1/4 "also is the LEM (Lipid Energy Model) mutually exclusive with high LDL being atherogenic?"
Yes and no.
Yes -- in that the two should be treated as separate questions. It may well be that LEM is true, yet high LDL is independently atherogenetic and vice versa.
However...
Yes and no.
Yes -- in that the two should be treated as separate questions. It may well be that LEM is true, yet high LDL is independently atherogenetic and vice versa.
However...
https://twitter.com/vardaanbhat/status/1632248580886114305
2/4 No -- in that it was actually metabolic dynamics having an impact on lipid profiles that led me down the road we're at now.
Function vs dysfunction (or successful regulation vs unsuccessful regulation) having an upstream impact on lipid levels should be strongly considered.
Function vs dysfunction (or successful regulation vs unsuccessful regulation) having an upstream impact on lipid levels should be strongly considered.
3/4 But currently, it is assumed these influences are either irrelevant or the impact known -- at least to the extent that it is commonly assumed high LDL is pathogenic in every context (hence, little need to prospectively study metabolically healthy populations with high LDL)
4/4 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 their LDL-C levels are in the highest 0.1% of the population (~260 mg/dL thus far)
Actively excluding those with dysfunctional lipid metabolism of genetics (ie monogenetic FH) or of acquired disease (ie atherogenic dyslipidemia)
Yet their LDL-C levels are in the highest 0.1% of the population (~260 mg/dL thus far)
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