1/ Yes, the topic of a "hyper-response" with high #LDL #Cholesterol (LDLc) on #keto has been coming up a lot this summer, particularly for #LMHRs -- and that's a good thing. More discussion and research desired!

I'll try to unpack the key differences in 3 standing hypotheses...
2/ Conventional: higher LDLc "hyper-response" (HR) mainly due to higher consumption of saturated fat (SF)

@DrNadolsky hypothesis: HR due to higher SF, but also genetics

Me: HR affected by many things, but generally more influenced by Lipid Energy Model (LEM) than SF or genetics
3/ Starting with a few key influences we all agree on...

These things likely have a significant detectable increase on LDL compared to reverse:

1) Swapping unsaturated fat with SF
2) Reducing fiber
3) Less resistance training
4/ The question of genetics is an interesting one, and I definitely think many SNPs impact lipid levels. Some impact these levels a lot, but they are very rare.

This brings us to the major difference between my friend and colleague @DrNadolsky's hypothesis and mine...
5/ I commonly predict if I could choose the cohort (lean, metabolically healthy, more aerobic than resistance training) and the dietary intervention (very low carb, high fat, carnivore-ish diet), then I believe the majority would demonstrate a #LMHR-like phenotype.
6/ I think @DrNadolsky would take me up on this bet as, per retweet above, the expectation is that this response is predominantly genetic influenced (such as via ABCG8 hyper-absorption,etc) and should be rare to observe emergence of this HR, including in my suggested design above
7/ Hopefully we'll get to test this "gym hypothesis" in time to see if indeed there is emergence of the #LMHR profile across a varied genetic cohort.

(As an aside, I love when something is this distinctive and testable. Should be fun when we really get something solid together)
8/ [Addendum] -- @DrNadolsky has corrected me that he is considering other aspects beyond higher consumption of saturated fat -- but the rare gene interaction is still very much central to the hypothesis.

Still testable to the experiment described above...

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More from @realDaveFeldman

Jul 27
1/ 🙏 Happy Accident 🧵

I’m incredibly thankful for that day back in March 2015 when I got an A1c of 6.1 for the second year in a row.

Why?

It led to my finding #lowcarb as a possible means to prevent the onset diabetes…
2/ Shortly after starting, I had immediate family members with health issues be inspired to do likewise.

One of those immediate family members had an A1c of 8.1 at the time. Two were hypertensive, and taking medication for it. And these are just the immediate family members…
3/ off the top of my head, I think there are roughly 2 dozen people between both close friends and family who are sustained lower carb now than they were before For weight loss, or other reasons of health gain.

To be sure, it hasn’t worked for everyone, nor would I expect that.
Read 6 tweets
Jul 8
2 x 2 poll — answer all four.

1/ looking to a population that has this combination of lipid levels:

⬇️⬇️ very low LDL-C & ApoB
+
⬆️⬆️ very high HDL-C
+
⬇️⬇️ very low triglycerides

… you would expect to see what prevalence of heart disease compared to the general population?
2/ looking to a population that has this combination of lipid levels:

⬇️⬇️ very low LDL-C & ApoB
+
⬇️⬇️ very low HDL-C
+
⬆️⬆️ very high triglycerides

… you would expect to see what prevalence of heart disease compared to the general population?
3/ looking to a population that has this combination of lipid levels:

⬆️⬆️ very high LDL-C & ApoB
+
⬇️⬇️ very low HDL-C
+
⬆️⬆️ very high triglycerides

… you would expect to see what prevalence of heart disease compared to the general population?
Read 5 tweets
Jul 6
1/ Interesting thread via @NutritionMadeS3. I invite everyone to read through his before reading the remaining of mine here below…
2/ naturally, you’re discussing a topic that’s very near and dear to my research, @NutritionMadeS3. I’m certainly very interested in metabolic health as it relates to lipid profiles — particularly the “triad” of high LDLc, high HDLc, and low TG. (See mdpi.com/2218-1989/12/5…)
3/ But we should agree to recognizing a common problem. Rather than take several tweets in this thread to explain it, let me open with our conversation from last month where I posed this question for you regarding #LMHRs and #ASCVD at several points:
Read 9 tweets
Jun 30
1/3 Okay, here's my daily breakdown for the #IsItSaturatedFat Experiment.

I'm going to consume 1,000 calories for @KerrygoldUSA! 🧈🧈🧈

That's 140g of butter per day!
2/3 However, I'll be likewise supplementing 728 calories from dextrose, thus consuming much of my remaining dietary energy from carbs.

Per the #LEM, I believe this will have a substantial lowering impact on my LDL-C relative to the increasing influence via ⬇️LDLr of butter
3/3 Note I'm performing this experiment in the spirit of both learning and keeping it fun. ☮️

While I'll concede I might have been caught off guard for a moment yesterday, I'm now thankful this can provide us a new opportunity for discovery and furthering the discussion. 🔬🔬🔬
Read 4 tweets
Jun 29
1/ 🚨New N=1 Experiment: #IsItSaturatedFat🚨
🙏retweet🙏

Yes, I'm doing a new N=1 -- and it's going to be a biggie!

My good friend and colleague, @DrNadolsky completed his recent #MakingLMHR experiment concluding the added 2 sticks of butter as the reason for his LDL increase. Image
2/ He's already conceded he's left out all the context on aiming for #LMHR profile, the relevance of RER, and the #LEM (so no need for people to keep pinging me on the IG video). I've chatted with him privately and we'll leave it at that. 👍

3/ However -- this actually affords us a huge new opportunity.

@DrNadolsky's claim isn't just his own, it's just about everyone else's outside the low carb community.

Simply stated: high #LDL #cholesterol seen in #LMHRs is predominantly due to high consumption of saturated fat.
Read 6 tweets

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