#61

I too have an APOB of 125 and high TC and LDL-c. Docs want to put me on statins. However, I have non CAC score, BP 100/69, very low BMI and HDL of 80 TG of 82.
Just recently ran across the ABOP/APOA ratio indicator and I have almost zero risk based on this. Check APOA

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#62

A small 90 person observational study shouldn’t make or break your decision to go on a cholesterol lowering medication IMO, especially if your doctor suggests otherwise. Thousands of participants in with really good clinical study design (randomized controlled trials), show they’re beneficial for all cause mortality, heart disease, etc.

#63

Just pay attention to your liver when taking red yeast rice due to possible liver damage for some people.

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#64

There is also this:

137,100 men and women aged 25–84 years were followed an average 17.8 years

#65

I’m not a cardiologist, doctor, or researcher.

Apolipoprotein A-I concentrations and risk of coronary artery disease: A Mendelian randomization study

https://www.atherosclerosis-journal.com/article/S0021-9150(20)30081-2/fulltext

#66

Maybe your cardiologist read the article below:

Comparison of Conventional Lipoprotein Tests and Apolipoproteins in the Prediction of Cardiovascular Disease

https://www.ahajournals.org/doi/10.1161/CIRCULATIONAHA.119.041149

Results:

ApoB, LDL-C, and non–HDL-C were highly correlated (r>0.90), while HDL-C was strongly correlated with ApoA1 (r=0.92). After adjustment for classical risk factors, 1 SD increase in ApoB, direct LDL-C, and non–HDL-C had similar associations with composite fatal/nonfatal CVD events (hazard ratio, 1.23, 1.20, 1.21, respectively). Associations for 1 SD increase in HDL-C and ApoA1 were also similar (hazard ratios, 0.81 [both]). Adding either total cholesterol and HDL-C, or ApoB and ApoA, to a CVD risk prediction model (C-index, 0.7378) yielded similar improvement in discrimination (C-index change, 0.0084; 95% CI, 0.0065, 0.0104, and 0.0089; 95% CI, 0.0069, 0.0109, respectively). Once total and HDL-C were in the model, no further substantive improvement was achieved with the addition of ApoB (C-index change, 0.0004; 95% CI, 0.0000, 0.0008) or any measure of LDL-C. Results for predictive utility were similar for a fatal CVD outcome, and in a discordance analysis. In participants taking a statin, classical risk factors (C-index, 0.7118) were improved by non–HDL-C (C-index change, 0.0030; 95% CI, 0.0012, 0.0048) or ApoB (C-index change, 0.0030; 95% CI, 0.0011, 0.0048). However, adding ApoB or LDL-C to a model already containing non–HDL-C did not further improve discrimination.

Conclusions:

Measurement of total cholesterol and HDL-C in the nonfasted state is sufficient to capture the lipid-associated risk in CVD prediction, with no meaningful improvement from addition of apolipoproteins, direct or calculated LDL-C.

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