1/4 Retweeting via @Lpa_Doc -- click within to read 3 part thread. 👇

Also, per our video abstract:
"We remind viewers that existing guidelines and every major scientific institution around heart disease strongly advises against high cholesterol levels."
2/4 And,"While these data on our patient are comprehensive and provide potential new insights, they are limited in scope and timespan. It’s certainly possible this patient is an outlier, or that their progression of plaque will take place later, or many other such possibilities."
3/4 In short, while we appreciate the opportunity to explore the Lipid Energy Model (#LEM paper forthcoming) and share novel data (such as this case study), we continue to emphasize this is uncharted territory and largely considered substantially risky within Lipidology.
4/4 Please read full case report for the context of this patient and considerations taken by him and his care team to date.

doi.org/10.3389/fendo.…

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More from @realDaveFeldman

Apr 17
1/4 FWIW -- the recent WDHR study using CCTA provided some very powerful data on this very question: jamanetwork.com/journals/jaman…

[Note the mean age was 58] -- "Second, we observed absence of plaque in 46.2% of patients with LDL-C levels of at least 190 mg/dL."...
2/4 ... "This proportion was similar to that in patients with lower LDL-C levels. Third, CCTA-ascertained absence of CAC indicated no detectable plaque in 86.8% of patients, including those with LDL-C levels greater than 190 mg/dL."
3/4 To be sure -- "However, the prevalence of noncalcified plaque increased with higher LDL-C levels."

This isn't too surprising where not stratifying for metabolic health and other such higher associative indicators at those levels...
Read 4 tweets
Apr 13
1/ A lot of times polls like these are more interesting for the talk they generate than even the results themselves.

Here are a few featured comments and my added thoughts...
2/ A lot of people wanted greater specificity on what I meant by "rich" -- I left this more to the reader's interpretation. IMO, I'd have thought this would be in a highest quantile, such as top 1/3rd or 4th of typical aggregate diet.

3/ @MichaelMindrum mentioned the poll results might skew a bit too much toward expectation of SFA not causing CVD given those likely following my account -- I don't disagree.

Hence my interest in direct study on health conscious populations consuming high SFA (like many #LMHRs)
Read 5 tweets
Apr 8
📊Polls ahead of #KetoSaltLake

Poll (1/4)
Lean Mass Hyper-responders (#LMHRs) are defined by:

+⬆️#LDL #Cholesterol at 190mg (5.17mm) or higher,
+⬆️#HDL-C 80 (2.07) or higher &
+⬇️#Triglycerides of 70 (0.79) or lower

In your opinion, cardio risk level of this profile is likely
Poll (2/4)
Many demonstrating the #LMHR phenotype (but not all) consume a diet...

High in animal protein
High in red meat
High in saturated fat

In your opinion, if we were to further stratify the #LMHR population to those with the above diet, their cardio risk level would be...
Poll (3/4)

When did you first hear of the Lean Mass Hyper-responder profile?
Read 5 tweets
Mar 9
1/ The scientist in me is looking forward to this new, real world data emerging on #HealthConscious #Carnivores.

It will help provide data that helps confirm/disconfirm the long standing assumption that "healthy user bias" has been effectively adjusted for by researchers...
2/ If you're not familiar with "healthy user bias" (HUB), it's a known potential confounder where those who are doing what they feel is healthy in one regard (such as avoidance of red meat), can often have other likewise "healthy habits", such as more exercise, less smoking, etc
3/ This is a big problem with epidemiology given the overlap is quite common.

To mitigate this, there are efforts to adjust for these confounders such as through statistical techniques (ie sensitivity analyses)
Read 6 tweets
Mar 8
1/ Yes! @NutritionMadeS3 -- please stay with this, it's important.

This goes back to what we were talking about last summer and why I keep drawing the distinction...

In fact, if you (and everyone else reading) would care to indulge me -- I'll unpack further...
2/ Let's definitely grant for a moment that ApoB containing lipoproteins (which we'll call ApoB-Lp) are participants in the process of ASCVD.

Can we likewise consider there are disease states (whether genetic or acquired) that result in both changes in serum ApoB-Lp *and* ASCVD?
3/ Monogenetic FH is certainly one I'd Put on the table.

In particular, a likewise constituent participant in the process of ASCVD are macrophages. Macrophages are nucleated immune cells and can thus suffer the same dysfunctional lipid metabolism we see with hepatocytes of MoFH.
Read 14 tweets
Feb 27
🎙An absolute *must listen*!!! 🎙

1/ This podcast episode via @HCTriage, the third in a series on #ScienceTransparency, the #ReproducibilityCrisis and how we got here is easily one of the richest, and most articulated explanations I’ve heard yet podcasts.google.com/feed/aHR0cDovL…
2/ Again, an incredible triumph in science communication by @crashcoursestan @olsenvideo @DrTiff_Phd among others.

👏 👏 👏
3/
@BrianNosek:
“The big challenge as we see it is that the values that we have for how we think science should operate are not aligned with the culture, the incentives, and the policy landscape for driving how science does operate.”
Read 8 tweets

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