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    Just viewed video of Dr. Rhonda Patrick interviewing Dr. Ron Krauss, M.D. (the director of atherosclerosis research at Children’s Hospital Oakland Research Institute, Adjunct Professor at UCSF and UC Berkeley) and is/was affiliated with the Berkeley Heart Lab. The discussion covers many topics primarily related to lipids, nutrition, heart disease and statins. It is interesting to hear from someone who is doing cutting edge research. However, it is about 2.5 years old. Video title: "Dr. Ronald Krauss on LDL Cholesterol, Particle Size, Heart Disease & Atherogenic Dyslipidemia"

  • #2
    Thanks for the video. Unless I missed it, Dr. Krauss never uttered a word about inflammation or insulin resistance which are the main root causes of CVD. He seems to think having lipid abnormalities are the root causes.


    • #3
      John, there was talk about inflammation and diabetes in conjunction with cvd. He is both a practicing physician and a researcher. After writing this I clearly remember the discussion of inflammation and cvd. He discusses both the positive and negative role inflammation plays in human biology. He also discusses why humans have more cvd than other species. I enjoyed the discussion from a researchers perspective.


      • #4
        Thanks, John. I’m glad to hear that he did.


        • #5
          I learned a lot recently from podcasts by Peter Attia on this topic, the first podcast with Ron Krauss and the second was a series of podcasts with Tom Dayspring. I like Rhonda Patrick's foundmyfitness videos in general, but I learned a lot more on this topic from those recent podcasts done by Peter Attia. Both Ron Krauss and Tom Dayspring have been among the leaders in the mainstream of lipid research and use of the ever expanding knowledge for diagnostic purposes over the last 30-40 years. Peter Attia goes through his philosophy of necessary but not sufficient to explain why mutliple conditions are required for cardiovascular disease; not just a bunch of lipids or inflammation or endothelial dysfunction alone. I thought that the Ron Krauss podcast was very good for background info, but I learned more specifics from the five-podcast series with Tom Dayspring.

          I would highly encourage anyone who is interested in understanding lipids and cardiovascular health to use these as a learning experience. Peter Attia likes to explore the personal history and passions of his podcast guests, and so a person could look though the extensive show notes and identify those areas which are of the most interest to the listener. On the Tom Dayspring series, I would start with the second podcast and actually skip to the third one if a person wants an in-depth explanation of why HDL-C is not as useful a marker as most people/physicians still think. I think that the notion of LDL-P (apoB) being a much better predictor of cardiovascular health over LDL-C has been accepted by a larger group at this point, but many doctors still treat their patients using the results of a standard lipid panel. Both Ron Krauss and Tom Dayspring emphasize the importance of triglyceride levels in order to understanding cardiovascular health risks. Tom Dayspring goes further to explain (with good diagrams) how high TG (>130 mg/dL) often leads to an excess of vLDL particles, in particular in insulin resistance, which have an apoCIII but not an apoE protein. These collapse down to become the small dense LDL that aren't cleared well by the liver, and as a side note is likely why niacin is known to be effective in reducing sdLDL by its reduction of TG levels. I had always thought that LDL particles contained cholesterol in order to transport it to tissues that need it. So wrong I found out.


          • #6
            In the fourth episode:


            Attia and Dayspring discuss in detail the use of niacin. Their conclusion seems to be that the serious side effects of niacin (worsening of insulin resistance, et al) don't justify taking it if you are already reducing your ApoB particles with a statin and that fenofibrate would be preferred. I'm taking 2g of immediate release niacin now with 20mg of rosuvastatin, and I'm considering dropping the niacin.

            Would appreciate a discussion by John L. and Dr. Brewer about this.


            • #7

              There is certainly disagreement on this topic as Peter Attia mentioned, and to understand that better listen to the last 15 minutes of the Peter Attia podcast with Ron Krauss on Heart Disease that specifically covers niacin in-depth (Ron Krauss uses it himself as do many physicians). I think that the answer is, as in many cases for individuals, "it depends". If a person already has a significant amount of insulin resistance, a high dose of niacin might increase blood glucose levels enough to make a difference. In other people, it is likely ok. I wouldn't make any major changes to my medications, and at 2 gm/daily niacin is effectively a medication, without talking to your doctor.


              • #8
                Dayspring is a lipidologist. He’s been preaching for years primarily about treating lipids with medications to improve CV outcomes. He seldom discusses controllable root causes such as inflammation, obesity, insulin resistance, lack of exercise, hypertension, poor diet, etc.

                His theory on Lp(a) not be a risk factor if our LDL is below 160 mg/dL doesn’t hold water either. Lp(a) is an independent and residual risk factor at any LDL level.

                As one doctor told me about ten years ago, we can make our labs look as pretty as we want them to look with medications BUT we will still be diseased. There are no magic pills that can correct those controllable risk factors.


                • #9

                  You are absolutely right that correcting a poor lifestyle trumps just almost anything that can be done with medications, and conversely medication cannot overcome a poor lifestyle. Tom Dayspring is a lipidologist, and primary care physicians referred their patients to him when necessary for advice on lipids. I would look to the primary care physicians to emphasize the lifestyle stuff and let the lipidologist do their thing. You could make the point that he was overweight for a long time, but I don't hold that against his advice.

                  I do also agree that anything like Lp(a) not being a risk factor if LDL (I gather you mean LDL-C) is below 160 mg/dL doesn't hold water as that statement makes no sense to me. Where did you hear/read that because that is not what I have heard/read him to say in several papers and videos (years before the podcast series I mentioned)?

                  I also agree that there are no magic pills, but the continuing use of just a standard lipid panel by many primary care physicians tends to mask the potential lipid problems like Lp(a).


                  • #10

                    Thanks. Here is an excerpt from Dayspring:

                    "In most of the epidemiological studies the risk of elevated apo(a) depends in a linear fashion on the LDL-C concentration. Indeed, data from the large Physicians Health Study, revealed that Lp(a) conveyed no risk if the LDL-C was less than 160 mg/dL. In the Women’s Health Study Lp (a) conveyed no risk unless it was extremely elevated (>90th percentile) and the LDL-C (apoB) was also elevated. Thus elevated Lp(a) in the face of normal LDL-C is not a risk factor.

                    1) Men: High Lp(a) predicts risk of angina, and the risk is substantially increased with high concomitant LDL-cholesterol (reported as > 160 mg/dL). The study found that Lp(a) concentration strongly contributed to CHD risk when LDL-C was concomitantly increased, consistent with several other studies. In other words the risk of Lp(a) is not there if LDL-C is OK (< 160 mg/dL). The men with the highest risk had Lp(a) concentrations > than the 80th percentile and LDL-C > 160 mg/dL. The reference is: Apolipoprotein(a) Size and Lipoprotein(a) Concentration and Future Risk of Angina Pectoris with Evidence of Severe Coronary Atherosclerosis in Men: The Physicians’ Health Study Nader Rifai et al. Clinical Chemistry 2004;50:1364–1371.

                    2) Women: In this cohort of initially healthy women, extremely high levels of lipoprotein(a) (90th percentile), measured with an assay independent of apolipoprotein(a) isoform size, were associated with increased cardiovascular risk, particularly in women with high levels of LDL-C. However, the threshold and interaction effects observed do not support routine measurement of lipoprotein(a) for cardiovascular stratification in women. Lipoprotein(a), Measured With an Assay Independent of Apolipoprotein(a) Isoform Size, and Risk of Future Cardiovascular Events Among Initially Healthy Women Jacqueline Suk Danik, et al. JAMA. 2006;296:1363-1370"

                    Here is the complete article written by Dayspring:


                    • #11

                      Thanks for including the link to the article, and thank you for pointing out things that really let me make my point. My point is that context matters. If I may try to state your point, you don't believe that Tom Dayspring sufficiently understands lipids because of what you perceive to be a gross misunderstanding of Lp(a) risk from quoting parts of that article. I couldn't find the exact date for this article, but it appears to be about 12 years old. From item 1) Men, the reference is stated for a 2004 study. Did Tom Dayspring not understand the named study results? I don't think so. If you think so, please let me know where he misread the study (and this is the critical part because you criticize him for that statement). Context matters.

                      The really important thing is to understand that science doesn't stand still, and lipid science has made remarkable advances in the last 12 years. You may remember the days when many people wrote a lot of critical articles on NMR being unreliable and without a common standard. Things have changed. Lipid science also went through a period of development and testing of CETP inhibitors which many people in the lipid world (and several big pharma companies) believed would give a 1-2 punch of statin and CETP to tame cardiovascular disease. Ultimately that didn't work out, and the lipid world learned more which is how science works. Now, let's talk about Lp(a). How many physicians even knew about Lp(a) 12 years ago? Very few at a best case, and those that did used the articles written by Tom Dayspring and others to gain some knowledge on that subject. How much knowledge did lipidologists have about Lp(a) back then. Again very limited by the studies available at that time. Context matters..

                      If you were to compile the lipid information gained over the last 12 years, you would end up with a different view today than what Tom Dayspring said 12 years ago based upon that valid study at the time that he used. He has said this himself, including in this podcast if you listened to it. That is why I agreed in today's understanding that the sentence you quoted out of context made no sense because it doesn't (today). Context matters.

                      If a person want's today's understanding of lipids, you need to dig around for more recent information and attach more importance when multiple mainstream leaders in the lipid field tell us something new. Both Ron Krauss and Tom Dayspring emphasize that LDL-P (apoB) is the marker that we need to pay attention to more than LDL-C and HDL-C as part of a standard lipid panel. In addition, they both say that triglycerides are important to understanding lipid problems, and many people exhibit the high triglycerides/low HDL-C marker as part of metabolic syndrome. Lowering triglycerides often raises HDL-C. Does that mean that more of that HDL-C is actually leaving the body. Nope, and that is the point that they are making. There are NO functional tests now for how much of that HDL-C gets taken out of circulation. Hopefully one day there will be, but like a lot of metabolic issues being studied the functionality of HDL hasn't been easy to tease out.

                      If you did listen to the podcast, you would understand that an Lp(a) inhibitor is being developed and will go through a testing phase that hopefully will help many with Lp(a) to substantially lower those particles. Facts matter within the appropriate context.


                      • #12
                        Are you referring to the anti-sense drugs? Yes, they are in trials now, I believe. I look forward to news. I've got a few patients with the very high Lp(a) levels, one over 500. These are from a well-known gene pool of French Canadians. They often get aortic valve calcification at a young age. Most of the other Lp(a) patients I've seen are in the 50-150 range. Most of those folks can do usually do fairly well with lifestyle and other countermeasures. They tend to get into trouble with their IR starts kicking up. It will be so good, though, if the anti-sense drugs turn out to be a definitive treatment.


                        • #13
                          Dr. Brewer,

                          Yes, to my understanding this is one of the newer anti-sense drugs. The company is Ionis/AKCEA, ironically formally known as ISIS (reason for name change obvious). Below is the link to the Phase II results. Interestingly, this company is also working on an apoCIII lowering drug. People who naturally have lower apoCIII levels tend to live longer and have less heart disease.