Friday, 18 May 2018

Is Lipid Level or Inflammation the Critical Factor for Cardiovascular Disease Risk?




re-posting from here

No orthodoxy lacks accompanying heretics; it often seems that science is a business of proceeding abruptly and messily from one steady state consensus to another via the mechanism of heresy. It is of course worth bearing in mind that most heretics do turn out to be wrong, and are consequently forgotten by all but the most painstaking of scientific historians. In the paper I'll point out today, the orthodoxy of blood lipid levels as a cause of cardiovascular disease is challenged. The heresy is to suggest that it isn't the lipids at all, but all down to a matter of chronic inflammation.
This is a tough topic to arbitrate, because raised lipids, such as cholesterol, and raised inflammation go hand in hand. Dietary approaches to tackling cholesterol levels are minimally effective in the grand scheme of things, as dietary content is only a small factor in the lipid content of blood, but they also, inconveniently, tend to move the needle on inflammation as well. The calorie content of the diet, considered over the long-term, is linked to lipids and inflammation in equal measures via the amount of visceral fat tissue an individual carries. Therapies that are available and widely used to reduce blood cholesterol, such as statins, are shown to have anti-inflammatory effects. Therapies under development, such as delivery of the APOA1 protein that makes up the HDL particles responsible for dragging cholesterol out of vulnerable cells and transporting it to the liver, also have significant anti-inflammatory effects. You can probably see the challenge.
On the one hand, it doesn't seem completely unreasonable to mount the argument that lipid levels are a smokescreen, and we should be caring about chronic inflammation. We know that chronic inflammation is very damaging, and contributes to the progression of all of the common age-related diseases. When it comes to cardiovascular disease, and particularly atherosclerosis, it seems hard to write off a role for lipid levels in blood, however. Atherosclerosis is caused by oxidized lipids that overwhelm the cells sent to clean them up when they irritate blood vessel walls; the fatty deposits that narrow blood vessels are made up of lipids and dead cells. More lipids means more overwhelmed cells. Lower lipid levels means fewer oxidized lipids. But does that simple calculus hold up when looked at in detail? To answer that question, we need more data on highly effective therapies that are either anti-lipid or anti-inflammatory, but not both.
Inflammation, not Cholesterol, Is a Cause of Chronic Disease

= = =

our answer:

In our work

In vivo anti-atherogenic properties of cultured gilthead sea bream (Sparus aurata) polar lipid extracts in hypercholesterolaemic rabbits

we have shown that fish polar lipids do not affect significantly levels of LDL but increase levels of HDL and  reduce atherosclerotic lesions.

The diets employed led to significant increases (day 45 vs. day 0) in TC, LDL-C, HDL-C and TAG concentrations in animals of both groups (Table 1). TC, LDL-C and TAG levels did not exhibit significant differences between groups A and B by day 45. On the other hand, HDL-C levels exhibited significant increase in group B compared to group A by day 45 (p < 0.05) (Table 1).
Table 1. Basic plasma lipid profile in rabbits of both groups.

Time (days)A (n = 6)B (n = 6)
TC (mg/dl)062 ± 2066 ± 18
451906 ± 821a1555 ± 122a
LDL-C (mg/dl)019 ± 167 ± 5
451707 ± 742a1300 ± 126a
HDL-C (mg/dl)029 ± 430 ± 7
4582 ± 26a,b138 ± 30a,b
TAG (mg/dl)0141 ± 49146 ± 66
45652 ± 316a588 ± 141a
Results are expressed as mean ± SD.
A: atherogenic diet; B: atherogenic diet enriched with GSBPL.
a
Denotes statistical significance within same group (day 45 vs. 0; p < 0.05), according to the Wilcoxon test.
b
Denotes statistical significance between groups A and B (day 45; p < 0.05), according to the Mann–Whitney U-test.


Fig. 1. Representative optic micrographs × 100 of aortic wall sections stained with haematoxylin and eosin from the two experimental groups, where atherosclerotic lesions appear as foam cells (). (A) Group A (atherogenic diet); (B) Group B (atherogenic diet enriched with GSBPL).

We can thus suggest that it is NOT the cholesterol but the anti-inflammatory impact of fish lipids.
We have further studied that here.

Fish polar lipids retard atherosclerosis in rabbits by down-regulating PAF biosynthesis and up-regulating PAF catabolism

 

 

  
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