LONGECITY

We now know why SFAs got painted with the "bad fat" brush: It was because they raised LDL during a time when we did not know that LDL could be both good and bad -- we thought LDL was always the "bad lipoprotein." We now know (hopefully MR too!) that there is good and bad LDL, and SFAs only raise the good kind.

Why do you think is LDL-C associated with CHD? Obviously you consider LDL increases due to SaFA harmless. What do you believe is responsible for the harmful increases in LDL-C that are related to heart disease?

We now know why SFAs got painted with the "bad fat" brush: It was because they raised LDL during a time when we did not know that LDL could be both good and bad -- we thought LDL was always the "bad lipoprotein." We now know (hopefully MR too!) that there is good and bad LDL, and SFAs only raise the good kind.

Why do you think is LDL-C associated with CHD? Obviously you consider LDL increases due to SaFA harmless. What do you believe is responsible for the harmful increases in LDL-C that are related to heart disease?

It's the particle number that is the culprit. You can have high LDL-C with low LDL-P if you have large particles. You can also have low LDL-C and have high LDL-P if you have small particles.


The below video explains, which is based on the cholesterol series here:


http://youtu.be/8GDx5sObceI

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I understand that particle number is the actual problem and that lowering triglycerides will lower particle number even if ldl-c doesn't decrease. However as far as I see LDL-C DOES correlate with particle number as well. So all other things staying equal, shouldn't a rise in ldl-c be a bad thing? Doesn't this theory still support MUFAs over SaFAs?

However as far as I see LDL-C DOES correlate with particle number as well.

I believe the conclusion that Peter made was that LDL-C does not track with with LDL-P. So one can have a large LDL-C spread over a few large particles (low LDL-P). The high LDL-C would typically be considered a health risk but the more reliable LDL-P says otherwise. Similarly one could have a low LDL-C (considered low risk) but spread over a large number of particles - high LDL-P - an actual high risk indicator. The point was that what we see from actual stats is that just as many (slightly more I believe) die from CVD with low serum cholesterol as for those with high cholesterol. In other words the level of serum cholesterol LDL-C is a meaningless indicator of CVD risk. The dietary conclusions from Peter is that high carb intake tends to result in high LDL-P and that high fat/low carb tends towards low LDL-P.

So all other things staying equal, shouldn't a rise in ldl-c be a bad thing? Doesn't this theory still support MUFAs over SaFAs?

The entire MUFA/SAFA argument appears to be irrelevant where increased CVD risk is concerned, which they do. The only reason fats were implicated in CVD risk was because they caused a rise in total cholesterol. That was before we knew anything about HDL/LDL and now particle counts. From what we know now fats in the presence of carb restriction offer lower CVD risk whether MUFA or SAFA.
Edited by Cris Barrows, 18 June 2013 - 03:57 PM.

This is perhaps simpler to follow than Peter's talk.

Corrected statement on post #94 that I can't edit - sigh!

The entire MUFA/SAFA argument appears to be irrelevant where increased CVD risk is concerned. The only reason fats were implicated in CVD risk was because they caused a rise in total cholesterol, which they do. That was before we knew anything about HDL/LDL and now particle counts. From what we know now fats in the presence of carb restriction offer lower CVD risk whether MUFA or SAFA.