Man – the backwards animal
As a rule, we approach problems backwards.
For example, we readily believe the notion that a molecule, LDL-cholesterol, which carries important nutrients to cells, is actually atherogenic per se.
Not even remotely credible. Evolution would have selected against it long ago.
More likely the atherogenicity is due to an adulteration of LDL-cholesterol, such as the chemical reaction between methylglyoxal and LDL-cholesterol.
If the rate of the reverse reaction is negligible, the net rate of this adulteration reaction is given by:
R = k*A1*A2
Where R is the rate of the forward reaction, k is the average rate constant, A1 is the chemical activity of LDL-cholesterol, A2 is the average chemical activity of the principal adulterants.
Each chemical activity is factorable into an activity coefficient and a concentration.
I would not choose to attack A1 unless it is severely out of bounds, as it is in familial hypercholesterolemia, and indeed people with LDL-cholesterol levels that can be 5 times normal or more suffer the consequences of the more rapid adulteration reaction (more rapid onset of heart disease).
I would attack A2 by:
a. Reducing the rate of formation of adulterants.
b. Reducing their activity coefficients.
c. Increasing the rate of turnover of adulterants.
d. Increasing the rate of excretion of adulterants (e.g. produce more urine per day).
e. Increasing the rate of the chemical inactivation of adulterants (e.g. by increasing free arginine in the bloodstream).
f. And many more.
There are apt to be fewer harmful side effects attacking A2 than attacking A1, which is what backwards people do
Reducing A1 has had both beneficial side effects (for example the beneficial effects of statins on NO metabolism) and harmful side effects (reduction of important metabolites of the mevalonate pathway such as CoQ10, squalene, dolichols). Were it not for the beneficial side effects of statins, scientists may have long ago abandoned reducing A1 except in severe cases.