No Lower Limit? Strikingly Low LDL-C Levels Boost Cardiovascular Protection With No Added Safety Risk

yes, I do. ApoB=72, and rest below. BTW I’m lucky my LPa is a very desirable 13. So, not going to have a CVD event anytime soon, and most likely NEVER LOL.

HDL-Cholesterol

Aug 29, 2026

47mg/dL

Normal

Triglycerides

Aug 29, 2026

77mg/dL

Optimal

Total Cholesterol

Aug 29, 2026

147mg/dL

In range

HDL as % of Total Cholesterol

Aug 29, 2026

32%

In range

Total Cholesterol/HDL Ratio

Aug 29, 2026

3.1ratio

Optimal

LDL/HDL Ratio

Aug 29, 2026

1.81ratio

Optimal

LDL-Cholesterol

Aug 29, 2026

85mg/dL

Normal

VLDL-C (Calculated)

Aug 29, 2026

15mg/dL

Optimal

Non-HDL Cholesterol

Aug 29, 2026

100mg/dL

Optimal

Triglyceride/HDL Ratio

Aug 29, 2026

1.64ratio

Optimal

Lp(a)

Aug 29, 2026

13nmol/L

Optimal

I agree, mostly. You could toss a few of your key metrics into a Risk-adjusted ApoB model and likely be fine managing to that single metric.

The formula:

RW-ApoB (mg/dL) = 0.736 * ApoB (mg/dL) + 11.65 * (TG (mmol/L) + 0.215 * Lp(a) (nmol/L)

. . . puts more than half of the MACE risk into a single tracking metric with (as thought contemporaneously) no loss and some benefit.

Not covered in this metric are conditions exemplified by a person with “perfect” lipid metrics drops dead of a MACE. A few of those cases await explanation or involve unusual, one-off circumstances but most of them involve long term high systemic inflammation. I’m very close to concluding that inflammation, rather than being an accelerant of MACE, is actually in the causal chain. Making this case, however, involves many arguments and footnotes. For now, it seem certain sustained elevated inflammation strongly exacerbates MACE. What to track? GlycA covers more of your risk bases than other inflammation metrics.

RW-ApoB and GlycA low? If yes, monitor and move on to something else.

1 Like