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    Old 11-26-2003, 04:03 PM   #16
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    Re: Fish Oil*Friend or Foe?

    Continuing with the previous post .......

    Conveniently enough, chylomicrons contain cholesterol and lecithin. This brings up another inaccuracy in the link offered on this thread. There is no exchange of apolipoproteins between HDL and VLDLs or chylomicrons. Rather, there is an interaction so the apolipoproteins in HDL can act on cholesterol and phospholipids in chylomicrons and VLDL remnants. If anything, there is a "transfer" of cargo (through the action of LCAT) and the nascent HDL becomes a mature HDL particle carrying cholesteryl esters. The mature HDL, now rich in cholesterol returns to the liver, where cholesterol is unloaded and where some of it is converted into bile salts.

    From all this, it's easy to see why VLDLs, triglycerides and LDL levels are decreased on a carbohydrate restricted diet. The increase in HDL levels are not explained that easily, particularly because there is more than one HDL subtype.

    And here is more along the same lines where Orion responded in the same thread regarding dietary fats:

    Remember the sequence of events from the ingestion of dietary fats. Dietary lipids pose a special problem for the digestive process because of their insolubility in water. Their digestion begins with their emulsification by bile salts and bile phospholipids. A specialized enzyme in the small intestine takes care of neutral fats. What results from all this process are mainly fatty acids, monoglycerides, glycerol, cholesterol and phosphate. Now, those products need to be transported where they're needed. To do that, the cells in the intestinal epithelium re-pack them into triglycerides (cholesterol is not re-packed into anything but added to the carbo as it is). The "re-packing" process involves the making of chylomicrons, which will transport triglycerides and cholesterol through the lymph system and to the blood. You could think of this as a "delivery" system. Chylomicrons "deliver" or "unload" triglycerides on tissues like fat cells, heart and skeletal muscle. Of course, the size of chylomicrons decreases because they don't have much cargo to transport. Those chylomicron remnants end up in the liver as it was described in my previous post. Chylomicron remnants still contain some triglycerides and cholesterol and that is taken up by the liver. At this point, there is no LDL to talk about.

    LDL (as well as VLDL) transports triglycerides, cholesterol and phospholipids from the liver to other tissues. Chylomicrons, on the other hand, transport triglycerides, cholesterol and other lipids from the intestine to the tissues before ending up in the liver. In other words, LDL transports endogenous lipids, whereas chylomicrons transport dietary ones.

    The first lipoproteins made to transport endogenous lipids is VLDLs (in the liver), which are rich in triglycerides and don't contain much free cholesterol but more cholesterol ester. If we ought to talk about relative abundance, then triglycerides will be the main component, then phospholipids (licithin perhaps), then cholesterol ester, then free cholesterol, and then of course a minute amount of their characteristic apolipoproteins, B-100, C-III, E, and C-II (in comparison with the amount of lipids). VLDLs then move around delivering triglycerides to tissues. Those tissues where triglycerides are delivered are equipped with a specialized enzyme that brakes them so what the cells really take up are fatty acids. When triglycerides contained in VLDLs are degraded, these lipoproteins change their density and become a more "intermediate" density particles (rightly named ILDLs but I didn't mentioned that before to avoid more confusion), before becoming LDLs. When ILDLs have lost almost all their triglycerides, they become cholesterol-rich lipoproteins, with little triglyceride content, more cholesterol ester, indeed mature LDL particles. LDLs now are the delivery system for cholesterol to the tissues. It's a relatively small particle compared to VLDL, so in case you're wondering why is not VLDL the one that delivers cholesterol, size is a problem! The protein B-100 in LDL, which is now a smaller particle, is recognized by specific receptors (LDL-receptors) in the membranes of cells of extrahepatic tissues. This is very important becuase it ensures that it is LDL what's recognized and not chylomicrons, for example. Interestingly enough, and appropriately so, the liver has specific receptors for chylomicrons and that makes sure that chylomicron remnants end up there and not in the extrahepatic tissues. Nature is clever huh! So, continuing with the sequence of events, when LDLs are recognized by those cells that have LDL-receptors, the whole LDL-cholesterol particle is taken up and dealt with. LDL particles that are not taken up, may return to the liver where they are taken up by the same process and their contents recycled. The key, again, is to understand that LDL lipoproteins are the way endogenous lipids are transported. That means that their cargo has to be made somewhere in the body, and that somewhere is the liver.

    After this recap, we can go back to your questions, which starts with an important premise... if you keep your carbs low.... This actually means that there won't be much endogenous lipids being made, or endogenous cholesterol either. Cells, unless there is something wrong with their programming, don't normally waste energy in making things they don't need, and the synthesis of VLDLs is linked to the need of transport of lipids from the liver to the tissues. Under carbohydrate restriction, triglycerides decrease but that doesn't necessarily translate into less LDL, as many of us have seen with our own results. In fact, a recent study (published in Clinical Biochemistry) that analyzed the LDL profiles of diabetic and non-diabetic individuals, found at least seven different LDL "subclasses". Two of those represent the pattern "A" or large particles, and the other five represent the pattern "B" of small LDL particles, which are the ones associated with increase risk of coronary artery diseases. Probably, what would change more dramatically is the amount of VLDL, which contain more triglycerides, which in turn is what decreases dramatically under carbohydrate restriction (triglyceride synthesis is a reflection of carbohydrate metabolism, not fat metabolism).

    Now... and I left this bit to the end, you asked if the type of fat has some bearing in all this. The answer seems to be "yes". Just as not all fats are created equal, not all fats are used in the same way either. Mary Enig has described this in detail, and the simplest way to explain it is by saying that the length of the fatty acids has a lot to do with the way they're used. Thus, some fats will be more likely to be stored, and some other more likely to be used for heat production (some won't even go through the same oxidation process as long chain saturated fatty acids do, and they will produce more heat than a usable form of energy for the cells... ATP). There is an interesting study in rats, where the animals (which are normally prone to be obese) were fed a low calorie, high fat diet. Talk about confusion... how come something can be low calorie but high in fat? Well, what they did is to give 40% less calories to those rats, but more than 60% of those less calories came from saturated fat. Of course, those rats didn't become obese and adapted quite well to that kind of caloric restriction (which brings us back to the concept that a calorie is not a calorie, is not a calorie).

    So, all this fits very well into what we always like to repeat on this board. We don't care much about the amount of fat, but we do care about the quality of it because it won't be treated in the same way, and we an use that knowledge to tailor our food intake so we make the best of our adequate amount of protein and moderate amount of fat with the benefits of not too much carbohydrate around.


    To begin with, the link between fat and cholesterol may be the fact that cholesterol is made out of a very well known molecule: Acetyl-CoA. Fat metabolism produces Acetyl-CoA, therefore, fat metabolism leads to cholesterol and the more Acetyl-CoA is produced, the more cholesterol is made. Nothing could be more far from the truth. While it's true that Acetyl-CoA is the starting block in the synthesis of cholesterol, it is not true that only fat metabolism produces Acetyl-CoA. In fact, glucose metabolism also produces Acetyl-CoA, and when there is excess glucose being obtained from excess carbohydrates in the diet, the amount of Acetyl-CoA obtained from that is significantly higher. Moreover, the key regulatory enzyme in the synthesis of cholesterol is activated by insulin and inhibited by glucagon... and what insulin does to fat oxidation? It shuts it down. So, where is the link?

    In the clinic, the assumptions are different. The measurement of cholesterol in the clinic is based on the use of a formula, the Friedewald formula, and the clinical utility of such formula (which by the way goes back to 1972) is based on two assumptions, as explained by Sniderman et al (they published a review on the "Achilles heel" of the Friedewald formula). The first is explicit: assumes that the ratio of triglyceride to cholesterol in VLDLs is constant (which is not... see previous post). The second is implicit: assumes that LDL-cholesterol is the most accurate measure of risk related to LDL. Sniderman writes Both assumptions are demonstrably wrong and the errors that result are common and important and can lead to less than ideal clinical decision-making and clinical care.
    The tragedy of science is the slaying of a beautiful hypothesis by an ugly fact. T H Huxley

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    Old 11-26-2003, 06:51 PM   #17
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    Re: Fish Oil*Friend or Foe?

    Hmmm...Well, naturally I am inclined to agree.

    Old 11-27-2003, 05:32 AM   #18
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    Re: Fish Oil*Friend or Foe?

    Originally Posted by ARIZONA73
    Hmmm...Well, naturally I am inclined to agree.
    Me too. Which allows me to reiterate my worn out mantra about the calculated relationship of LDL to trigs being, at minimum, a huge compromise and more likely borders on ridiculous.

    Last edited by pcovers; 11-27-2003 at 05:33 AM.

    Old 11-27-2003, 05:47 AM   #19
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    Re: Fish Oil*Friend or Foe?

    In regards to LDL particle size, wouldn't you think that LDL which is predominantly Pattern A(large particles)would provide conditions that will favorably promote increased levels of HDL? This makes sense to me, since high triglycerides seem to be more strongly correlated with low HDL, and small LDL particle size. Niacin appears to clearly illustrate such an effect. It raises HDL, while simultaneously increasing LDL particle size. Statins don't even do that. So, does one have anything to do with the other, or is it merely a coincidence? I'm inclined to believe there may be a connection.

    Old 11-27-2003, 06:08 AM   #20
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    Re: Fish Oil*Friend or Foe?

    Thanks for that great reprint, pcovers. I've dropped it onto my desktop for a more "awake" reading later. It deserves several reads!
    It even touches on to my "problems" with low triglyceride readings on high fat diets.

    But then like all long articles advocating low-carb, some points will have me tearing my HAIR out:

    Well, what they did is to give 40% less calories to those rats, but more than 60% of those less calories came from saturated fat. Of course, those rats didn't become obese and adapted quite well to that kind of caloric restriction (which brings us back to the concept that a calorie is not a calorie, is not a calorie).
    Uhhhh....didn't she (Mary Enig) just illustrate that a calore IS a calorie IS a calorie?

    Ok at least we are all agreed: that odious cholesterol formula is nonsense and probably shouldn't be repeated.
    I for one am through with it and it shall never again pass my lips (well, fingers).

    A Happy Thanksgiving all. (Eat that L-tryptophan!)

    Last edited by zip2play; 11-27-2003 at 06:18 AM.

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