2/ We've had an ongoing debate on how much (or little) #saturated fat consumption is responsible for high #LDL#cholesterol levels we typically see for #LMHRs.
Whereas I (we) believe #LEM to have greater relevance overall.
3/ Could @DrNadolsky emulate the #LMHR phenotype while *not* being fat adapted? (or at least, to get his #LDL#cholesterol that high?)
He consumed two sticks of butter a day to test this! 🧈🧈
Yes, the experiment went more toward my prediction, so alas, I won't be flying there.
4/ However, @DrNadolsky is now doing another experiment on the heals of this one where he's going keto with some added elements you may find interesting. But I'm leaving it to him to share.
(Not as excited about this 2nd one, but still very much interested in the data)
5/ Again, my sincerest thanks to @DrNadolsky for performing this experiment and contributing his share of #CitizenScience. 🙏🙏🙏
Lastly, if you want to read more on the #LEM I was speaking to above, be sure to see our recent paper on it here:
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.
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. 👍
2/ If replacing M/PUFA with SFA but keeping all else equal (including -- importantly -- carbs) for this exact context, this might have a marginal impact on TC/LDL/HDL. But would it command a higher magnitude of increase? I'd be doubtful...
However, if replacing carbs with fat...
3/ ... Thus going lower carb, we get closer to the model around LEM and its explanation regarding TC/LDL-C/HDL-C changes toward the outcome magnitude of the LMHR phenotype.
Hence the value of looking to RER for this experiment to confirm/disconfirm fat-adaptation.
1/5 This is BIG & I've really been looking forward to it. @DrNadolsky will be looking to see if he can reach a #LMHR phenotype while not being low carb or keto (or at a minimum, increase LDL-C to 200)
In short, can high consumption of saturated fat w/o being fat-adapted = #LMHR?
3/5 But more importantly, this gets to a very common assumption regarding #LMHRs -- that their phenotype can be mostly explained by higher consumption of saturated fat.
3/ To be sure, I'd echo @NutritionMadeS3's qualifier in the video that this is expected at a population level. So the exceptions don't prove the rule (in either direction).
Hence the enormous importance of studying those with extremely high LDL/ApoB at a population level...
1/ I'd love to take an opportunity to expand on this important topic, and if I may, suggest something important to watch for with some newly emerging data.