I was reading a medical study on treatment targets and found this fascinating insight:
"Conclusion & Future Perspective
It is usually argued that the introduction of apoB as a marker of risk and target of therapy would lead to confusion of both physicians and patients. For more than two decades, a great effort was devoted to education on the issue of the role of 'bad cholesterol' (LDL-C) in the development of atherosclerosis and the necessity of cholesterol-lowering therapy in the prevention of CVD. Thus, most authorities in this field think that it is necessary, at least for an interim period of time, to introduce apoB assessment to the routine lipid profile.
ApoB is a marker of the risk of atherogenic particles, especially LDL risk, and cannot substitute the whole lipid profile, especially at baseline examination. Thus, as this article suggests, apoB should be a part of the routine lipid panel at baseline. However, when apoB is the target, total cholesterol, LDL-C and non-HDL-C need not be measured on routine follow-up visits. Thus, apoB could unify all lipid targets representing the proatherogenic lipoprotein particle risk into one parameter.
Estimation of baseline TGs is useful, as a mild-to-moderate increase in TGs is a good marker of insulin resistance and its associated risk factors and also as a marker of increased risk of CVD. Even in patients treated with statins to achieve very low levels of LDL-C of less than 70 mg/dl, high TG levels represent a considerable residual risk. "
The study went on to conclude...
"Several observations have shown that for many antiatherogenic roles of HDL, apoA-I is more important than HDL particle cholesterol content. Thus, in future, HDL-C assessment could probably be substituted with apoA-I assessment until better methods for the evaluation of HDL functionality are developed.
At present, the apoB:apoA-I ratio seems to be the best marker of cholesterol balance. It was shown to be the best marker of risk of MI and CVD in the AMORIS and INTERHEART studies, and also the best marker of treatment effects in the AFCAPS/TexCAPS study and in combined data from the TNT and IDEAL studies. Thus, for the future, the apoB:apoA-I ratio is a promising marker of both risk and treatment effect."
In summary, the ApoB measures atherogenic particles in your bloodstream. These are the particles that cause plaque accumulation which leads to artery narrowing and increase the risk of a heart attack and stroke. LDL-C is an estimated value and also includes NON-atherogenic particles, therefore it is not the optimal lipid value as a treatment target.
The ApoB/ApoA-1 ratio provides the balance between atherogenic and and anti-atherogenic particles in your bloodstream and appears to be the optimal treatment marker.
If you are not currently measuring ApoB and ApoA-1, you should ensure you begin doing so at your next blood test. You should then ensure that you get a copy of your blood test so you can record and monitor these values over time. By checking your blood lipids on a quarterly basis, it provides you with the motivation to stick to your cardio-protective diet. Such a diet should include the avoidance of sugars and simple-carbohydrates as the weight of evidence in CVD research is beginning to lean more toward the impact of sugar than saturated fat.
That said, I spoke with a research doctor at McGill University today who indicated that although sugar is probably the main culprit in CVD, it may also depend on the individual as some people are also affected by dietary saturated fat consumption. Therefore it is NOT open season for the consumption of saturated fats, moderation should be practiced. In either case, unless you combine daily rigorous exercise with a cardio-protective diet, it won't matter what you eat. Exercise is a baseline minimum to validate the benefits of either diet noted.
Be disciplined and continue to educate yourselves.