1/ Reminder: "Lean Mass Hyper-responder" is literally defined as a combination of LDL ≥ 200, HDL ≥ 80, and Triglycerides ≤ 70.
In other words -- by definition -- #LMHRs are not hypertriglyceridemic (high triglycerides). They are the opposite. (See CholesterolCode.com/lmhr)
2/ For example, in the first of this case series a woman is identified as hypertriglyceridemic (triglycerides of 1109). This is if 15 fold higher than the TG max cap of #LMHR.
3/ Moreover, we actually addressed this particular case of hypertriglyceridemia in our Letter to the Editor of this very case series. In fact, it's how we set up the question on what to consider when triglycerides are low instead
1/ It’s ironic, I came across an email I wrote almost 3 years ago when I was first pushing for a “Study on atherosclerosis in LMHRs”. For that first 1.5 years I tried to raise interest and money from inside the system. Some of these details I’ll go into with the book eventually..
2/ Not at all calling anyone out — just noting that it took me a while to realize it was likely a dead end.
For almost all of them, the answer to this question was already known: High LDL LMHR = high atherosclerosis
(And FWIW, it’s possible they’re right— we’ll soon see...)
3/ Then I had the crazy idea to start a charity and announce at #LowCarbHouston in Oct 2019 that we’re going to just try to straight up raise the money to do this study through crowdfunding.
I saw this paper linked by @BioLayne (hat tip!) in a twitter discussion and had to stop and read most of it. Basically SFA vs PUFA infused muffin RCT. There's quite a lot of interesting data within. And it's publicly available, btw (no firewall)...
... The lipid profile changes for the SFA group are unsurprising to me, ofc. But I was surprised they went with ALT as the proxy for "liver fat accumulation". Relative change 53%, but I didn't find the absolute values listed for ALT between groups? Maybe in the supplement...?
... They had a subgroup of 10 (5 of each) where the did PET-MRIs (need more of this in studies) to detect "change in hepatic palmitate uptake" -- which tends to be a stronger proxy for liver fat accumulation, but it showed no association.
1/ Whether in agreement or not, @DBelardoMD's statement does represent the existing position of mainstream medicine, particularly lipidology. (Tho she's adding a bit more "color" to it, ofc :) )
My retweets like these are to further generate cross exposure to other voices...
2/ ... Think of it as working toward breaking down some of the echo-chamber-ism.
If you follow me, you're going to get this on a regular basis because I feel hearing every side is important (I have many friends who are LDL skeptics who definitely don't agree with me on this!)
1/ Still one of my favorite studies in relation to the #LipidEnergyModel. One might wonder what happens to animals who become fat adapted due to fasting for a long period.
2/ They were comparing bears in captivity and the wild. And in both, lipid levels during hibernation are "considerably higher than what is normally found in humans"
3/ In spite of the high lipid levels alongside other risk factors, they found no signs of atherosclerosis in brown bears.
... And obligatory disclosure -- @siobhan_huggins and I are trying to see if we can get this offered through OwnYourLabs.com, but my comment above is not a pitch for OYL specifically, there are many ways to get a @BostonHeartDX lab done, in many cases thru your doctor...
... For anyone reading this who has a doctor who uses @BostonHeartDX, you can consider asking if you can get it ordered (and if they cover it). That's likely to be the best option.
(Also obligatory this-isn't-medical-advice, just an assay I hypothesize has enormous value)