[coldfire]

פורסם במקור על ידי m0she

מתוך מטה אנליזה על 90,000 נבדקים ב14 מחקרים שונים על סטטינים (1):

Statin therapy can safely reduce the 5-year incidence of major coronary events, coronary
revascularisation, and stroke by about one fifth per mmol/L reduction in LDL cholesterol, largely irrespective of the initial lipid profile or other presenting characteristics. The absolute benefit relates chiefly to an individual’s absolute risk of such events and to the absolute reduction in LDL cholesterol achieved. These findings reinforce the need to consider prolonged statin treatment with substantial LDL cholesterol reductions in all patients at high risk of any type of major vascular event.

בנוגע לאומגה 3 יש לך cofounder הוא האומגה 3 עצמו. הוא מעלה LDL אבל יש לו אפקטים רבים אחרים (למשל אנטי דלקתיים ואנטי קרישתיים) שמאפשרים לו להיות מועיל למרות שהוא גרם לעליה קצרה בLDL.

מתוך סקירה של הפתוגנזה של אתרוסקלרוזיס (2):

In patients with hypercholesterolemia, excess LDL infiltrates the artery and is retained in the intima, particularly at sites of hemodynamic strain. Oxidative and enzymatic modifications lead to the release of inflammatory lipids that induce endothelial cells to express leukocyte adhesion molecules. The modified LDL particles are taken up by scavenger receptors of macrophages, which evolve into foam cells.

אפשר להמשיך אבל זה חסר פואנטה, אתה מחפש בנרות מחקרים שאתה לא יודע לקרוא ומתווכח סתם. תקרא בעיון על הפתוגנזה של אתרוסקלרוזיס, על המרכיב הדלקתי שהLDL משפעל ותחזור אליי.

1. 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: 1267–78
2. Inflammation, Atherosclerosis, and Coronary Artery Disease. N Engl J Med. 2005 Apr 21;352(16):1685-95

אין וויכוח ש statins עוזרים במניעת מחלות לב. אבל זה לא בגלל השפעות על LDL:

Statins reverse or impede the progression of atherosclerosis in
rabbits, without any accompanying change in serum cholesterol.
59
Kano H, Hayashi T, Sumi D, et al. A HMG-CoA reductase inhibitor
improved regression of atherosclerosis in the rabbit aorta without
affecting serum lipid levels: possible relevance of up-regulation of
endothelial NO synthase mRNA. Biochem Biophys Res Commun
1999;259:414-419.
60
Soma MR, Donetti E, Parolini C, et al. HMG CoA reductase inhibitors: in
vivo effects on carotid intimal thickening in normocholesterolemic rabbits.
Arterioscler Thromb Vasc Biol 1993;13:571-578.

Improvements in arterial function: In elderly diabetic patients,
cerivastatin increased dilation of the brachial artery (improved
blood flow) after only three days, before any change in cholesterol
61
levels had occurred. In healthy young males with normal
cholesterol levels, improved endothelial function was observed
within 24 hours of treatment with atorvastatin; again, this
62
improvement preceded any drop in serum cholesterol levels.
61
Tsunekawa T, Hayashi T, Kano H, et al. Cerivastatin, a
hydroxymethylglutaryl coenzyme a reductase inhibitor, improves
endothelial function in elderly diabetic patients within three days.
Circulation 2001;104:376.
62
Laufs U, Wassmann S, Hilgers S, et al. Rapid effects on vascular function
after initiation and withdrawal of atorvastatin in healthy,
noncholesterolemic men. Am J Cardiol 2001;88:1306-1307.


Longer-term improvements in arterial function: In human
volunteers with slightly elevated cholesterol, researchers found
that 4 weeks of simvastatin therapy significantly enhanced forearm
blood flow. The improvement increased with continued
administration of simvastatin despite no further reduction in serum
cholesterol, and there was no relation between the decrease in
63
cholesterol and improvement in endothelial function.
63
O’Driscoll G, Green D, Taylor RR. Simvastatin, an HMG-coenzyme a
reductase inhibitor, improves endothelial function within one month.
Circulation 1997;95:1126-1131.

Anti-clotting effects: Statins have been shown to reduce
platelet production of thromboxane, an eicosanoid that encourages
blood clotting. This effect was not seen with older drugs that
lowered total or LDL cholesterol such as cholestyramine,
64
cholestipol, and fibrates. Puccetti et al. observed that simvastatin,
atorvastatin, and fluvastatin reduced platelet reactivity before
significant reductions in LDL cholesterol occurred.65,66
64
Schror K. Platelet reactivity and arachidonic acid metabolism in type II
hyperlipoproteinaemia and its modification by cholesterol-lowering
agents. Eicosanoids 1990;3:67-73.
65
Puccetti L, Pasqui AL, Pastorelli M, et al. Time-dependent effect of statins
on platelet function in hypercholesterolaemia. Eur J Clin Invest
2002;32:901-908.
66
Puccetti L, Sawamura T, Pasqui AL, et al. Atorvastatin reduces platelet-
oxidized-LDL receptor expression in hypercholesterolaemic patients. Eur
J Clin Invest 2005;35:47-51.

In humans, statin therapy produces significant reductions in C-
reactive protein, a marker of inflammatory activity that has
repeatedly been associated with increased cardiovascular risk. This
statin-induced reduction in CRP levels is not correlated with any
68-71
decrease in LDL cholesterol levels.
68
Ridker PM, Rifai N, Pfeffer MA, et al. Long-term effects of pravastatin on
plasma concentration of C-reactive protein. Circulation 1999;100:230-
235.
69
Albert MA, Danielson E, Rifai N, et al. Effect of statin therapy on C-reactive
protein levels: the Pravastatin Inflammation/CRP Evaluation (PRINCE):
randomized trial and cohort study. JAMA 2001;286:64-70.
70
Jialal I, Stein D, Balis D, et al. Effect of hydroxymethyl glutaryl coenzyme A
reductase inhibitor therapy on high sensitive C-reactive protein levels.
Circulation 2001;103:1933-1935.
71
Plenge JK, Hernandez TL, Weil KM, et al. Simvastatin lowers C-reactive
protein within 14 days: an effect independent of low-density lipoprotein
cholesterol reduction. Circulation 2002;106:1447-1452.

The numerous actions of statins unrelated to lipid lowering are
no doubt a major reason why almost all of the major controlled,
randomized trials with these drugs have shown no association
between the degree of total or LDL cholesterol lowering and the
50, 88-92
CHD survival rate. In most of these studies, the risk of a fatal
heart attack was similarly reduced whether total or LDL cholesterol
levels were lowered by a small or large amount.
88
Sacks FM, Pfeffer MA, Moye LA, et al. The effect of pravastatin on coronary
events after myocardial infarction in patients with average cholesterol
levels. N Engl J Med 1996;335:1001-1009.
89
Sacks FM, Moye LA, Davis BR, et al. Relationship between plasma LDL
concentrations during treatment with pravastatin and recurrent coronary
events in the Cholesterol and Recurrent Events Trial. Circulation
1998;97:1446-1452.
90
The Long-Term Intervention with Pravastatin In Ischaemic Disease (LIPID)
Study Group. Prevention of cardiovascular events and death with
pravastatin in patients with coronary heart disease and a broad range of
initial cholesterol levels. N Engl J Med 1998;339:1349-1357.
91
Heart Protection Study Collaborative Group. MRC/BHF Heart Protection
Study of cholesterol lowering with simvastatin in 20,536 high risk
individuals: a randomized, placebo-controlled trial. Lancet 2002;360:7-22.
92
Ravnskov U. Implications of 4S evidence on baseline lipid levels. Lancet
1995;346:181.

שוב, אני יכול להמשיך.

לגבי האומגה-3, אתה בעצמך אמרת כגרע שיש לו אפקטיים אנטי דלקתיים למרות שהוא מעלה את ה LDL. יש מצב שזה אומר ש LDL הוא לא מה שגורם ישיר לדלקות ומחלות לב?

משעשע שאתה מביא לי ציטוטים על אנשים עם בעיה גנטית נדירה.

אבל אתה רופא, אז אתה תמיד צודק. כי אתה יודע לקרוא מאמרים ואחרים לא.