Anybody interested in a lipid chat with Dave Feldman?

[MarcR]

Mike, you already got my best advice:

I wonder if Dr. Richard Bernstein's insights would apply to your situation.

You indicated that you have "been following Bernstein for a number of years now." When I read the table of contents from his book, I see an awful lot of detail that seems relevant to your questions.

Your description of your insulin trial was brief, and your role in the process appeared to be passive:

I was put on insulin in the hospital and continued afterwards. I started gaining weight and could not control eating.

It sounds as though your dose may not have been dialed in. Bernstein devotes four chapters just to exogenous insulin - I think he shares detailed protocols designed to balance physiology, food, glucose, and insulin precisely and consistently.

So ... when you say you have been following Bernstein, does that mean that you have bought, read, and implemented the strategies described in the book,

Dr. Bernstein's Diabetes Solution - A Complete Guide to Achieving Normal Blood Sugars

and that they have failed to resolve your concerns?

[mike]

Mike, you already got my best advice:

I wonder if Dr. Richard Bernstein's insights would apply to your situation.

You indicated that you have "been following Bernstein for a number of years now." When I read the table of contents from his book, I see an awful lot of detail that seems relevant to your questions.

Your description of your insulin trial was brief, and your role in the process appeared to be passive:

I was put on insulin in the hospital and continued afterwards. I started gaining weight and could not control eating.

It sounds as though your dose may not have been dialed in. Bernstein devotes four chapters just to exogenous insulin - I think he shares detailed protocols designed to balance physiology, food, glucose, and insulin precisely and consistently.

So ... when you say you have been following Bernstein, does that mean that you have bought, read, and implemented the strategies described in the book,

Dr. Bernstein's Diabetes Solution - A Complete Guide to Achieving Normal Blood Sugars

and that they have failed to resolve your concerns?

Let me re-phrase the Bernstein mention. He was one of the first I read quite a number of years before. I went back to my phone and re-downloaded it from my library. This was years before I was ever on insulin. I've been following his advice to limit peaks in blood sugars for 10-15 years. The link you first gave me was a list of foods that he avoids, and I'm as strict or more. I looked briefly at the list of tests he advises, and I do pretty much all of them. I didn't see anything for IR testing, but I'll look some more.

In regards to insulin, I had reasonable control for the first 16 years of my T2D journey, but then I had a small brain-stem blood clot, and after that the meds did not seem to work as well. Of course my exercise level also dropped... I year later I had a negative reaction to new T2D drug that caused my TG to be too high to measure, and put me into the hospital, where they put me on insulin. After, I then saw the doctor who treated me at the hospital for another year privately. I started on low dose of basal insulin, and then had to up the dose as my blood sugars went up, then he added fast acting insulin before meals, and likewise, the dose had to be raised. This doctor is VERY highly rated, but he couldn't explain it. I think I gave insulin a fair shot. I decided on a different track. I dropped the insulin all together, and my blood sugars did not change. My weight started dropping without effort. It is becoming clear that like AD, T2D is not just one disease, but a number of similar diseases.

I'm not expecting you to solve my issues Marc, but I do appreciate being able to bounce ideas off you and the others here.

[MarcR]

The video recording of the webinar is available here:

Dave Feldman: Lipids, Health, and ApoE4 Webinar

We're working on show notes and will post again when they are available.

[Julie G]

I didn't perceive anyone to be espousing that point of view at the webinar, but my own views are close enough that I feel the need to clarify.

This is what I think:

1. Using drugs that interfere with lipid biochemistry probably increases all cause mortality (ACM).
2. Using lifestyle to reduce or increase LDL or LDL-P may reduce or increase ACM.
3. Using lifestyle to optimize the biomarkers in the metabolic syndrome definition while trusting one's body to manage LDL and LDL-P almost certainly reduces ACM.

"Arbitrarily raising TC" would fall under item 2.

I really like your take on this, Marc. I didn’t mean to imply that Dave was recommending “arbitrarily raising TC” to improve odds of longevity. Like everyone, I tend to apply my own experience to various hypotheses to see if it fits. Indeed, optimizing my metabolic profile has definitely corroborated Dave's energy model in terms of TG/HDL with a current ratio of 0.256 (TG-50, HDL-95), but my LDL-P has had an interesting trajectory that might track with my Babesiosis. When I was at the height of my infection, my LDL-P was also at it's highest. Now that I've healed from that, my LDL-P has dropped fairly dramatically (1380 to 890.) It's hard for me to reconcile my experience with Dave's ACM data. Why would healing an infection statistically put me at higher risk of death? That said, TC may be too rough of a measure to capture my experience as my overall TC is far from low largely due to HDL.

It's interesting to apply the ACM data to the the studies we have of indigenous hunter-gatherers with a high percentage of ε4. The Innuits support Dave's data, but what about all of the studies of those (like the Nigerians & Papua New Guineans) with low LDL that supposedly remained free from chronic disease?

It makes me wonder what type of evolutionary advantage our enhanced responsiveness to dietary fat and increased cholesterol absorption have provided us? Perhaps our ancestral "thrifty allele," was maximized for efficiency when food was scarce?

And Attia starting his podcast with the reasons why he doesn't agree with Feldman, without Feldman being able to respond was better!? You let Dave rebut those three points in our podcast - I think that is just continuing the dialog. It will be these guys that will battle it out, trying to prove their own theories, and likely falsify someone else's.

Don't get me wrong, Mike. I loved Dave's rebuttal to Peter. I just think that the topic is unresolved enough that we could all benefit from further back and forth.

[JimBG]

Julie I agree that we could benefit from more back and forth on this topic. Dave raises some very good points and has some compelling data from his own self experimentation. He has done a great deal of research in developing his energy model and I am certainly not well versed enough to effectively challenge it. That said I can make the following observations after listening to the whole webinar:

1) I don't believe that Attia nor Dayspring think that think that high LDL particle count is the sole cause of CVD. Attia has said that endothelia health and inflammation are also important factors. LDL particles are necessary but not sufficient.
2) Both Attia and Dayspring have noted that drug studies reporting ACM have not been statistically "powered" enough for that outcome. I would like them to elaborate more on that. I am not an expert in this area but my sense is that there is insufficient data
to be sure that the ACM is not more significant than chance variation. How long the study and how many individuals would be required I have no idea.
3) Dave's energy model and his resultant thinking that LDL particle counts do not matter seems to be limited to a subset of individuals who are lean mass hyper responders. And who also have naturally high HDL C and low Trigs. And after collecting data for a year or so on himself and some others he postulates that their CVD risk is low. Maybe yes. Maybe no. Time will tell. And my sense his thinking is that pharmaceutical interventions to improve the HDL C and Trig ratio are likely not effective. So what about the rest of folks who are not in this subset? Shouldn't they be concerned about high LDL P?
4) As a former risk manager and also having a background in chemical engineering I respect his approach in looking for root causes, taking a fresh problem solving perspective and challenging current dogma. That said I can't help but coming away with the view that based upon his personal experience, engaging a handful very smart folks, doing a great deal of reading of related studies over the last couple of years, as well as accumulating some of his own anecdotal data, that his will overturn key features of the vast body of knowledge accumulated over decades by many scientists, doctors and researchers who have devoted their entire lives to this field. In my opinion that is very unlikely.

[MarcR]

3) Dave's energy model and his resultant thinking that LDL particle counts do not matter seems to be limited to a subset of individuals who are lean mass hyper responders.

I understand his argument much differently. He starts from the observation that cardiovascular risk tracks much better with triglycerides and HDL than it does with LDL. If you look at LDL in a vacuum, there's a weak relationship, but once you add trigs and HDL the relationship disappears and reveals LDL by itself as nothing more than a surrogate for high trigs and low HDL. These analyses come from the same datasets, MESA, WHI, etc. etc. If you look at trigs, HDL, and LDL together, you see that LDL doesn't affect CVD risk. Only if you ignore trigs and HDL does LDL appear to matter.

This leads to two obvious questions:

1. Why would we manipulate LDL when all of the CVD risk actually goes with trigs and HDL?
2. How do we live in such a way as to bring our trigs into double digits and our HDL into high double digits?

Those are the key issues.

Now, the low CVD risk group with low trigs and high HDL can be divided into two subgroups. Most people in this group have low LDL; a smaller subgroup has high LDL. The latter group gets flagged by the LDL guidelines and is told by primary care doctors to take statins. This is the group Dave identifies as Lean Mass Hyper Responders (LMHR).

The analysis of LDL against all cause mortality (ACM) is just an additional source of comfort for those in the LMHR group. It's not central - the core point remains that LDL is not correlated with CVD risk if you include trigs and HDL in the statistical analysis.

And who also have naturally high HDL C and low Trigs.

In 2003 my trigs were 373 and my HDL was 36 for a ratio of 10.36. The results were so bad that I didn't visit the doctor for six years. Since 2009, six months after I began my journey back to good health, I have tested lipids nine times, and that ratio has varied from 0.33 to 1.10. I am far from alone in learning that intermittent fasting, avoiding processed food and seed oils, and exercising can make a huge difference in that CVD risk marker. For many people, attaining a low trigs/HDL ratio is a lifestyle choice.

[mike]

Very nice summary of Dave's talk, thanks Marc!

[JimBG]

Marc …. thanks for your clarifications on his argument. They are helpful. And I have no doubt that lifestyle changes make a huge difference in lowering CVD risk. And congrats on your progress to good health! I also endeavor to practice the same lifestyle items you mention. I still believe that although the Trig/HDL ratio is an important marker it is not the end all be all. CVD is a very complex disease and a long term process. Looking a one risk marker, while helpful, is in my opinion likely not sufficient. And for some people life style changes alone may not be enough to address their CVD risk.

[DaveKeto]

Don't get me wrong, Mike. I loved Dave's rebuttal to Peter. I just think that the topic is unresolved enough that we could all benefit from further back and forth.

Let me just cast a very, very strong vote here for the same.

Throughout my life, I've always valued debate as a learning tool like no other. Not he rancorous, cable TV style talk-over-each-other kind. Rather, the respectful examination of arguments from both sides.

In fact, I've started a series, #CholesterolScience, where I'm intentionally seeking out opinions across the spectrum to advance this discussion further. Currently, I've interviewed Spencer Nadolsky https://www.youtube.com/watch?v=6UsnzkpMmDI, Ivor Cummins https://www.youtube.com/watch?v=RxRzj_i9fJg, and Joel Kahn https://www.youtube.com/watch?v=JHzfU7TgcGo -- with Dr Tro Kalayjian coming this Wednesday)

More than anything, I'd like to get some of these tougher questions explored.

[DaveKeto]

3) Dave's energy model and his resultant thinking that LDL particle counts do not matter seems to be limited to a subset of individuals who are lean mass hyper responders.

I understand his argument much differently. He starts from the observation that cardiovascular risk tracks much better with triglycerides and HDL than it does with LDL. If you look at LDL in a vacuum, there's a weak relationship, but once you add trigs and HDL the relationship disappears and reveals LDL by itself as nothing more than a surrogate for high trigs and low HDL. These analyses come from the same datasets, MESA, WHI, etc. etc. If you look at trigs, HDL, and LDL together, you see that LDL doesn't affect CVD risk. Only if you ignore trigs and HDL does LDL appear to matter.

This leads to two obvious questions:

1. Why would we manipulate LDL when all of the CVD risk actually goes with trigs and HDL?
2. How do we live in such a way as to bring our trigs into double digits and our HDL into high double digits?

Those are the key issues.

Now, the low CVD risk group with low trigs and high HDL can be divided into two subgroups. Most people in this group have low LDL; a smaller subgroup has high LDL. The latter group gets flagged by the LDL guidelines and is told by primary care doctors to take statins. This is the group Dave identifies as Lean Mass Hyper Responders (LMHR).

The analysis of LDL against all cause mortality (ACM) is just an additional source of comfort for those in the LMHR group. It's not central - the core point remains that LDL is not correlated with CVD risk if you include trigs and HDL in the statistical analysis.

And who also have naturally high HDL C and low Trigs.

In 2003 my trigs were 373 and my HDL was 36 for a ratio of 10.36. The results were so bad that I didn't visit the doctor for six years. Since 2009, six months after I began my journey back to good health, I have tested lipids nine times, and that ratio has varied from 0.33 to 1.10. I am far from alone in learning that intermittent fasting, avoiding processed food and seed oils, and exercising can make a huge difference in that CVD risk marker. For many people, attaining a low trigs/HDL ratio is a lifestyle choice.

Fantastic summary, Marc. I think you illustrated my position perfectly.