Chiming in because I'm an ApoB evangelist. I think it's THE metric that matters most for cardiovascular risk, and it's what I track most closely. Semaglutide 1.0 mg, 7 months: | Marker | Baseline | Month 7 | |--------|----------|---------| | ApoB | 132 mg/dL | 94 mg/dL | | LDL-C | 142 mg/dL | 108 mg/dL | | LDL-P (NMR) | 1680 nmol/L | 1120 nmol/L | | Small Dense LDL | 48% | 28% | Note the small dense LDL percentage dropped from 48% to 28%. This is hugely significant. Small dense LDL particles are the most atherogenic — they penetrate the arterial wall more easily and are more susceptible to oxidation. The shift from small/dense to large/buoyant pattern is a direct result of triglyceride reduction and improved insulin sensitivity. If your doctor only checks standard lipid panel, ask for NMR LipoProfile or ApoB. It tells a completely different story than LDL-C alone.

Nina, excellent data. The pattern shift from predominantly small dense LDL (Pattern B) to large buoyant LDL (Pattern A) is one of the most clinically meaningful changes we see with GLP-1 therapy + weight loss. For the thread: here's a quick reference for lipid targets in 2025: | Marker | General Population | Moderate Risk | High Risk (CVD/Diabetes) | |--------|-------------------|---------------|------------------------| | LDL-C | <130 mg/dL | <100 mg/dL | <70 mg/dL | | ApoB | <120 mg/dL | <90 mg/dL | <65 mg/dL | | Non-HDL-C | <160 mg/dL | <130 mg/dL | <100 mg/dL | | Triglycerides | <150 mg/dL | <150 mg/dL | <150 mg/dL | | HDL-C | >40 M / >50 F | — | — | | Lp(a) | <75 nmol/L | — | — | ApoB and non-HDL-C are particularly valuable because they capture ALL atherogenic particles — VLDL, IDL, LDL, and Lp(a) — not just LDL.

Dr. Park, quick question — should I be concerned that my Lp(a) is 156 nmol/L? My PCP didn't seem worried but everything I read says that's high. It hasn't changed on semaglutide (was 152 at baseline).

Terry, yes — an Lp(a) of 156 nmol/L is significantly elevated (>75 nmol/L = high risk). Your PCP may not have been aware of recent guidelines. Lp(a) is: - ~90% genetically determined - Not meaningfully affected by diet, exercise, or current medications (including GLP-1s and statins) - An independent risk factor for ASCVD and aortic valve stenosis - Currently only reducible by PCSK9 inhibitors (~25-30% reduction) and upcoming antisense therapies (pelacarsen, olpasiran — in Phase 3 trials showing 80-98% reduction) With your Lp(a) at 156, I would recommend aggressive management of ALL other modifiable risk factors — keep ApoB <80, optimize blood pressure, don't smoke, exercise regularly. Your overall risk is higher than someone with the same LDL but normal Lp(a). Consider asking for a referral to a lipidologist or preventive cardiologist who can do a comprehensive ASCVD risk assessment including Lp(a) context.