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  • #16
    Originally posted by Artbuc View Post
    Peter Attia is saying LDL-P is the total number of LDL particles of all sizes and that LDL size is not a risk factor. He is very adamant on this point.
    Yes, and with a fixed amount of cholesterol contained in LDL, the higher the LDL-P number, the smaller each particle has the potential (like quantity more highly dispersed) to be which increases it's ability to deposit behind a single cell membrane..... causing damage and the foundation for plaque collection. Am I wrong on this? I read the blog linked earlier once, about 5 months ago, but I thought I had retained it fairly well.

    On the other hand, you're right. Had I just left "small particle" out of my original statement then message conveyed.
    Went Primal: 20 DEC 2011
    Starting: 6'1" 220 lbs
    Starting Energy: "bleh...."
    Current: 183 lbs @ 8.33% BF (Jackson/Pollock 4 caliper method)
    Current Energy: "WOOHOO!" See my journal HERE.

    "Paleo? Try it, but be wary of the cult mentality that comes with it. Paleovangelists are everywhere and a bit scary."

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    • #17
      Ha, scratch that, I found it.....

      "The common denominator is that both sets of patients in (1) and (2) have high LDL-P. What Iím going to attempt to show you today is that once adjusted for particle number, particle size has no statistically significant relationship to cardiovascular risk."

      Good catch, thanks for the correction!
      Went Primal: 20 DEC 2011
      Starting: 6'1" 220 lbs
      Starting Energy: "bleh...."
      Current: 183 lbs @ 8.33% BF (Jackson/Pollock 4 caliper method)
      Current Energy: "WOOHOO!" See my journal HERE.

      "Paleo? Try it, but be wary of the cult mentality that comes with it. Paleovangelists are everywhere and a bit scary."

      Comment


      • #18
        And scratch that back, I knew I wasn't crazy.... The example he used:

        "Hereís the example: Consider 2 patients, both with the same total content of cholesterol in their LDL particles, say, 130 mg/dL. Furthermore, assume each has the ďidealĒ ratio of core cholesterol ester-to-triglyceride (recall from Part I and III of this series, this ratio is 4:1). Iím going to explain in a subsequent post why this assumption is probably wrong as often as itís right, but for the purpose of simplicity I want to make a geometric point.

        1.LDL-C = 130 mg/dL, Pattern A (large particles) Ė person on the left in the figure below
        2.LDL-C = 130 mg/dL, Pattern B (small particles) Ė person on the right in the figure below

        Under the set of assumptions Iíve laid out, case #2 is the higher risk case. In other words, at the same concentration of cholesterol within LDL particles, assuming the same ratio of CE:TG, it is mathematically necessary the person on the right, case #2, has more particles, and therefore has greater risk"

        His point was, all other things equal, that smaller particle size would result in a higher particle count. That's what I had stuck on the brain.
        Went Primal: 20 DEC 2011
        Starting: 6'1" 220 lbs
        Starting Energy: "bleh...."
        Current: 183 lbs @ 8.33% BF (Jackson/Pollock 4 caliper method)
        Current Energy: "WOOHOO!" See my journal HERE.

        "Paleo? Try it, but be wary of the cult mentality that comes with it. Paleovangelists are everywhere and a bit scary."

        Comment


        • #19
          Yes, but the key point is that it is total LDL-P, not particle size which drives risk, at least according to Attia. Others do not agree with him. In the example you used, it is just a mathematical reality that at the same LDL-C, if someone has small particles they will necessarliy need more LDL partcles to carry the given amount of cholesterol and thus have higher risk of CVD. This is why I think we should not be so quick to condemn statins. If Attia is right about LDL-P, and we don't have a way to reduce LDL-P (at least I have never seen anyone site a study or claim they know how to), the only way we can reduce risk is to reduce the amount of LDL-C. Attia also says (based on my memeory) that LDL-C has NOTHING to do with accumulation of plaque. To be honest, I do not know how to square these two statements. Attia says plaque accumulation is a purely gradient driven process. Simply put, the more particles you have bouncing around, the more will penetrate, cause foam cells and accumulate plaque. Just seems to me that if those LDL particles are carrying less cholesterol, I would have less plaque. Maybe someday Attia will address this.
          Last edited by Artbuc; 08-18-2012, 05:07 AM.

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          • #20
            Well, trigs are carried in higher density in LDL particles. Insulin resistant people have higher trig counts, as well as people on high carbohyrate diets. I assume because unsulin signaling is preventing the use of fatty acid in the energy process leaving a higher concentration of trigs in the blood stream, but that's my non-scientific best guess. I don't have any clue as to why that actually is. The higher your trig count, the more dispersed your cholesterol (at a given amount at any time) is in LDL. Higher trig=higher LDL-P as best I can tell. Somebody feel free to smack me if I'm wrong. He does mention specifically that small particle LDL can be a very early indicator of insulin resistance and all the metabolic mallodies that follow it.
            Went Primal: 20 DEC 2011
            Starting: 6'1" 220 lbs
            Starting Energy: "bleh...."
            Current: 183 lbs @ 8.33% BF (Jackson/Pollock 4 caliper method)
            Current Energy: "WOOHOO!" See my journal HERE.

            "Paleo? Try it, but be wary of the cult mentality that comes with it. Paleovangelists are everywhere and a bit scary."

            Comment


            • #21
              Cholesterol is such a wacky number that I see manipulating ....or even testing it to be a waste of energy. It has almost no correlative value, and certainly not causative value. Your cholesterol is EXACTLY what it needs to be based on your current lifestyle and circumstances. The only caveat to this may be hard wired genetic familial hypercholestorolemia. Otherwise, it is meaningless and you should just concentrate on eating a low carb primal diet.

              Comment


              • #22
                Bonz, your posts prompted me to reread Attia plus some other stuff. Don't know how I missed it before, but statins do reduce LDL-P. Somehow I got the idea that statins reduce only LDL-C.

                Comment


                • #23
                  He does seem to imply that statins lower LDL-P along with LDL-C in patients whose P and C numbers are concordant (both indicate high risk for CVD), but he's less clear on whether this is the case when those numbers are discordant (i.e. "normal" LDL-C indicators in patients who have metabolic syndrome or diebeties whose high LDL-P (>1300 mmol/L) go unnoticed). I can assume this is because statins are never prescribed because those patients go undiagnosed.
                  Went Primal: 20 DEC 2011
                  Starting: 6'1" 220 lbs
                  Starting Energy: "bleh...."
                  Current: 183 lbs @ 8.33% BF (Jackson/Pollock 4 caliper method)
                  Current Energy: "WOOHOO!" See my journal HERE.

                  "Paleo? Try it, but be wary of the cult mentality that comes with it. Paleovangelists are everywhere and a bit scary."

                  Comment


                  • #24
                    Originally posted by Neckhammer View Post
                    Cholesterol is such a wacky number that I see manipulating ....or even testing it to be a waste of energy. It has almost no correlative value, and certainly not causative value. Your cholesterol is EXACTLY what it needs to be based on your current lifestyle and circumstances. The only caveat to this may be hard wired genetic familial hypercholestorolemia. Otherwise, it is meaningless and you should just concentrate on eating a low carb primal diet.
                    This ^

                    And familial hypercholesterolemia is pretty damn rare.
                    Durp.

                    Comment


                    • #25
                      Originally posted by BONZ View Post
                      He does seem to imply that statins lower LDL-P along with LDL-C in patients whose P and C numbers are concordant (both indicate high risk for CVD), but he's less clear on whether this is the case when those numbers are discordant (i.e. "normal" LDL-C indicators in patients who have metabolic syndrome or diebeties whose high LDL-P (>1300 mmol/L) go unnoticed). I can assume this is because statins are never prescribed because those patients go undiagnosed.
                      So, I guess Attia must be a big supporter of statins if they reduce LDL-P which is the primary marker for CVD? I'll have to go through his blogs and see what he says about statins.

                      Comment


                      • #26
                        Originally posted by Neckhammer View Post
                        Cholesterol is such a wacky number that I see manipulating ....or even testing it to be a waste of energy. It has almost no correlative value, and certainly not causative value. Your cholesterol is EXACTLY what it needs to be based on your current lifestyle and circumstances. The only caveat to this may be hard wired genetic familial hypercholestorolemia. Otherwise, it is meaningless and you should just concentrate on eating a low carb primal diet.
                        I'm highly inclined to agree with you..... Seems to me the human body itself is the best regulatory agent you have and tends to let you know when you're giving it the wrong inputs.
                        Went Primal: 20 DEC 2011
                        Starting: 6'1" 220 lbs
                        Starting Energy: "bleh...."
                        Current: 183 lbs @ 8.33% BF (Jackson/Pollock 4 caliper method)
                        Current Energy: "WOOHOO!" See my journal HERE.

                        "Paleo? Try it, but be wary of the cult mentality that comes with it. Paleovangelists are everywhere and a bit scary."

                        Comment


                        • #27
                          From Part IV of the Attia presentation (which is really interesting, thanks for the tip):

                          Empirically, we know that the most successful pharmacologic interventions demonstrated to reduce coronary artery disease are those that reduce LDL-P and thus delivery of sterols to the artery.
                          EDIT: Came across this paper, which suggests that a combination of HDL-C and Tri measurements are a suitable proxy for LDL-P measurement.

                          http://www.theheart.org/article/767865.do

                          "At any given LDL-C level, if you have two people and one has increased LDL-P while the other has normal LDL-P, the one with the increased LDL-P is at greater risk of CAD, and this tends to coincide with people who have metabolic dyslipidemia [which usually includes low HDL-C levels and high triglycerides]," he said.

                          "Recognition that patients with low HDL-C and/or high triglycerides often have elevated numbers of LDL-P without having elevated LDL-C may enable their LDL-related CAD risk to be managed more effectively," the authors write.
                          Last edited by DeeDub; 08-18-2012, 10:50 AM.

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