Anyone who is interested in nutrition science must read above article, because it sheds light on good science that has been ignored by US dietary guidelines. 180 researchers & scientists from around the world, and their grad students, signed a letter trying to get this paper retracted, and it was a whole year-long battle. But ultimately, the paper survived, with exact corrections, but none of them affected any of the key allegations in the paper. And this paper has now been peer reviewed by pretty much everybody on the planet.
0 評論
Nutrition coalition shared a paper with me recently & I was surprised to find that current nutrition advise for familial hypercholesterolemia (FH) is evidence-free! I extracted the key points from above paper & pasted below:
Atherogenic dyslipidaemia risk triad: triglycerides, high-density lipoprotein (HDL) and small, dense LDL. LDL-C is contained in heterogeneous particles which range in size and composition from a small, dense, triglyceride (TG) rich LDL (sdLDL) to a large, buoyant, cholesterol-enriched LDL (lbLDL). This distinction between LDL particle subclasses is important because sdLDL, unlike lbLDL, is a component of an atherogenic dyslipidaemia risk triad (ADRT), composed of elevated levels of TGs and sdLDL, in conjunction with low levels of HDL.8–10 23 Each of the three components of the ADRT, individually, has been associated with increased risk of CHD. For example, sdLDL, unlike lbLDL, is a unique marker of CHD risk, independent of LDL-C.24 Another study demonstrated that FH individuals, distinguished solely on the basis of having high TGs (>200 mg/dL), exhibited three times greater occurrence of a myocardial infarction (MI), compared with FH individuals with low TGs (<200 mg/dL).25 It is noteworthy that the association of high levels of TGs in FH with a high rate of MI occurrence was independent of their LDL-C levels (figure 1). Overall, the ADRT is a highly reliable measure of CHD risk in FH, as well as non-FH, individuals. Lipoprotein a Lipoprotein a [Lp(a)] is one of the most robust of all markers of CHD risk in FH and non-FH populations.26 Lp(a) contains a plasminogen-like glycoprotein, known as apolipoprotein (a), which is bound to the apolipoprotein B-100 of an LDL particle. Elevated levels of Lp(a) are more closely associated with CHD than is LDL-C. For example, Seed et al,27 showed that FH individuals with CHD had significantly greater levels of Lp(a) compared with FH without CHD; the association of Lp(a) with CHD in FH was independent of their LDL-C levels (figure 2). Haemostatic balance between coagulation and fibrinolysis A powerful influence on the development of CHD is the interplay between processes that promote clot formation (coagulation) and those that cause clots to lyse (fibrinolysis). There is extensive evidence, at cellular, metabolic and genetic levels of analysis, that the haemostatic balance in FH is shifted toward hypercoagulation. These findings were reviewed by Ravnskov et al,18 who found strong evidence of hypercoagulation, and not LDL-C, as a cause of CHD in FH. A subset of the literature is provided below.
Non-lipid CHD risk factors FH individuals are as susceptible to non-lipid CHD risk factors as non-FH individuals. The following is a subset of the literature that has documented this finding:
This blog is going to be a bit technical & intended for health care professionals who want more in-depth information about biomarkers that predict cardiovascular risk.
Canadian guidelines have included Apo-B as a biomarker to predict CV risk along side LDL-C but the US is lagging behind for reasons that are not clear. Click the word "Apo-B" & see the document about the details. I also have some cartoons that explains biochemical structure of lipoproteins. Click the word "cartoon" to see them. |
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Eat animal fats
Don't fear fat. Eating saturated fat will not make you fat. Eating refined carbs will.