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Ahmed Profile picture
Ahmed
@TheCuriousAhmed
Nov 24, 2018 • 17 tweets • 8 min read
Both ApoB and LDL-P measure the same target i.e LDL particle concentration, yet discordance between the two metrics usually occur.

An example, this study (Krauss et al) we analyzed earlier, SFA significantly increased ApoB, but not LDL-P.
1/
 On the other hand, in this study (Maki et al), MUFA decreased ApoB, yet increased LDL-P.

This study seem to indicate that LDL-P doesn't necessarily go with the same direction as ApoB.
2/
Oct 16, 2018 • 11 tweets • 20 min read
@puddleg @MorganPfiffner @DaveKeto @kirbz83 @DoctorTro @MMAdailyfeed @martijnkatan @Karageorgos15 I don't know how I forgot about this study. Very relevant to this discussion
ncbi.nlm.nih.gov/m/pubmed/10856…
It includes details on cholesterol esterification, intracellular TG accumulation and ApoB secretion. @puddleg @MorganPfiffner @DaveKeto @kirbz83 @DoctorTro @MMAdailyfeed @martijnkatan @Karageorgos15 ApoB secretion correlated more with intracellular TG accumulation than with cholesterol esterification.
Sep 1, 2018 • 8 tweets • 3 min read
How different saturated fatty acids affect blood lipids? What are the worst saturated fatty acid? A quick look. There's now a consensus for ApoB being the crucial marker for CHD, not LDL-C, if that's the case, what are the worst saturated fatty acid based on this marker? Clearly most SFAs are bad, most of them increase LDL-C, but again, it's the ApoB what does matter.
Aug 29, 2018 • 45 tweets • 9 min read
Lipoprotein lipase, the major player in the LMHR phenotype, apparent atheroprotection, despite higher LDL-C, thread.

To begin with; I was supposed to post this thread 2 weeks ago, but due to circumstances it was delayed.
This is an extensive thread comprised of 5 sections. Section 1: discusses the mechanisms.
Section 2: the effect of insulin.
Section 3: the relationship with other blood markers.
Section 4: the effect of diet.
Section 5: the impact in atherosclerosis.
Section 6: longevity syndrome (separate thread - in progress)
Jul 4, 2018 • 19 tweets • 6 min read
We suggest dyslipidemia -not LDL- is the predictor of CHD, increased LDL levels is often a component of dyslipidemia, to unmask confounding, other components of dyslipidemia - i.e high TG, low HDL - should be controlled. In the upcoming posts, we show studies that controlled for the other lipid markers.
Summary:-
Dyslipidemia, caused by insulin resistance and/or inflammation, is more plausible to be the cause of CHD, instead of LDL as a part of homeostatically regulated system.