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    Old 11-23-2003, 07:29 AM   #1
    jerry78
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    Fish Oil*Friend or Foe?

    It is a known fact that fish oil supplements, in the correct daily doses, can indeed lower triglycerides; however, did you know that there are studies that show they can also INCREASE the levels of LDL?

    So, what is the current thinking on this? Which is worse: High TRi's or high LDL ?

     
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    Old 11-23-2003, 07:40 AM   #2
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    Re: Fish Oil*Friend or Foe?

    Probably high triglycerides. At least, that's my opinion.

     
    Old 11-23-2003, 08:07 AM   #3
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    Re: Fish Oil*Friend or Foe?

    Quote:
    Originally Posted by jerry78
    It is a known fact that fish oil supplements, in the correct daily doses, can indeed lower triglycerides; however, did you know that there are studies that show they can also INCREASE the levels of LDL?

    So, what is the current thinking on this? Which is worse: High TRi's or high LDL ?
    aaaarrrrrgggghhhhh!!!!!! (amidst images of me pulling my hair out)

    Using the means by which 99% of all lipid profiles numbers are determined, the rule, not the exception, but the rule states that if trigs go down ldl goes up. No wonder studies would show this. Thre is nothing else hey could possibly show except this. Simple math:

    LDL=TC(minus)HDL(minus)(Trigs/5)

    Anyway you look at it, if trigs go down, ldl goes up. So, it would be a correct statement to say that if fish oil reduces trigs, all else being equal, ldl will of a certainty go up. The real question is, what does it matter given how ldl is determined.

    Last edited by pcovers; 11-23-2003 at 08:09 AM.

     
    Old 11-23-2003, 08:14 AM   #4
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    Re: Fish Oil*Friend or Foe?

    Hmm, jerry,

    My first thought was to dismiss your claim but after a little snooping I am forced to agree with you.

    Quote:
    Effects of dietary saturated, monounsaturated and n*3 fatty acids on fasting lipoproteins, LDL size and post*prandial lipid metabolism in healthy subjects.

    Rivellese AA, Maffettone A, Vessby B, Uusitupa M, Hermansen K, Berglund L, Louheranta A, Meyer BJ, Riccardi G.

    Department of Clinical and Experimental Medicine, School of Medicine, Federico II University, Via S. Pansini 5, 80131 Naples, Italy. [email][email protected][/email]

    BACKGROUND: The influence of the quality of dietary fat on some aspects of lipid metabolism*i.e. lipoprotein concentrations, post*prandial lipids and LDL size*is not completely understood, especially in healthy individuals. OBJECTIVES: Aim of this study was to evaluate the effects of different types of dietary fat (monounsaturated vs. saturated fatty acids, and n*3 or placebo supplementation) on fasting lipoproteins, LDL size and post*prandial lipids in healthy people. DESIGN: One hundred and sixty*two individuals were randomly assigned to follow two isoenergetic diets, one rich in saturated fatty acids (SFA diet) and the other in monounsaturated fatty acids (MUFA diet). Each group was further randomised to receive supplementation with fish oil (3.6 g/day) or placebo. RESULTS: The type of diet significantly affected LDL cholesterol and triacylglycerol content, which was higher with the SFA diet and lower with the MUFA diet. The changes between the two diets were statistically significant for cholesterol (P<0.01) and triacylglycerol (P<0.03). VLDL cholesterol and triacylglycerol were significantly reduced and LDL cholesterol significantly increased by fish oil supplementation. Plasma triacylglycerol was significantly lower in those taking n*3 fatty acids, also 1 and 3 h after a test*meal. Neither type of diet nor n*3 supplementation affected LDL size. CONCLUSIONS: A moderate substitution of saturated fatty acids with monounsaturated fatty acids has beneficial effects on lipid metabolism also in healthy individuals. A moderate supplementation of long*chain n*3 fatty acids in healthy individuals reduces both fasting and post*prandial triacylglycerol concentrations but increases LDL cholesterol, irrespective of the type of diet.

    PMID: 12618280 [PubMed * indexed for MEDLINE]
    sorry, I couldn;t just give a link....the linking seems to be more tightly curtailed the last couple days.
    ps......those n*3's are Omega 3 oils.

    Last edited by zip2play; 11-23-2003 at 08:15 AM.

     
    Old 11-23-2003, 11:30 AM   #5
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    Re: Fish Oil*Friend or Foe?

    Quote:
    Originally Posted by pcovers
    aaaarrrrrgggghhhhh!!!!!! (amidst images of me pulling my hair out)

    Using the means by which 99% of all lipid profiles numbers are determined, the rule, not the exception, but the rule states that if trigs go down ldl goes up. No wonder studies would show this. Thre is nothing else hey could possibly show except this. Simple math:

    LDL=TC(minus)HDL(minus)(Trigs/5)

    Anyway you look at it, if trigs go down, ldl goes up. So, it would be a correct statement to say that if fish oil reduces trigs, all else being equal, ldl will of a certainty go up. The real question is, what does it matter given how ldl is determined.

    Pcovers:
    I hear what you are saying; however, the formula is not the only way to calculate LDL. There is a blood test called DIRECT MEASURE LDL, and I'm not sure, but I would think that in these studies, the researchers would be more inclined to utilize the direct measure method.
    By the way, a direct LDL measure is also available at any high-tech hospital blood lab, it is just a matter of you physician requesting it on your lipid lab script.

     
    Old 11-23-2003, 12:19 PM   #6
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    Re: Fish Oil*Friend or Foe?

    This throws a monkey wrench into my plans to lower both triglycerides and LDL by taking fish oil supplements. It is more important to me to get my LDL down as my triglycerides are barely over the norm.

    These patients were on a diet rich in saturated fat. A change in diet to lower saturated fat intake at the same time will effect a decrease in LDL.
    ----------------------------------------------------------------------------

    Effects of Omega-3 Fatty Acids and Lipoproteins
    The addition of omega-3 fatty acids to the diet lowers triglyceride levels, an effect that is pronounced in those with marked hypertriglyceridemia.3 The triglyceride-lowering effect is not seen with plant sources of n-3 PUFA.4 In those patients with type V hyperlipidemia, the use of fish oil supplements is an important therapeutic option.5 Connor6 listed the following putative mechanisms of dietary n-3 PUFA on lipoprotein metabolism in humans: (1) inhibition of VLDL triglyceride synthesis, (2) decreased apoprotein B synthesis, (3) enhancement of VLDL turnover with an increased fractional catabolic rate of VLDL, (4) depression of LDL synthesis, and (5) reduction of postprandial lipemia.

    A critical review by Harris2 has clarified the discrepancy among fish oil studies reporting effects on LDL cholesterol (LDL-C). He noted that in the majority of studies reporting reductions in LDL-C levels, the saturated fat intake was lowered when subjects switched from the control diet to the fish oil diet. When fish oil is consumed and saturated fat intake is constant, LDL-C levels either do not change or may increase.

    Although fish oil is not recommended in the treatment of hypercholesterolemia, it does have a role in the treatment of lipoprotein disorders characterized by severe hypertriglyceridemia. It can be quite useful in those severely hypertriglyceridemic (triglyceride >1000 mg/dL) patients for whom attempts to correct secondary causes (through diet, exercise, and gemfibrozil) have proved inadequate.7 Although a negative aspect is the concomitant elevation in LDL-C that occurs when fish oils are given to these patients with lower plasma levels of triglyceride, this is usually not a problem for those with severe hypertriglyceridemia, because LDL-C values are usually quite low. It can be a problem for those with more modest elevations of triglycerides in whom the elevation of LDL-C will actually move the patient away from the desired LDL-C goal.

    Last edited by JacquelineL; 11-23-2003 at 03:30 PM.

     
    Old 11-23-2003, 01:09 PM   #7
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    Re: Fish Oil*Friend or Foe?

    I think that an elevated triglyceride level poses a significant risk, since it contributes towards LDL as VLDL. This can result in a shift in LDL particle size towards that of Pattern B, a predominantly smaller particle size which carries significantly higher risk. While we all have LDL which is composed of varying particle sizes, some people are predominantly Pattern A (large particle size), while others may be Pattern B. It has been said that Pattern B can carry as much as 3 times the risk as Pattern A. That tells me that someone who is Pattern B and has an LDL of 70 may carry as much risk as someone else who has an LDL of 210, but is Pattern A. Generally speaking, Pattern A is more strongly correlated with high HDL and low triglycerides, while Pattern B is more common with low HDL and high triglycerides. But a calculated LDL tells us essentially nothing. A measured LDL provides a much clearer picture of actual risk.

     
    Old 11-24-2003, 05:57 AM   #8
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    Re: Fish Oil*Friend or Foe?

    Quote:
    Originally Posted by ARIZONA73
    But a calculated LDL tells us essentially nothing. A measured LDL provides a much clearer picture of actual risk.
    I have been thinking about this for several months and have come to the conclusion that you have hit the nail SQUARE on the head, Arizona.
    Back in the dark ages they got themselves a way to easily measure CHOLESTEROL. But then they found that there are several components to it such as HDL and LDL....hmmm but these didn't add up so they threw in triglycerides as a fudge factor....oops tpoo high, but if we divide by 5, hmmmm.

    OK, so now they had a first approximation analysis. BUT then turning it backwards (as if it could be dealt with in pure numbers like A +B =C) to determine LDL by working in the TRI/5 is pure hokum.

    In your bloodstream there are PARTICLES of LDL....if your vision was good enough you'd SEE them. Adding some extra triglyceride molecules won't make these particles of matter disappear, only SEEM to disappear on paper because the "equation" fiddling is bad science.

    So for several weeks now, everytime I saw LDL = TC - HDL -(T/5) my eyes just glazed over


    This same line of reasoning goes to VLDL's as well....they are VERY REAL MOLECULES: triglycerides/5 is NOT REAL just a convenience that's probably CHEAPER to measure.

    Last edited by zip2play; 11-24-2003 at 06:01 AM.

     
    Old 11-24-2003, 08:25 PM   #9
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    Re: Fish Oil*Friend or Foe?

    Quote:
    Originally Posted by pcovers
    Using the means by which 99% of all lipid profiles numbers are determined, the rule, not the exception, but the rule states that if trigs go down ldl goes up. No wonder studies would show this. Thre is nothing else hey could possibly show except this. Simple math:

    LDL=TC(minus)HDL(minus)(Trigs/5)

    Anyway you look at it, if trigs go down, ldl goes up...
    I've seen that statement made before, but I don't see how you can come to that conclusion by just looking at a simple mathematical equation. The equation doesn't mean that if triglycerides go down that LDL must go up. HDL and total cholesterol can also change resulting in no direct correlation between LDL and triglycerides. And no studies that I am aware of support this statement either. Now LDL particle size and triglycerides are closely related, but not the total amount of LDL.

    The LDL equation starts with the following equation:

    Total Cholesterol = HDL + LDL + VLDL

    Solving for LDL and substituting trig/5 for VLDL results in the common form of the equation shown above:

    LDL = Total Cholesterol - HDL - triglycerides/5.

    This equation is just used as a convienence and cost saving measure since LDL is more difficult to directly measure than the total or any of the other subcomponents.

    As an example, if triglycerides went down 50 points and HDL went up 10 points and total cholesterol remained unchanged, then the LDL number would not change. And this is a fairly common response to a low carbohydrate diet (reduces triglyceride levels) that includes plenty of red meat and animal fats (natural saturated fat promotes elevated HDL levels).

    Back to the LDL particle size and triglyceride connection. I have read several study abstracts on Medline and other sources that show a close correlation between low triglyceride levels (in general <100 mg/dl) and the predominate LDL particle size being the larger pattern A which is not considered harmful. And high triglyceride levels have been shown to be strongly associated with the predominate LDL size being the smaller denser pattern B with is highly subject to oxidation and most often associated with atherosclerosis. This may be related to what is happening with the fish oil/triglycerides/LDL studies. Anyone note the LDL particle size associated with the fish oil supplementation?
    __________________
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    Last edited by arkie6; 11-24-2003 at 08:34 PM.

     
    Old 11-25-2003, 05:03 AM   #10
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    Re: Fish Oil*Friend or Foe?

    Quote:
    Originally Posted by arkie6
    I've seen that statement made before, but I don't see how you can come to that conclusion by just looking at a simple mathematical equation. The equation doesn't mean that if triglycerides go down that LDL must go up. HDL and total cholesterol can also change resulting in no direct correlation between LDL and triglycerides.
    I think one reason for your confusion over my position is that you left out the key qualifying statement I made. To restate, I said:

    So, it would be a correct statement to say that if fish oil reduces trigs, all else being equal, ldl will of a certainty go up.

    I am not saying that ldl will go up in reality, I am stating that using the accepted equation for determining calculated ldl, the number reported to doctor and patient for LDL will be higher. I say, "all else being equal" because we can play if's and but's all day with TC and HDL. If HDL goes up, if TC goes down, if this or if that occurs. The bottom line remains the same, if HDL and TC remains the same (that is the "all else being equal" part) and trigs goes down, calculated LDL goes up...and this seems to be an odd notion that to lower trigs will necessarily cause ldl to increase.

    Last edited by pcovers; 11-25-2003 at 05:09 AM.

     
    Old 11-25-2003, 06:45 AM   #11
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    Re: Fish Oil*Friend or Foe?

    Total cholesterol is cheaply measurable; HDL is cheaply measurable; thus TC/HDL is a valuable and accurate marker for the health of the blood-lipid stream.
    Triglycerides are easily measurable but are not really lipoproteins (cholesterol- protein-glyceride complexes).
    They have a distinct value taken alone.

    But apparently LDL and even more pointedly VLDL are expensive to measure and most useful only for lab work and the Triglycerides/5 is a fudge factor to give the measurables, TC and HDL, some (cheaply measured) relationship to one another.

    TC measures total cholesterol and it was measured for half a century before the other components even had names. Thus TC = TC and little else. The TC = HDL + LDL + VLDL is just not a fact, and VLDL = TRI/5 is preposterous on it's face!


    Scientists LOVE grand unifying theory even if it flies in the face of reality! Gee I wonder what genius invented the "5" fudge factor...maybe he saw a miniscule 5 under an electron microscope?....maybe it's ok, string theory had 20 or more fudge factors (but then they fixed it)...
    Lots of this haze will go away when they FINALLY start measuring and reporting actual LDL for our blood tests. Then everything will be as it really is and there will be no need for first approximation "equations." Just dealing with TC, HDL, LDL, and Tris all as measure will be REAL....and get "realer" if they add a measured VLDL.

    At that point those who may want to continue dividing Triglycerides by 5, or 9, or 11.7 for themselves will be free to do so without messing up all our lab printouts with hokum.

    Last edited by zip2play; 11-25-2003 at 07:07 AM.

     
    Old 11-25-2003, 09:41 AM   #12
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    Re: Fish Oil*Friend or Foe?

    Quote:
    Originally Posted by zip2play
    Total cholesterol is cheaply measurable; HDL is cheaply measurable; thus TC/HDL is a valuable and accurate marker for the health of the blood-lipid stream.
    Triglycerides are easily measurable but are not really lipoproteins (cholesterol- protein-glyceride complexes).
    They have a distinct value taken alone.

    But apparently LDL and even more pointedly VLDL are expensive to measure and most useful only for lab work and the Triglycerides/5 is a fudge factor to give the measurables, TC and HDL, some (cheaply measured) relationship to one another.

    TC measures total cholesterol and it was measured for half a century before the other components even had names. Thus TC = TC and little else. The TC = HDL + LDL + VLDL is just not a fact, and VLDL = TRI/5 is preposterous on it's face!


    Scientists LOVE grand unifying theory even if it flies in the face of reality! Gee I wonder what genius invented the "5" fudge factor...maybe he saw a miniscule 5 under an electron microscope?....maybe it's ok, string theory had 20 or more fudge factors (but then they fixed it)...
    Lots of this haze will go away when they FINALLY start measuring and reporting actual LDL for our blood tests. Then everything will be as it really is and there will be no need for first approximation "equations." Just dealing with TC, HDL, LDL, and Tris all as measure will be REAL....and get "realer" if they add a measured VLDL.

    At that point those who may want to continue dividing Triglycerides by 5, or 9, or 11.7 for themselves will be free to do so without messing up all our lab printouts
    with hokum.

    In my opinion on all this, I would say have a direct measure of LDL performed on your lipid panel before you even think about popping fish oil pills to lower Tri's.
    Then, if your direct measure LDL is in a favorable range, there would be no problem on a low Tri level affecting a calculated measure.

     
    Old 11-25-2003, 12:42 PM   #13
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    Re: Fish Oil*Friend or Foe?

    Here's some information regarding the increased risk associated with small LDL particle size, and its relationship to elevated triglycerides. I believe this supports the argument that LDL should me measured instead of merely calculated, and a particle size assessment should be determined. I think that niacin is an invaluable cardiovascular supplement that not only increases HDL levels, but increases LDL particle size as well. The addition of fish oil can help lower triglycerides, and further reduce the risk of heart attack. Together, they appear to be a formidable one-two punch.
    [url]http://www.lbl.gov/Science-Articles/Archive/cholesterol-particles.html[/url]

     
    Old 11-26-2003, 06:39 AM   #14
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    Re: Fish Oil*Friend or Foe?

    I am hazy on the small, dense LDL:
    Quote:
    LBL scientists were the first to establish a link between a predominance of smaller, denser LDL particles and heart disease. The researchers matched 312 of the subjects who had heart attacks during a 7 1/2 year period by age and smoking status with 312 health control subjects.

    The researchers then determined each person's LDL particle-size profile and divided the subjects into five groups (quintiles). The lowest quintile--those with the smallest and most dense LDL particles--had more than three times the risk of heart attack as the quintile with the largest LDL particles.
    Is there a continuous spectrum where LDL becomes denser and denser and then becomes HDL (perhaps low-density HDL?)
    Or are LDL and HDL different in kind.
    If a continuous spectrum, one might think that increasing density (and/or decreasing size) is a GOOD thing.
    But the evidence that high density LDL is the very worst kind proves that untrue.
    Can anybody shed some light?

    And running with Arizona's lateral pass , since fish oils have been seen to decrease arterial disease, maybe what Omega-3's are doing is to increase LDL, but primarily the larger, less dense fraction, those with the least deleterious effect.
    I guess though, with the paucity of evidence we shouldn't attempt TOO many conclusions until we all get labs and can set up some GOOD experiments!

    Last edited by zip2play; 11-26-2003 at 06:45 AM.

     
    Old 11-26-2003, 03:57 PM   #15
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    Re: Fish Oil*Friend or Foe?

    Quote:
    Originally Posted by zip2play
    I am hazy on the small, dense LDL:

    Is there a continuous spectrum where LDL becomes denser and denser and then becomes HDL (perhaps low-density HDL?)
    Or are LDL and HDL different in kind.
    If a continuous spectrum, one might think that increasing density (and/or decreasing size) is a GOOD thing.
    But the evidence that high density LDL is the very worst kind proves that untrue.
    Can anybody shed some light?
    HDL is not just a denser form of LDL. HDL and LDL have different proteins attached which respond to different cell receptors. They serve very different functions.

    Orion, the resident scientist over at the Protein Power bulletin board, posted the following response to a question about an article in Redflagsweekly by Malcom Kendrick. I think his response will answer your question in greater depth and detail than I ever could. Here it is:

    Indeed, cholesterol and other lipids are carried in the blood plasma from one tissue to another as plasma lipoproteins, which are in turn macromolecular complexes of specific carrier proteins called apolipoproteins (apo designates the protein in its lipid-free form) with various combinations of phospholipids, cholesterol, cholesterol esters, and triglycerides. Apolipoproteins combine with lipids to form several classes of lipoprotein particles. In fact, what cholesterol tests measure is the different types of particles (that is a particle with a lipid core surrounded by proteins in the surface). Different combinations of lipids and proteins produce particles of different densities, ranging from very low-density lipoproteins (VLDL) to high-density lpoproteins (HDL).

    What's important to realize is that each class of lipoprotein has a specific function, determined by its point of synthesis, lipid composition and apolipoprotein content. The apolipoprotein composition is not just a protein cage to transport the lipid core composed by different lipids. The apolipoprotein composition actually confers a targeting mechanism to the lipoprotein particle, which directs its fate from the intestine to the various tissues where lipids need to be unloaded. At least nine different apolipoproteins are found in lipoproteins of human plasma. Some of them have a known function, for some others that's still unknown. These protein components act as signals, targeting lipoproteins to specific tissues or activating enzymes that act on them. This is a key concept to understand the mechanisms by which lipoproteins transport lipids to different tissues.

    The link oversimplifies the rather complex mechanism by which Chylomicrons are formed, as well as the mechanism by which they disappear. Contrary to what it is said there, I have not read any reference that talks about de novo VLDL. Lipoproteins are characterized by their apolipoprotein composition as well, not only for the lipids they carry. To illustrate this, let's see the apolipoprotein composition of human plasma lipoproteins:

    ApoA-I (present in HDL. Function: Activates LCAT -I'll explain this later)
    ApoA-II (present in HDL. Function: unknown)
    ApoA-IV (present in Chylomicrons, HDL. Function: unknown)
    ApoB-48 (present in Chylomicrons. Function: unknown)
    ApoB-100 (present in VLDL, LDL. Function: binds to LDL receptor)
    ApoC-I (present in VLDL, LDL. Function: unknown)
    ApoC-II (present in Chylomicrons, VLDL, HDL. Function: activates lipoprotein lipase)
    ApoC-III (present in Chylomicrons, VLDL, HDL. Function: inhibits lipoprotein lipase)
    ApoD (present in HDL. Function: unknown)
    ApoE (present in Chylomicrons, VLDL, HDL. Function: triggers clearance of VLDL and chylomicron remnants).

    Note those apolipoproteins present in chylomicrons and VLDL. Only Chylomicrons contain ApoB-48, unique to this class of lipoproteini and it is that apolipoprotein and their particle size what characterizes chylomicrons. VLDL, on the other hand, share ApoB-100, and for a reason. It is ApoB-100 what binds to the LDL receptor and helps clear LDL and VLDLs.
    If we make a recap of the fate of lipids, then we read that all starts with the formation chylomicrons, which move dietary triglycerides from the intestine to other tissues. It is also inaccurate to call triglycerides to VLDLs. The chemical structure of triglycerides is quite simple: three fatty acid molecules bound to a glycerol molecule. VLDLs, on the other hand, have an apolipoprotein combination that can't be dismissed, thus making it a clearly different chemical entity.
    Chylomicrons are not synthesized everywhere. They're made by the epithelial cells that line the small intestine. They then move through the lymphatic system and enter the bloodstream. From the list above, you'll also notice that chylomicrons also contain ApoC-II. It turns out that ApoC-II activates lipoprotein lipase (lpl) in the capillaries of adipose tissue, heart, skeletal muscle and lactating mammary tissues, which makes sense because lpl allows the release of free fatty acids to the tissues. So, chylomicrons transport fatty acids (among other lipids) to be either consumed or store as fuel. The remnants of chylomicrons, now depleted from mostof their triglyceride content but still containing cholesterol, ApoE and ApoB-48, move through the bloodstream to the liver, where they are taken up, degraded in lysosomes (these are the organelles inside the cells that degrade different things like protein or lipids by the use of enzymes), and their constituents recycled.

    If the diet contain more than enough fatty acids (more than needed immediately as fuel), they are converted into triglycerides in the liver and packed with specific apolipoproteins into VLDLs. Excess carbohydrate in the diet also leads to the making of triglycerides in the liver and exported as VLDL. This is one of the reasons why reducing carbohydrates in the diet dramatically decreases the amount of triglycerides and also the amount of VLDLs. VLDLs als contain some cholesterol and esters of cholesterol (cholesteryl esters) as well as ApoB-100, ApoC-I, ApoC-II and ApoC-III and ApoE (see the list above). These lipoproteins are transported in the blood from the liver to muscle and adipose tissue, where activation of lpl by ApoC-IIa causes the release of free fatty acids from the triglycerides of the VLDL. Whereas adipociytes take up fatty acids to resynthesize triglycerides (storage), muscle cells take them up for oxidation to supply energy. Most VLDL remnants are removed fro circulation by hepatocytes which take them up and degrade them.

    The loss of triglycerides converts some of the VLDLs into LDLs, which are very rich in cholesterol and cholesterol esters. So, when people talk about "LDL", what they actually mean is LDL-cholesterol particles. LDL also contain ApoB-100, which is the "signal" to be taken up by cells in the body through a specific receptor. When this lipoprotein finds its receptor, the cell takes up the whole particle in a process called "receptor-mediated endocytosis". Once inside the cell, the particle is degraded, cholesterol and cholesterol esters used for what they're needed, and the protein remnants degraded. The amount of LDL receptors on the cell membrane depends on how much cholesterol is needed by the cell. If there is continuous production of cholesterol, the cell doesn't really "sense" the need to take it up from the blood and the receptors are not made (downregulation). Should the cholesterol machinery inside the cell come to a halt (for example by inhibiting the key enzyme in its synthesis with a statin drug), the cells "starves" of cholesterol and needs to increase the number of receptors on the membrane to "catch" whatever cholesterol may be around! That's how statin drugs act to decrease the amount of LDL in the blood. Interestingly, that enzyme is activated by insulin... sooo... if you reduce your levels of insulin (of course by restricting carbohydrates), you also reduce the amount of LDL in the same way the statin drug would do, only in a natural way.

    One of the easiest ways to understand the dynamics of lipoproteins in relation to cholesterol and triglycerides, is to think that VLDLs (and LDLs), transport cholesterol and triglycerides to the tissues, and HDL (as we'll see in a little bit), transports cholesterol from the tissues back to the liver, thus "scavenging" cholesterol and helping with its removal. Another important point is to understate that if there is little cholesterol or triglycerides to send to tissues (for example because they are not being made, which could be because there is no excess carbohydrates in the diet and no extra fat than what's needed), then the synthesis of the required apolipoprotein and thus the synthesis of the associated lipoproteins is decreased. Likewise, if there is an increase of transport of cholesterol back to the liver (where it has to be used for making bile acids, for example), then there is an increase demand on the synthesis of the apolipoproteins and the lipoprotein carrier... HDL.

    The life of HDL starts in the liver and small intestine as small, protein-rich particles (see the list above... HDL contains several types of apolipoproteis). Nascent HDLs contain little or no cholesterol. They also contain a very special , ApoA-I, and a very special enzyme named lecithin-cholesterol acyl transferase, or LCAT. ApoA-I acivates LCAT and what does LCAT do? It converts cholesterol and licithin (which real name is phosphatidylcholine) into cholesterol esters. LCAT takes lecithin and cholesterol as substrates and converts them into cholesterol ester and a lecithin derivative (lisylecithin). That may also explain the effects of lecithinin in lowering cholesterol levels.
    __________________
    The tragedy of science is the slaying of a beautiful hypothesis by an ugly fact. T H Huxley

     
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