Read on Twitter
1/🧵 I'm definitely a fan of both @DominicDAgosti2 and @DrRagnar (obviously), so I was excited to see them chatting about #lipids, #LMHRs, and Dom's consideration of increasing carbs to lower his #ApoB
If no one minds, I'd like to add some thoughts...
If no one minds, I'd like to add some thoughts...
2/ First -- I'm extremely excited to share @DominicDAgosti2 may be the most notable N=1 I've waited for regarding #ResistanceTraining change & #LDL/#ApoB in a #ketogenetic context
Those who've followed me for a while know exactly what I'm talking about...
Those who've followed me for a while know exactly what I'm talking about...
https://twitter.com/realDaveFeldman/status/1363717241129209856?s=20
3/ When chatting with Dom in SD last year for dinner, he mentioned focusing less on maintaining such a sizable muscle mass as he typically does, and I predicted he'd likely see his LDL/ApoB as considerably higher with this change if still #keto. This podcast appears to confirm...
4/ If fact, I was trying to get a comparable experiment (even if just for 2 weeks) with @jerryteixeira to test this part of the hypothesis 👇
(Lifters always love when I emphasize this as a "confounder" in lowering LDL -- but it makes perfect sense, IMO)
(Lifters always love when I emphasize this as a "confounder" in lowering LDL -- but it makes perfect sense, IMO)
https://twitter.com/realDaveFeldman/status/1466120798645612554?s=20
5/ @DrRagnar mentions lower insulin as relevant where observing ApoB and its association with atherosclerotic risk.
"If you have pristine metabolic health, I still think your risk is higher than somebody with the same metabolic health, but with a lower ApoB."
"If you have pristine metabolic health, I still think your risk is higher than somebody with the same metabolic health, but with a lower ApoB."
6/ To be sure, I'd hope the Lipid Energy Model could add to this discussion, of course.
Metabolism and ApoB are not at all mutually exclusive. I know they are often treated as discreetly separate risk factors, but I think lipid profiles are more often a consequence than a cause
Metabolism and ApoB are not at all mutually exclusive. I know they are often treated as discreetly separate risk factors, but I think lipid profiles are more often a consequence than a cause
7/ Prolonging the process of delivering triglycerides from ApoB lipoproteins means they will remain in circulation for longer (all else being equal), which will coincide with higher remnants and TG, alongside lower HDLc due to lower turnover.
All these are collinear w/ MetSyn.
All these are collinear w/ MetSyn.
8/ Our #LMHRstudy is the first of its kind.
Actively excluding those with dysfunctional lipid metabolism of genetics (ie monogenetic FH) or of acquired disease (ie Atherogenic Dyslipidemia)
Yet baseline avg LDLc levels are in the highest 99.9% of the population (~260 mg/dL)
Actively excluding those with dysfunctional lipid metabolism of genetics (ie monogenetic FH) or of acquired disease (ie Atherogenic Dyslipidemia)
Yet baseline avg LDLc levels are in the highest 99.9% of the population (~260 mg/dL)
9/ In other words, to this point we've never prospectively studied a population with extremely high LDLc/ApoB where ASCVD risk factors were low, including those around metabolism that may be directly contributing to the character and residence times of ApoB lipoproteins directly.
10/ The irony is that this was only possible due to the rise in popularity of the #keto diet.
... A diet popularized in part by @DominicDAgosti2 himself, no less.
... A diet popularized in part by @DominicDAgosti2 himself, no less.
• • •
Missing some Tweet in this thread? You can try to
force a refresh
