Discussions that mention gemfibrozil

High Cholesterol board

Hi Lenin,

Now that I am home, I can finish with where I was going--and that relates more to what you were asking.

I think the breakdown from adipose tissue, where FFAs are removed is done so by VLDL and HDL, but I need to look a bit further to find out if I understood that correctly. I wanted to mention something about the HmG-CoA reductase inhibitors, and how it affects the whole pathway to squalene, then cholesterol formation...I did, at least, mention the high levels of squalene and cholesterol on the skin. Now, wouldn't it be even more bizarre if the relative composition of skin acids correlated well with the fatty acid intake? Perhaps I should write a NIH grant to.... Back to the subject

I am pulling the following info from a bunch of sources, and if you want a specific one later, just let me know:

Plasma lipid concentrations are impacted by the amount and type of fats (no surprise there). The amount of fat directly relates to amount of CMs in the blood. The problem with our Western diet is that we consume so many fats that the CM remnants are found at high level, and these are atherogenic and promote thrombosis. Liquidprofiler corrected me in that the clearance of TG from CMs does take more than the 4-6 hrs as originally thought--again, this is probably a product of the high level of fats ingested as well as slow clearance...and this is even moreso true in hypertriglyceridaemic people...yet again, back to fat types...

Sat Fats--Here was the surprising fact to me--> Among sat fats, not all sat fats are metabolized and affect the lipoproteins equally. Sat fats result in LDL elevations and are thrombogenic. In the mid 80s, a couple of manuscripts by Brown and Goldstein showed that the effect of sat fats was to influence the liver's LDL receptors, decreasing their synthesis-->decreases LDL removal-->increases LDL in the blood. Even though I mentioned that little dietary cholesterol effects are noted, it seems that I was wrong (in part). Apparently, when you combine this effect of sat fats with dietary intake of cholesterol, the LDL receptor was further reduced, and again, greater plasma LDL concentration results.

Some of these fats also result in an increased synthesis of LDL by the liver, e.g. coconut oil. That is too bad, because I love coconut--> Mounds bars, coconut cakes for my birthday. Anyway, as you can see I am getting hungry.

You brought up stearic acid (C18:0) so..that actually was found to have a neutral effect on plasma lipid levels, as was C8:0, and C10:0 acids. It was lauric (C12:0), myristic (C14:0), and palmitic (C16:0) that increased the levels. Goodbye Mounds bars (loads of C12,C14)... Oh, those C8 and C10 acids are water soluble, and the body handles them like carbs rather than fats. I don't know, at this time, which foods contain more of those than others. BUT, I do know where to get that information!!! It's available in the USDA nutritent database, through the government site. Butter: C14,16,18, Palm oil is C16...you get the drift--but note, C16:0 is the most common sat fat in our foods! I won't get into trans fats, but sat fats won't impact Lp(a) like trans will, and trans will, without any doubt, elevate the plasma lipids.

Monounsat acids, of which oleic acid (C18:1) that I mentioned this morning as a skin emanation, is a omega-9 and the only significant dietary monounsat. fatty acid. In general the effects of these acids on lipid profiles is neutral, but they do lower the levels more than sat fats--not sure that made sense? It's a comparison thing, not an absolute thing. In other words, if you took in no fats, there would be no elevation, etc. Mono, unlike poly, did not lower HDL levels, also.

Now, I mentioned this before, in relation to its impact upon CETP, but w-3 fish oils (these are actually polyunsats-- C20:5)m these monounsat fats do not improve plasma TG levels. Omega-3s are also antithrombotic, but that is a discussion for another time, another day. We could go into the Mediterranean diet too, and some other facts about it, but let us leave that alone for now too.

Polyunsat acids are only obtainable from dietary intake, but necessary to make cellular membranes and prostaglandins. The most common are the omega-6 (like linoleic, C18:2) that I mentioned above, and arachadonic acid (C20:4). Linoleic is converted to the latter above by the liver. I will leave the discussion of EPA/DHA out for now (fish oils) out for now for the same reason as I wrote above in the monounsat section. Besides, you already know about those effects well ;)

Large intakes of these acids reduce LDL in normal and hypercholesterolaemic people, but this is different than hypertriglyceridaemic or combined hypercholesterolaemic individuals (oops, I fit here...or once did I should say). Again, only omega 3s help the hypertriglyceridaemia via lowering VLDL levels (OK, and it accelerates liver catabolism of VLDL). In some people, though the LDL goes up as the measured plasma TG drops (type IV hypertriglyceridaemia) when fish oil is added, or gemfibrozil is added. Yet, in type V, there is a lowering of TG and lipid levels when 10-15g is added, per day. Yes, huge dose....fish oil promotes clearing the CMs after a fatty meal (perhaps this paper is hinting that we take our capsules with the meal??) Finally, there is not TG lowering from omega 6 vegetable oils.

But again, I am on a tangent.

Anyway, Lenin my friend, I hope you have a good weekend. Eat fish, take your capsules, and drink a few glasses of wine. I will check in from time to time, but I have to fly to D.C. on Monday and won't return until Friday.

Oh red wine, resveratol, antioxidants. If one is concerned about blocking CETP to increase HDL, then it does not matter if the wine is red or white, or for that matter, what form the alcohol comes in. The benefit comes to those who drink moderately, which if not mistaken from the gram conversion, translates to 3/4 a bottle of a wine. As I was saying, raise a few glasses...if that is your thing.

Now, who rambles?? ;)