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  • LDL Test Question

    Dr Brewer:

    i hope you can help clarify something. Per your suggestion, I had the Inflammation and NMR Panels done at Cleveland. Inflammation tests show low risk, LIpid panel also looks good generally, however, I'm confused about what the sdLDL test indicates and how it relates to the LDL-P, Small LOL -P and LDL Size tests.

    For example, I've read one account saying that the percentage of small dense particles to LDL-P is important, but the sdLDL a better read of percentage than dividing Small LDL - ​​​​​P / LDL - P
    I appreciate any clarification you can provide. My PCP is not clear on some of these distinctions. Thank you.
    Last edited by Joby; 03-29-2019, 07:15 PM.

  • #2
    It's true that sdLDL ( small, dense LDL) is the type of LDL that is more likely to be slip through damaged intima & lodge as plaque. However, these particle fractionation exercises usually end up as more of a distraction from the primary goal. If you're able to control the basics, the basics take care of the fractionation challenges.

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    • Robin
      Robin commented
      Editing a comment
      Yep, keep the lining healthy and NOTHING slips through the cracks.

  • #3
    Some LDL family particles will always get through, it is just a matter of how many and whether those are adequately removed by HDL particles over time to prevent plaque build up sufficiently to result in a heart attack or stroke.

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    • #4
      Good point.

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      • #5
        Thank you all or your comments. It's a challenge to get HDL over 40. Last read was 36. Tried Niaspan years ago, no improvement. 8 hours exercise weekly, using whole food, plant based diet to keep inflammation and LDL low. Though, would like to see HDL at 50.

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        • #6
          If your triglycerides are high, let's say over 130 mg/dL, then you might be able to raise your HDL-C by lowering your triglycerides. Higher triglycerides, in particular over 130 mg/dL, lower your HDL-C level as a common part of the metabolic syndrome. If your triglycerides aren't high, then you may genetically have low HDL-C. The thing with HDL-C is that it is a valuable marker, but imprecise marker for some people. Not everyone with lower HDL-C has cardiovascular disease, and it has to do with HDL particle functionality. I posted a link to a good article on HDL particle functionality below.
          https://insight.jci.org/articles/vie...form=hootsuite

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          • #7
            Fatmax - I've been on the Plant based approach since last June. A month after I started, my HDL hit the high of 40 and triglycerides hit a low of 88. Great numbers for me. More recently, I've increased fat intake with nuts, seeds and avocado, along with salmon and sardines. I know Keto is popular on Dr Brewer's site. I'll recheck lipids in June and see how they look. I take 5 mg Crestor.

            Tom - as noted above, triglycerides are low, increasing a bit to 110 while HDL dropped to 36 last Dec. Howevet, labs were done right after completing 20 days of high dose Prednisone, for an unrelated issue. I read that Pred can increase triglycerides and lower HDL Generally,. I think the lower HDL is genetic.

            Thx for the article. I saw on the Cleveland Heart Lab site, they have a functional HDL test due sometime soon.

            Thx again guys!!
            Last edited by Joby; 04-30-2019, 11:10 PM.

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            • #8
              Fatmax said, "Don't worry about cholesterol or LDL-C. I take 20mg rosuvastatin and 2g niacin daily plus supplements."

              That statement is highly problematic. That dosage of Rosuvastatin is 4X the amount that Dr. Brewer recommends for inflammation. At that dosage you can pretty much inject pure cholesterol into your blood stream. If you truly didn't care about LDL-C or cholesterol you certainly wouldn't be popping 20mg a day.

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              • #9
                James - I do watch TC and small dense LDL, in particular. I did my first VAP Cholesterol test in 2002 and my LDL pattern was B, more smaller particles. A later test showed A/B , as my lipid levels improved a few years later. On my current diet TC dropped to 116, while sdLDL- C measured at 19.5%, lower risk. So, I'm comfortable the Plant based diet has been helpful, although per my original question, I'm not clear how sdLDL relates to LDL- P, Small LDL - P (558) AND LDL size (20) . Also, I prefer to keep Creator dose at 5mg.

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                • #10
                  If a person can tolerate a higher dose of a statin, then there are additional benefits from lowering LDL particle numbers in addition to the lower inflammation. Some people do have issues with rising liver enzymes (in particular ALT) and generally feeling not quite right on a higher dose of a statin in addition to what a relatively few people have experienced with muscle breakdown. In theory statins should only work on the liver, but as has been seen there are some off-target effects in muscle in particular.
                  There are more people, who have been on a keto diet for months, experiencing significant increases in their LDL particle numbers along with LDL-C. There are a lot of theories on whether this is healthy or not long-term, but nobody knows for sure because it hasn't been studied over a long enough period. Taking a higher dose of rosuvastatin (actually 40 mg/day is the highest) would probably tamp down on this to a degree. In the end it is all just one big experiment with each of us making their choices.

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                  • #11
                    Fatmax, this is from the article you posted: "...As anticipated, lower on-treatment LDLC levels and lower on-treatment hsCRP levels were both associated with significantly better clinical outcomes, even after adjusting for clinical characteristics and for baseline lipid and inflammation levels (both probability values <0.001).23 Although LDLC and hsCRP reductions were only weakly correlated in individual JUPITER patients (r values <0.15), best clinical outcomes were observed among those receiving rosuvastatin who achieved low levels of both variables; in fully adjusted analyses, a 65% reduction in the hazard of vascular events was observed among those allocated to rosuvastatin who achieved both LDLC <70 mg/dL and hsCRP <2 mg/L (HR, 0.35; 95% CI, 0.23 to 0.54) whereas a smaller 36% reduction in hazard was observed among those who achieved neither target (HR, 0.64; 95% CI, 0.49 to 0.84; P across treatment groups <0.0001). Moreover, a 79% relative hazard reduction was observed among those who achieved the even more aggressive targets of LDLC <70 mg/dL and hsCRP <1 mg/L (HR, 0.21; 95% CI, 0.09 to 0.51;"

                    So whether you acknowledge it or not, lower LDL-C levels in conjunction with lower hsCRP levels do have a significant impact on the reduction of cardiovascular events, even according to your own research.

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                    • #12
                      Fatmax - Thx for sending the link. I’ve seen Dr Davis’s info and asked Dr Joel Kahn, who’s advice helped me develop my WFPB diet, about this. In short, he doesn’t agree with Dr Davis’s approach. I have no intention of starting an argument, Obviously, you’ve had success with your approach, presumably using Dr Davis’s suggestions. I’ve had success with Dr Kahn’s. Although my HDL is lower than I’d like, 36-40, it is better than 24-28, which was typical over the long term, before the diet change

                      My intent is to clarify different dr’s have different approaches. The important point is that each of us is motivated to follow some approach, and if found to be helpful, stick with it.

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                      • #13
                        Interesting. But again, also, not surprising. As we've shown on the FH vids, it's probably not as lethal as many thought (extremely high LDL). But I don't think it's good to have an LDL of 250, either. If I had it, I'd lower it.

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                        • #14
                          The issue with diets is that we need to be open to information and skeptical at the same time. I agree with the premise in William Davis's video that you referenced above that more attention needs to be given to triglyceride levels. This was first brought up as part of the metabolic syndrome, and for many high triglyceride levels will suppress HDL-C. However, I think it is not correct to say that there is no use in a standard lipid panel. Nuances and interpretation is important to understand what is happening and the corrections that need to be made. I think that it is more widely appreciated now that LDL-P is much more predictive of future cardiovascular risk than LDL-C, and part of that is due to the changes starting in the 80's with high carb/low fat diets that had a lot of unhealthy carbs. With that general unhealthy diet, other than the obvious obesity, triglycerides went up, VLDL went up, and there became discordance between the LDL-C and LDL-P relationship. At one time for most of the population those two numbers roughly would have a straight forward relationship. For the studies that included LDL-P measurements, LDL-P turned out to be a better predictor of cardiovascular risk than either LDL-C or HDL-C. If we are trying to tell people that we are following the science, then follow the science.

                          Dave Feldman is an interesting guy who has been a self-experimenter to his credit along with a big advocate for the keto diet. The one thing that I find interesting on these diet videos, is that rarely do the proponents have a in-depth discussion with someone who isn't already convinced about their outcome results. Because of this, it seems like that there is a lot of cherry-picking going on with data to analyze it this way and that way to eventually find something that supports their view. If what Dave Feldman said was so important, has his analysis been published by reputable journals? I don't personally have anything for or against keto dieting, and I am open to learning. I found the Peter Attia podcast with Dave Feldman to be most interesting. Peter Attia has interviewed a lot of knowledgeable people with different viewpoints on a variety of subjects, and he respectfully asks pointed questions to get to the basis of some of the claims that are oh so easy to make on the Internet.
                          https://peterattiamd.com/davefeldman/

                          As to cherry picking data, well how many of those NHAMES participants followed the keto diet? If the whole premise is to show that the increase in TC/LDL-C (really it is the LDL-P that counts) of people on a keto diet is healthy into old age, then I think it does matter what diet that the NHAMES participants were on. He boiled down a lot of data to find one thing that agrees with his premise. This reminds me of the super-centenarians who smoked. Did they live longer because they smoked, and thus everybody should embrace smoking? I think that the obvious answer is no. The problem with the analysis that Dave Feldman gave is assuming that we are all genetically the same. The fact that some people lived into old age with high LDL-C doesn't mean that we should all embrace high LDL-C (or even ignore it). As Dr. Brewer has pointed out, LDL-C doesn't matter as much if the other conditions that cause cardiovascular disease are well controlled. The problem is that many people don't seem to want to change their lifestyle enough to manage their cardiovascular inflammation and endothelium dysfunction, and so off to the primary care doctor to get a high dose statin. This is not an optimal solution, but it has put more years of life into some who would have otherwise died. This is science, good, bad and ugly as it is.
                          Last edited by Tom; 05-04-2019, 12:00 AM.

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                          • #15
                            Tom - good to read your thoughtful response. I can’t speak for other doctors, but one thing I like about Dr Kahn’s WFPB approach (included with Kahn are Drs Greger, Fuhrnan, Essylsten, Ornish etc) is their interest in reviewing scientific analysis, conducted in reputable journals, to reach conclusions. Dr Greger in particular, has a website filled with videos describing theses studies, and the related science. He often comments about some studies cherry picking to get selected results. An earlier comment suggested Kahn doesn’t follow science, and I believe this to be totally false.

                            These doctors are also advocates of tests Dr Brewer advocates, CCS, CIMT, inflammation and advanced lipid panels. LDL-P and particle size are key factors for them along with inflammation readings. In my view, they follow very defined medical and nutritional science, and demonstrate it in their writings and video. It was this attention to science, beginning with Essylsten, that got me interested in WFPB. I’m not criticizing Keto, it appears to work for some, it’s just not my preference.
                            Last edited by Joby; 05-04-2019, 04:43 PM.

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