1/ Medical Case
👉53y M, #LMHR w LDL 394, HDL 111, TG 40 for 4y on #keto diet
👉BMI 21.6
👉Prior to keto LDL was 98 mg/dl
👉CCTA shows no plaque, CAD-RADS = 0
👉Parents both lived to >80y w/o cardiac events Family hx of neurodegenerative diseases, including 2x of 👉Parkinson’s
2/ Patient doesn’t want to abandon diet because it makes them “feel my best.”
You’ll notice, there’s no poll associated with this case. Medicine isn’t a democracy and not all medical opinions on Twitter are equally informed. However, I wanted to share this case ...
3/ ...as a juxtaposition to the extremism I’m seeing ON BOTH SIDES: LDL/ApoB is benign v. lower is better (period). Neither is the case. A bit of nuance…
With respect to “LDL/ApoB is benign,” all things being equal, the data don’t support this view. It’s a risk factor...
4/ ... part of a causal pathway. Are there potentially more important risk factors? I think so, personally.
And should it Always be lowered medically. Well, if this were the case, everyone should be on meds to get levels to as close to 0 as possible. Which brings us to…
5/ “lower [ApoB] is better”
My issue with this catchphrase is that it is a blanket statement that discards competing medical considerations. I like this case as it highlights the fault of oversimplifications. Is having LDL in the basement, like 40, 30, or even 20 mg/dl, good?...
6/ For ASCVD let’s assume yes. But this patient has a clean CCTA and no fam hx of heart disease. By contrast, he has a family hx of PD for which low ApoB might increase risk (2019 data from Circulation Research, IF 17 AHA-associated journal: pubmed.ncbi.nlm.nih.gov/31382822/).
7/ So, is medicating down the LDL with a statin the best path, even were the patient agreeable? Open question without a clear answer.
IMHO "we" need to feel more conformable saying, honestly, “I don’t know, but here are the factors…”
8/Then the patient decides, which is always the case anyway
… “and let’s pursue more research that will help us cover clinical gray zones in future.”
2/ 2:45 I talk about how 30g inulin/d can increase inflammatory markers and markers of liver damage, here are those data. Look at the pink arrows and I explain what's going on.
3/ At 3:38 I discuss how Arabinoxylan fiber specifically, but not inulin fiber lowers LDL #cholesterol. You can see that very clearly here as the red line represents a plummeting of LDL vs. green line no real change. They are both fibers, but differentially impact lipids
Lipids & associated proteins have previously been identified as biomarkers of infection, including VLDL, HDL and various apolipoproteins, while both TAG and (serum) PUFA have been implicated as markers of severe disease outcomes
But what this paper adds
3/ Is an investigation (using mostly HEK293T-ACE2 and A549-ACE2 cells) of how the virus alters the lipidome and the importance of these changes in viral proliferation ... They found virus ⬆️TAGs, and PUFA chains were 2-8-fold more than saturated or monounsaturated species ...
2/ First and foremost, what did my diet look like?
Vegan and w/o no coconut to maintain low sat fat % <15% total fat. These are data from a day of soy protein, 1/4c tahini, 1lb eggplant, 100g broccoli, 6 Tbsp EVOO, 4 Tbsp avo oil, 2 oz ea macadamia and pecans, 200g asparagus
3/ I’m an example of an LMHR that eats a relatively low saturated fat diet at baseline. Even when >80% of my fat intake is MUFA/PUFA, my LDL can run >500. Thus, it’s not simply the sat fat. Even when fiber intake has been >30g with net carbs <30g, my LDL can easily run >350
1/ This ??? has come up before, can you be LMHR and not actually lean. Here is a good case!
Individual meets all criteria for LMHR, but BMI 27. So, by the formal definition, the answer is simply, "yes." But let's discuss the nuance...
2/ First, let's again redefine what an LMHR is: >=200mg/dl LDL, >=80mg/dL HDL, >= 70mg/dl TG. That's it. BMI is not part of the definition. The term, "LMHR" is historic based on the general pattern that persons who have this profile TEND to be lean and/or athletic, but ...
3/ That's not a hard and fast rule. So, one could fairly argue the term isn't perfectly descriptive, re "LEAN". This is nothing special -- it's just language. I could come up with any number of examples of imperfect terms, Syndrome X, Aplastic anemia, etc. And it well may be...
2/ What it IS:
We provide the first description of the long-awaited #LEM hypothesis, a model that attempts to explain:
(i) the inverse association between BMI and LDL-C on #lowcarb diets
(ii) the #LMHR phenotype, in which lean people on low carb exhibit very ⬆️LDL-C⬆️HDL-C⬇️TG
3/ These phenomena, presently, have no complete competing explanation:
If effect were purely genetic, the🧬s would need 2explain:
>how macronutrient change can alter, not just LDL-C, but HDL-C+TG as part of a triad
>correlation between BMI and lipid changes