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Aug 20

#CholesterolScience Show – With Ethan Weiss, MD

0:00 Intro and Ethan’s background

3:33 Cholesterol Skeptics and Concerned Medical Professionals – meeting in the middle.

8:20 How many patients does Ethan feel reach a decent level of knowledge about lipidology and cardiology?

10:15 Navigating the discussion on the benefits/risks of lipid changes from diet

17:15 When cholesterol is elevated for a metabolic reason alone – does it pose a greater risk?

23:00 Giving doctors the benefit of the doubt – are doctors just trying to help?

27:10 Dave’s disappointment with perceived lack of curiosity from the medicalsphere.

30:15 The difficulty in discussing possible benefits from lipoproteins and potential influence on all-cause mortality

36:50 Nuances of data collection and statin trials

Study mentioned: MRC/BHF Heart Protection Study of cholesterol lowering with simvastatin in 20 536 high-risk individuals: a randomised placebo controlled trial

Note from producer:
In the efficacy and safety statement for the trial mentioned it lists Merck Sharp & Dohme (manufacturers of simvastatin) as well as Hoffmann-La Roche (manufacturers of the vitamins used) as providing partial funding for the study:

The study is being funded by the UK Medical Research Council, the British Heart Foundation, Merck Sharp & Dohme (manufacturers of simvastatin[…]) and Hoffmann-La Roche (manufacturers of the vitamins[…])

doi: 10.1053/euhj.1998.1350

However in the published paper of the results it states the following:

The Clinical Trial Service Unit has a staff policy of not accepting honoraria or other payments from the pharmaceutical industry, except for the reimbursement of costs to participate in scientific meetings.

doi: 10.1016/S0140-6736(02)09327-3

44:56 If there were a trial that showed that people with high HDL, high LDL, and low triglycerides didn’t benefit from statins would [Ethan] want to know that information?

Study mentioned: Influence of Low High-Density Lipoprotein Cholesterol and Elevated Triglyceride on Coronary Heart Disease Events and Response to Simvastatin Therapy in 4S

52:40 Open data, machine learning, and possibilities moving forward

56:20 Non-HDL and mortality from the NHANES dataset

Twitter exchange mentioned:

58:30 Changes in ability to connect with researchers and scientists

1:00:05 What does Dave mean by risk?

1:04:10 Modifications to low carb to achieve lower LDL

1:08:55 What Dave has learned about the importance of rigorousness in self-experimentation

1:13:29 Can self-experiments have benefits applicable to people beyond the person doing them?

1:17:29 Cholesterol biosynthesis

1:18:40 Reverse causality – is there a possibility that the lipoproteins are reflecting a problem and not causing it?

Note from producer: I attempted a follow-up to see if I could find any studies looking at the impact of infusion of native mouse lipoproteins on atherosclerosis development, but I have not found any thus far.

1:24:33 Clotting, vascular injury, and engineering

1:29:55 The impact of placebo

Podcast mentioned: The Hidden Brain: The Untapped Potential of Placebos to Heal (transcript available)

1:33:23 The impact of seeing lipids change – could this impact the results of the study?

1:35:56 If it were dose dependency would all drugs that lower LDL have a likewise decrease in cardiovascular disease mortality?

1:38:46 Drug trials – ideals, replication, and funding

1:42:35 Wrap up and outro

Ethan Weiss Contact:

Twitter: @ethanjweiss

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Siobhan Hugginsbrad bakerG RBobSara Recent comment authors

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Antony Sanderson
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Antony Sanderson

Dave . . . you set out to have a “conversation” not a confrontation . . . You both achieved that magnificently. But this was not at the expense of ignoring difficult issues. Listening to the conversation set my mood to good for the rest of the day.

Bill Hare
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Bill Hare

Nice interview to dovetail with the Andre and Nick interview. I’m viewing the comment “So the key question is simple: When cholesterol is elevated for a metabolic reason alone – does it pose a greater risk?” I’m tending to consider it from the standpoint of – Does it provide a greater health benefit?? esp. in reference to KetoAF and PKD as therapeutic methods of treatment for multiple disease processes. That’s why I love the work that you and Siobhan are doing!!

JohnM
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JohnM

Re: elevated LDL for pathologic versus metabolic reasons

Peter at the Hyperlipid blog discussed this in a 7/6/08 post: “During glycation conditions the LDL cholesterol particle stops sticking to its normal receptor. Why? My answer is that under these conditions it is more advantageous for the body to have the LDL cholesterol particle in the blood stream than it is to have it endocytosed by an endothelial cell.

Finding high levels of LDL cholesterol is one of the more logical aspects of the hyperglycaemia of type 2 diabetes. Putting these patients on to LC diets usually drops their calculated LDL cholesterol levels along with their blood glucose levels. It probably markedly reduces AGE formation throughout their physiology. LDL can then get back to supplying normal lipid to normal cells through the LDL receptor.”
http://high-fat-nutrition.blogspot.com/search/label/AGE%20RAGE%20and%20ALE%20%281%29%3A%20The%20AGE%20of%20LDL

Assuming that essentially all people eating a SAD diet have elevated lipoprotein glycation, any blood panel returning an elevated LDL concentration should be viewed by a doctor as unhealthy as the assumption (absent other evidence) has to be it’s elevated for pathological reasons (ie, glycation). On the other hand, anyone who knows their LDL is not elevated due to glycation should not view the elevated LDL value as unhealthy.

Sara
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Sara

Regarding the vegan female researchers who went Keto for 2 weeks and showed improvement in their LDL’s, were they pre or post menopause?

Bob
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Bob

Echoing what JohnM posted. Wondering if you had a chance to view https://youtu.be/TRB0jOfymLk
Perhaps LDL is the particle we should fear when glycated and or oxidized when in a metabolically unhealthy state. If that’s the case then certainly it would be beneficial to remove these harmful particles. The irony of course being that statins seem only adept at removing the beneficial LDL (i.e. non oxidized)…Thoughts?

G R
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G R

“However, half of all myocardial
infarctions and strokes occur among apparently
healthy men and women with levels of low-density
lipoprotein (LDL) cholesterol that are below currently
recommended thresholds for treatment.”
from “Rosuvastatin to Prevent Vascular Events in Men and Women
with Elevated C-Reactive Protein” NEJM V359:21 November 20, 2008

brad baker
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brad baker

I have been low carb / Keto since April, lost 45 lbs. now normal weight at 165 for 5’8” male 58 yrs old. Stopped statins to get a baseline and Total Cholesterol. Sept 2019 results were; 272, LDL-C 178, HDL-C 74, LDL-P 2232, small LDP-P 908. I also had CAC score ran and 198 or 70th percentile with calcium in widowmaker LAD.

Prior to KETO was 205 lbs and pre diabetic. Do I go back on statins? Triglycerides are back to 100 from 475, Glucose normal at ~100. no longer pre-diabetic.

I like to low carb lifestyle and diet and can find very little reporting on those living Keto and also on Statins.