid levels in patients hospitalized with coronary artery disease: An analysis of 136,905 hospitalizations in Get With The Guidelines...
Conclusions In a large cohort of patients hospitalized with CAD, almost half have admission LDL levels <100 mg/dL.
More than half the patients have admission HDL levels <40 mg/dL, whereas <10% have HDL ≥60 mg/dL. These findings may
provide further support for recent guideline revisions with even lower LDL goals and for developing effective treatments to raise
HDL.
So of course they miss the obvious that 50% of those admitted with CVD did NOT have raised LDL (although they did have lower HDL) but instead use it as rational to consider tightening the guidelines still further :frusty:

Meantime I noted this statement in the "Results"...
Predictors for higher LDL included female gender, no diabetes, history of hyperlipidemia, no prior lipid-lowering medications, and presenting with acute coronary syndrome.
Chicken and egg? Maybe women are supposed to have raised cholesterol levels in response to underlying CVD/inflammation or whatever else may be going on?

But of course if you observe lots of fire-fighters around house-fires, the obvious conclusion is that by getting rid of fire-fighters you will reduce the number of house-fires :target:
 
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