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Could Cardiac Disease be a Fat Disease?

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  • Could Cardiac Disease be a Fat Disease?

    What I mean by that is if atherosclerosis isn't caused by cholesterol, yet cholesterol and triglycerides seem to have some correlation to arterial disease, why not look more at the triglycerides side.

    Chylomicrons are what transports triglycerides and cholesterol into the bloodstream. Once in the bloodstream, they supply triglycerides to cells and the liver (triglycerides and cholesterol). As triglycerides are removed from the chylomicrons, they eventually become remnants and are recycled by the liver.

    The liver produces vldl to carry triglycerides to cells. As fat is removed by the cells, the vldl becomes ildl and eventually ldl. Ldl is what's left from the vldl and is primarily cholesterol. As cholesterol is removed from ldl, it eventually becomes an ldl remnant and is recycled by the liver.

    So if LDL, which carries cholesterol, isn't the cause of plaque buildup in arteries; yet there appears to be a correlation between triglycerides, ldl, sdldl, etc to atherosclerosis, doesn't it seem that the fat side of the equation might be the problem?

    I'm having trouble finding articles that discuss what happens if chylomicron remnants and vldl remnants are not removed from the bloodstream by the liver and continue to circulate in the blood. Do they use the same docking points on the liver? What about sdLDL? Is it competing for the same ports? What happens when one has a leaky gut and substances from the gut leak into the bloodstream, some of which mimic liver docking points?

    Could it be that when the liver can't keep up with removing chylomicron remnants, vldl remnants, ldl, sdldl, and toxins from leaky gut, that these particles start damaging arterial walls which begins the plaque process. The arteries start to bleed and clotting takes place like with any wound. Eventually, it scabs over and new cell lining grows over the scab. But now this area is even more prone to damage and the plaque buildup continues. (Plaque contains both fat and cholesterol)
    This could also explains the inflammation issue as the toxins and wound healing would both cause low grade inflammation. I also wonder if high blood pressure may be a result as all the extra particles have to be pushed through blood vessels.

    It would be interesting to see if any studies have been done to see if patients with atherosclerosis have a leaky gut. My guess is it would be a much higher percent than the public at large. I have seen many blog posts that list heart disease as caused by a leaky gut, but so far haven't seen any scientific papers.

    Maybe a more accurate title would be: Could Cardiac Disease Be Caused By a Leaky Gut?

    Comments? I'm open to both positive and negative comments. It would be helpful to explain your comments so this can become a discussion.
    Last edited by rich; 07-11-2019, 09:32 AM.

  • #2
    I have been out cutting grass, where I always have my "best" ideas. I have revised my theory to make it all encompassing!

    As the number of, size of, and shape of, particles in the blood stream increase, the likelihood of damage to artery walls also increases.
    Under "normal" conditions, the particles in blood stream float along, rarely colliding with other particles. As the number and size of the particles increase, the number of collisions also increases. This includes collisions with artery walls. As the wall is almost continually bombarded with particles of various shapes and sizes, small openings occur in the cell wall and grow bigger until small particles like LDL start to get stuck in the openings. To heal the damage, inflammation occurs at the damage site and the healing process starts, first a scab and then new cell wall lining. It's like a cut that leaves a scar after healing. Sometimes the scar goes away or gets smaller over time, but not if the wound is continually being banged on and reopened.

    I had to try to figure out how diabetes would fit into my theory, but that was rather easy - increased glucose in the blood stream. Same with inflammation. Same with smoking. Similar with high blood pressure as now these particles are colliding with more force causing more damage.

    So how do a vegetarian or high fat keto diet work to reverse atherosclerosis? Fewer particles in the blood stream - vegetarian reduces the fat particles and keto reduces the glucose particles. BUT, to go back to my OP, if you have a leaky gut it is likely stlll a losing battle.
    Last edited by rich; 07-11-2019, 11:39 AM.

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    • #3
      Jeebus. Atherosclerosis is caused by long-term consumption of excess carbs.

      Comment


      • fatmax
        fatmax commented
        Editing a comment
        You said you had a genetic problem that prevented you from eating fat. Since there are only three macro nutrients, fat, carbs, and protein, you had to eat mostly carbs and protein to keep from starving. Consuming all those carbs over many years was unhealthful.

      • rich
        rich commented
        Editing a comment
        Where did you get that idea? Excess carbs are converted to fat.

        I never said I couldn't eat fat, I said I had a problem digesting and metabolizing SATURATED fat. Some of the saturated fat is digested and is metabolized, but some of it isn't. Unsaturated fat seems to be digested and metabolized just fine.

        You need to be at least a little objective. You have blinders on and it might get you in trouble. Show me the people eating a whole foods plant based diet that are having heart attacks.

    • #4
      Excess carbs generate excess insulin secretion. Excess insulin creates insulin resistance. Insulin resistance creates atherosclerosis. Ergo, excess carbs create atherosclerosis.
      Remove your blinders off and read some research, such as:

      https://www.crossfit.com/essentials/...-stupid-part-1

      Comment


      • #5
        Originally posted by fatmax View Post
        ...
        Dr. Juan Gallegos: It's not necessarily that it can't process it all, but the way, if you overcharge the system, then the processing of those things might be abnormal and that's part of the reason why people who have issues with their weight or have diabetes and high blood sugar can have something called fatty liver disease and that's because the fat starts accumulating inside the liver cells as they try to adapt to all this excess fat that's coming into the system, through your meal, but also through increased blood sugar that ultimately is transformed into fat deposits if it's not used elsewhere. https://healthcare.utah.edu/the-scop...ows=0_7frg4jjd

        The fatty acids needed to make triglycerides come from digesting the fatty foods you eat, but they can also be made in your body from the carbohydrates you eat. This conversion of carbohydrates to fatty acids is the basis of lipogenesis. This is an easy term to recall if you remember that the prefix 'lipo' refers to lipid, which is another name for fat, and 'genesis' refers to creation, so lipogenesis is literally the process of lipid creation. https://study.com/academy/lesson/lip...-function.html


        But this has nothing to do with this thread. I recommend you actually read my 2 posts.

        Comment


        • fatmax
          fatmax commented
          Editing a comment
          Best of luck to you.

      • #6
        This video on lipoprotein metabolism is by far the best I have seen at explaining how fats and cholesterol are processed. It's medical school level, but the instructor is so good it is fairly easy to pick up on the big concepts. I can only watch about 10 minutes at a time before overload sets in. I had read several articles about this subject (which is where my idea for this thread came from) before I found this video.

        You may have to reset the video to the beginning.

        Last edited by rich; 07-13-2019, 07:25 PM.

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        • #7
          I thought of a better way to say what I have been trying to say.

          Chylomicrons and vldl primarily carry fat to the cells. After giving up most of their fat, they becomes remnants. The same idea with LDL, but for cholesterol, not fat. It appears they all use ldl receptors on the liver.

          So my thought is if the chylomicrons and vldl remnants can't all be removed by the liver, then it is possible that ldl remnants (sdLDL) start stacking up causing ldl, ldl-p, sdLDL to all increase. So it would look like a cholesterol problem when really it is a fat problem.

          Comment


          • Tom
            Tom commented
            Editing a comment
            I just got back from being away for a week and looked at the video. In general I agree with what the presenter said, but I think that the presenter wasn't aware of the role of ApoCIII in both HDL and the LDL family of particles. https://www.ncbi.nlm.nih.gov/pubmed/11034934

            In addition the liver makes IDL and LDL particles separate from VLDL (i.e. not every IDL and LDL particle started out as a VLDL as the presenter seems to suggest). What we want is for the number of VLDL particles to be kept to the minimum because those are the ones that can end up with an ApoCIII protein, especially when the triglyceride levels are high (for many people TG >130 mg/dL). The presence of an ApoCIII protein will negate the positive clearance effect of an ApoE protein on the LDL family of particles (VLDL, IDL, and LDL) as noted in the above referenced study. Likewise the presence of ApoCIII proteins on HDL particles inhibits their clearance and therefore effectiveness in bringing cholesterol/cholesteryl ester back to the liver.

            As the presenter mentioned the HDL particles pass a good bit of cholesteryl ester via CETP to the LDL family particles which should take that cholesteryl ester back to the liver (in football terminology a forward pass). However, the amount of time that LDL family particles are in circulation makes all the difference between whether those get stuck in the sub-endothelium spaces (in football terminology a fumble). VLDL particles with the ApoCIII shed most of their triglycerides and eventually become the dreaded sdLDL which cannot easily be cleared by the liver because the ApoB docking area gets distorted as the LDL particle gets smaller to the sdLDL size.

            The presenter also doesn't discuss the LDL family of particles bringing phospholipids to the cells which is one of their two major cargos (triglycerides and phospholipids). Although LDL family of particles can drop off cholesteryl ester to cells that need it, most cells make enough on their own. As the presenter stated HDL particles generally service those tissues that don't produce enough cholesterol by dropping off cholesteryl ester.

            Chylomicrons don't last long in circulation (a matter of minutes rather than multiple hours/days), and unless a person has a genetic variation causing some issue chylomicrons aren't the problem. There are all sorts of genetic variations with both the LDL/HDL families of particles and the receptors which can cause severe lipid problems, but fortunately those occur for a relatively small population. Ron Krauss studied these variants while he was at the NHS for years, and if you want to hear a bit about those listen to the Peter Attia podcast with Ron Krauss.

            One more thing. You talked about endotoxins related to leaky gut. This is definitely a problem for developing cardiovascular disease for those who have leaky gut syndrome. Once an endotoxin binds to an LDL particle, it is very difficult for that LDL particle to be cleared by the liver. So guess where those long-lasting LDL particles can show up? Yep, deposited right in the sub-endothelium spaces where the immune system will react.
            Last edited by Tom; 07-21-2019, 07:47 AM.

        • #8
          Many of you are aware of the blog called Hyperlipid authored by Peter (Petro Dobromylskyj). I was reading through some of his posts and came across this:

          Now, a functional LDL-C receptor is utterly necessary for the anti-inflammatory effect of the chylomicron/endotoxin complex. If someone's ears don't prick up on this one they have clearly never heard of homozygous familial hypecholesterolaemia. The focus on elevated lipids (sigh) might just have missed the core of the problem, which is the failure to internalise lipoproteins. Interesting idea? It certainly is to me.
          https://high-fat-nutrition.blogspot....ch?q=endotoxin

          This appears to confirm what I theorized. if LDL-C receptors can't remove LDL fast enough, LDL is going to be high. Treatment should not be to lower cholesterol, but to remedy the cause of non-functional LDL-C receptors. In my case, I know I have a genetic predisposition for cells to have a resistance to absorbing saturated fat, which would likely mean an increase in chylomicron and vldl remnants without enough efficient ldl-c receptors to remove all of them. The result is LDL-C that can't be removed because receptors are also being used by chylomicrons and vldl. And also, as I posted earlier, according to Dr Rhonda Patrick, LPSs mimic liver ldl-c ports, so sometimes LPS will bind to LDL on the port it uses to bind to liver, causing sdLDL to become old and oxidized.

          Comment


          • Tom
            Tom commented
            Editing a comment
            It is a bit more complicated than LDL receptors not removing LDL family particles fast enough given what I said above about sdLDL as an example. Reducing LDL-C has clearly been shown to decrease heart attacks as noted during the PCKS9 inhibitor drug studies. So, its complicated. Dr. Brewer emphasizes a reduction in cardiovascular inflammation as a primary driver of cardiovascular disease and LDL-C as secondary except for those with FH (familial hypercholesterolemia). Most doctors go with the high dose statin approach to substantially reduce LDL-C levels. It is really LDL-P that is important vs. LDL-C, but that should be the focus of another post. That high dose statin will also substantially lower cardiovascular inflammation as long as the patient's lifestyle isn't too bad.

        • #9
          Tom, I appreciate your comments, but could it be that your comments are based on everything working the way it is supposed to? If everything was working properly, would there be plaque buildup in the arteries? Would remnants be considered highly atherosclerotic? I say no.

          So what happens when genetics or some other reason results in cells not efficiently absorbing fat from chylomicrons or vldl? Or what happens when a lps binds to ldl preventing it from being cleared by the liver? Or what happens if one has a leaky gut and toxins, undigested foods, bacteria, lps's, etc leak into the bloodstream? Or what happens if enough lipase is not being released? And I'm sure there are another 10 or 50 things that can go wrong.

          I'm finding article after article that says ldl is not the problem, but vldl remnants are. The only way I see them being a problem is if they are not being removed in a timely fashion. I think it's the same with LDL. If ldl is removed by the liver when it should be, then sdLDL should not be a problem. So if sdLDL is high, it seems to me there is a problem removing ldl.
          Last edited by rich; 07-22-2019, 04:17 PM.

          Comment


          • #10
            If everything works the way it should, yes we will all still get cardiovascular disease to a point as we age. It is just whether it is enough to cause the eventual problems that we notice as cardiovascular disease. For some people who have genetic variations affecting the transit time of chylomicron remnants, some of those remnants will end up in the intima-media space in high enough numbers to increase the level of cardiovascular disease. It is transit time that matters above all because those chylomicron remnants don't generally last for days like LDL particles (or even longer-lived sdLDL). Do some chylomicron remnants get into the intima-media space even in the best of cases? Yes, but not enough to be the driver of the disease process.

            The issue is what happens to most people vs. what happens to an individual. For an individual person, what you say can be true. However, that is not the case for most people (although leaky gut is likely more prevalent than severe genetic issues with lipid metabolism). A VLDL remnant is a problem because it becomes an sdLDL particle, so perhaps terminology differences account for the differences in thinking about this issue. How long does a VLDL remnant take to collapse down to an sdLDL? To my understanding not long enough for VLDL remnant particles to be nearly as significant an issue as sdLDL particles. Is an sdLDL not an LDL? Likewise, when an LDL particle gets attached to an endotoxin, is it no longer an LDL particle? I count all of those as LDL particles. I think that remnant term for VLDL (or any LDL family particle) is not helpful as it just confuses the underlying issues.

            We don't want a lot of VLDL "remnants" (i.e. soon to be long-lived sdLDL) circulating in our system. We don't want a lot of LDL particles with endotoxin's attached in our system. If a person's diet/lifestyle result in high triglycerides (e.g. greater than 130 mg/dL) then most of us will have lower HDL-C levels and make more VLDL particles which have an ApoCIII attached (ending up as sdLDL particles).

            I should make a late correction/comment to make sure that there isn't a misunderstanding. Not all VLDL particles end up as sdLDL, but those VLDL "remnants" that hang around are the ones likely to have the ApoCIII protein attached and do become sdLDL. We want VLDL particles to transition to IDL, then to LDL and finally be cleared by the liver. If triglycerides are kept low, that is more likely to happen.
            Last edited by Tom; 07-23-2019, 08:12 AM.

            Comment


            • rich
              rich commented
              Editing a comment
              "The issue is what happens to most people vs. what happens to an individual."

              I disagree. There are several SNPS that have to do with fat digestion and metabolization. If just 5% of the population had 1 or more of these SNPs, as well as a leaky gut, that might be as high as 10% of the people with CD.

              So with the results of a 23andme lab and a zonulin test, 2 fairly inexpensive tests, a knowledgeable doctor could rule them out or possibly in. An app could do the analysis in seconds. The treatment is cheap and fairly straightforward.

              I wish there was a good test for chylomicrons and vldl, as well as remnants. This would make it much easier to detect the problem.

              Something we didn't really discuss is the massive inflammation that both can cause. I think testing and treatment of leaky gut, if necessary, is critical for anyone with CD.
              Last edited by rich; 07-24-2019, 05:18 AM.
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