October 18, 2018


#23 – Tom Dayspring, M.D., FACP, FNLA – Part IV of V: statins, ezetimibe, PCSK9 inhibitors, niacin, cholesterol and the brain

"This is what it ultimately comes down to – and it's the way you practice – you've got to individualize everything." –Tom Dayspring

Read Time 78 minutes

In this five-part series, Thomas Dayspring, M.D., FACP, FNLA, a world-renowned expert in lipidology, and one of Peter’s most important clinical mentors, shares his wealth of knowledge on the subject of lipids. In Part IV, Peter and Tom review the history and current use of drugs to prevent cardiovascular disease. They also discuss why some drugs appear to be more effective than others, an in-depth conversation about niacin, cholesterol and brain health, and the futility of using CKs (creatinine kinase) and liver function tests to identify adverse effects in statins, to name a few topics in this episode.


We discuss:

  • Bile acid sequestrants and statins [2:00];
  • Ezetimibe (Zetia) [15:00];
  • PCSK9 inhibitors [27:30];
  • Fibrates [41:00];
  • Fish oil, DHA, and EPA [1:01:00];
  • Niacin [1:05:15];
  • PCSK9 inhibitors [1:23:45];
  • Cholesterol, statins, and the brain [1:30:00];
  • Elevated creatine kinase (CK) and liver function tests (LFTs) on statins [1:50:30]; and
  • More.



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Thomas Dayspring, M.D., FACP, FNLA

Thomas Dayspring, MD, FACP, FNLA is the chief academic officer for True Health Diagnostics, LLC. He provides scientific leadership and direction for the company’s comprehensive educational programs. Dr. Dayspring is a fellow of both the American College of Physicians and the National Lipid Association. He is certified in internal medicine and clinical lipidology.

Before relocating to Virginia in 2012, Dr. Dayspring practiced medicine in New Jersey for 37 years. Over the last two decades, he has given over 4,000 domestic and international lectures, including over 600 CME programs on topics such as atherothrombosis, lipoprotein and vascular biology, biomarker testing, and women’s cardiovascular issues.

Dr Dayspring is an Associate Editor of the Journal of Clinical Lipidology. He has authored or co-authored numerous manuscripts published across leading journals such as the American Journal of Cardiology, the Journal of Clinical Lipidology, and several lipid-related book chapters. He was the recipient of the 2011 National Lipid Association President’s Award for services to clinical lipidology. [truehealthdiag.com]


  • Employed full time for last three years by True Health Diagnostics, LLC, which provides biomarker diagnostics and clinical services to clinicians, patients, and healthcare organizations
  • 2017: small consulting project for Abbvie

Tom on Twitter: @DrLipid

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  1. Dr Dayspring is leaning way too heavily on the AIM HIGH and HPS2 trials in his condemnation of Niacin. Both studies are massive and expensive, but they are ridiculously designed and also have some minor executional flaws. So much so that their utility is marginal.

    Just consider the absurd premise. You’re starting with people in the lowest 5th percentile of LDL and trying to lower them even further. Where are you trying to go? To the first percentile?? Come on, that’s just nuts. The issue isn’t just that these patients are already drowning in statins, the issue is that they are on the steep part of the all mortality LDL U curve. So in that sense it is not too much of a stretch to say both studies are designed to kill people! Granted, no one has shown causality in the U curves, but you still cannot just blithely assume there *is* no causality. That’s just reckless. This whole notion of “reducing residual risk” from these levels of LDL is highly speculative. Who says the residual risk lies in LDL? That’s essentially assuming that all CVD risk lies in LDL. Where on earth has that been shown? I’m surprised Peter didn’t bring this up.

    On execution there’s plenty of published criticism: giving up to 200mg nicotinic acid to the placebo group, using laropiprant, the additional Zetia to lower LDL in the control group (wow, how bogus is that?).

    On top of that, Dr. Dayspring extrapolates these very narrow results to ALL possible patients. Just because niacin is not effective on someone soaked with statins in the lowest 5th percentile of LDL tells you nothing about how a non-diabetic with high LDL would respond. You don’t have to be an MD to see that, surely?

    Another concern is Dr. Daysprings speculative notion (1h:17m:55s) that despite lowering the causal LDL, Niacin is somehow secretly counteracting that benefit in two magical ways. The first magical way is that the counteraction is limited to only the cardiovascular system. Kind of odd, don’t you think? If Niacin is harmful then that harm could show up in the kidneys or liver, or a thousand other places, but somehow it confines itself only to cardiovascular. The second, is that the counteraction is so perfectly calibrated that it cancels the benefit of LDL reduction just perfectly, so perfectly that there is zero event reduction. What are the odds of that? Why not a little more, or a little less? I think Dr Dayspring is missing other more banal explanations, e.g. that residual risk does not lie in LDL.

    Dr Dayspring then goes on to nitpick all the negative side effects of niacin. Some of these are indeed valid, e.g. contraindication for diabetics and high triglycerides. But then, in fairness, you should talk about the negatives of statins: On this very channel you confirm that statins increase Lp(a), they increase coronary plaque as measured by calcium deposits (James O’Keefe interview), they reduce cholesterol production in brain cells (Alzheimer acceleration?), and, oh by the way, cause muscle pains.

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