Part 2 of an evergreen series: when we look at ApoB (instead of LDL-C) alongside fasting insulin, does the metabolic environment still play a role in how strongly ApoB associates with heart disease?
This is a clearer signal that metabolic context proxied by fasting insulin can materially change the observed association of ApoB with events. It aligns with the broader Feldman framing that particle number is necessary, but the surrounding metabolic environment influences the actual risk. The study does not prove risk level, but it is consistent with the hypothesis that context meaningfully modulates the relationship. Ongoing imaging and longer-term data in LMHR-like cohorts remain the more decisive tests. This continues to be a fascinating exploration.
I’m a 53 year old male on carnivore. I’m 5’8” and 160 lbs. hsCRP low, triglycerides 81, HDL 50 and fasting insulin (9.6 μU/mL) but all my other cholesterol numbers are considered high. How does this ApoB data also mix with high lp(a)?
Just had a CAC with a score of zero but my doctors say that means nothing and want me on high dose statins.
Thanks for reading and for being here — we really appreciate it.
One thing we’re always upfront about: TFP_ is educational and doesn’t offer medical advice or interpretations of individual results, and we don’t weigh in on personal treatment decisions in any direction.
Those depend on your full history and context, and that conversation belongs with a clinician who can see the whole picture.
Yep, I get that. Just wondering if you’ve also looked at patients with high levels of lp(a) as well. Was that a marker your study also considered? Could it explain some of the high ApoB cases that did have real world cardiovascular plaque increases?
This is a clearer signal that metabolic context proxied by fasting insulin can materially change the observed association of ApoB with events. It aligns with the broader Feldman framing that particle number is necessary, but the surrounding metabolic environment influences the actual risk. The study does not prove risk level, but it is consistent with the hypothesis that context meaningfully modulates the relationship. Ongoing imaging and longer-term data in LMHR-like cohorts remain the more decisive tests. This continues to be a fascinating exploration.
I’m a 53 year old male on carnivore. I’m 5’8” and 160 lbs. hsCRP low, triglycerides 81, HDL 50 and fasting insulin (9.6 μU/mL) but all my other cholesterol numbers are considered high. How does this ApoB data also mix with high lp(a)?
Just had a CAC with a score of zero but my doctors say that means nothing and want me on high dose statins.
APOLIPOPROTEINS & INFLAMMATION
Apolipoprotein B (ApoB): 233 mg/dL (ref <90) — H
Lipoprotein(a), Lp(a): 402 nmol/L (ref <75 optimal; >125 = high) — H
hs-C-Reactive Protein (hs-CRP): 0.6 mg/L (optimal <1.0)
LIPOPROTEIN FRACTIONATION — ION MOBILITY
LDL Particle Number: 2686 nmol/L (ref <1138) — H
LDL Small: 579 nmol/L (ref <142) — H
LDL Medium: 780 nmol/L (ref <215) — H
HDL Large: 5130 nmol/L (ref >6729) — L
LDL Peak Size: 217.2 Å (ref >222.9) — L
LDL Pattern: B (Pattern A large/buoyant is optimal)
Thanks for reading and for being here — we really appreciate it.
One thing we’re always upfront about: TFP_ is educational and doesn’t offer medical advice or interpretations of individual results, and we don’t weigh in on personal treatment decisions in any direction.
Those depend on your full history and context, and that conversation belongs with a clinician who can see the whole picture.
Wishing you all the best, Eric.
Yep, I get that. Just wondering if you’ve also looked at patients with high levels of lp(a) as well. Was that a marker your study also considered? Could it explain some of the high ApoB cases that did have real world cardiovascular plaque increases?