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The consumption of sugar (sucrose, high fructose corn syrup) increases plasma levels of triglycerides, VLDL and apo B, and reduces plasma levels of HDL-C and apo A-I. The consumption of fructose alone, though likely in dose-dependent fashion, has a similar, though perhaps less harmful, impact as that of fructose and glucose combined (i.e., sugar).

The addition of fat, in the absence of sugar and starch, does not raise serum triglycerides or other biomarkers of cardiovascular disease.

HDL is important, and more HDL particles are better than few.

But, raising HDL-C with a drug isn’t going to fix the problem.

One of his most popular (so far) being his series called The Straight Dope On Cholesterol – which at the time for many info-hungry folk seemed to take forever, but was worth the wait.

Read it in it’s entirety (thus far) here: – The point of this is to revisit this entire epic series but just remember the Cliff’s Notes highlights, with links back to the originals in case a refresh is needed.

The higher the level of serum triglycerides, the greater the likelihood of discordance between LDL-C and LDL-P (and apo B).

The greater the number (from 0 to 5) of inclusion criteria for metabolic syndrome, the greater the likelihood of discordance between LDL-C and LDL-P (and apo B).

The pool of cholesterol in our body is essential for life. Most of the cholesterol in our body was made by our body.This raises the question: if indeed LDL-P is always as good and in most cases better than LDL-C at predicting cardiovascular risk, why do we continue to measure (or calculate) LDL-C at all?HDL-C and HDL-P are not measuring the same thing, just as LDL-C and LDL-P are not.There is no way of determining which individual patient may have discordant LDL-C and LDL-P without measuring both markers.Discordance between LDL-C and LDL-P is even greater in populations with metabolic syndrome, including patients with diabetes.

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