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:
4/ Naturally, at a population level, #LMHRs shouldn’t be exempt from a high risk for cardiovascular disease despite having high HDLc and low TG where their LDLc and ApoB are at the very highest % of the population. This question gets to the heart of the thread of yours above👆
5/ i’ve actually been asking it of everyone for the many years it’s taken for us to get the LMHR study together. For many who favor lowering LDLc/ApoB, their answer is similar to your initial one here:
6/ But to be sure, I think we would agree that this doesn’t provide much specificity as to their overall differences in risk for developing ASCVD. Obviously there’s an extremely wide range of magnitude possible when stated in an open manner. But why?
7/ I suspect both of us would agree that very high LDL alongside *low* HDL and *high* TG would associate with a considerably high risk for cardiovascular disease.
Thus, would the high HDL and low TG criteria of the LMHR phenotype be the strongest modulator of risk? (not LDLc?)
8/ and to reemphasize, I don’t know the answer to that question yet. Yes, i’m hopeful for good news from our LMHR study, but we don’t know what we don’t know.
I just know if you’re opening the topic of lipid profiles instead of lipids in isolation, I’m always interested…:)
9/ But this key question of LMHRs and their risk at a population level should be an easy one to answer for every one of us who already has a strong opinion for this context.
(As always, I appreciate your work, @NutritionMadeS3 and I’m hoping you’ll come to be curious on mine)
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. 🔬🔬🔬
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/ 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.