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. 👍
5/ Using these #LEM principles, I'd hypothesize I could consume the same proportion of calories from butter @DrNadolsky was, yet have a moderate to low LDL-C (keeping total calories at maintenance levels).
I'll have the write up for this experiment released soon, but for now...
6/ What do you think - can this really be demonstrated through dietary intervention alone using principles as detailed in the Lipid Energy Model?
Can I consume that much butter per day and demonstrate a moderate to even low #LDL#Cholesterol?
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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.
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.