Paleo Diet and Paleolithic Diet Questions & Answers

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What are your thoughts? Does this fit within your paradigm? Any issues with the methods?

flag	asked Sep 29 at 13:50 cbucker 484●9

Jamie · Answer 1 · 2012-09-29 14:04:25Z UTC

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If these foams cells are anti-inflammatory, what then causes the inflammation. Doesnt this mean the lipid theory has another hole blown out of it?

If the precursor, truely is a precursor, then its levels should generally outstrip LDL when you have the ingredients for the precursor in abundance, given its materials > precursor > LDL, and when youve loads of precursor, the manufacture is stopped, and LDL cleared up.

Its very interesting research, but I am uncertain why the researchers are still buying the lipid hypothesis from the results. Seems to be a spanner in the works in a major way...

"n atherosclerotic lesions, Glass said the normal function of desmosterol appears to be "crippled.""

This seems to suggest an entirely seperate mechanism for heart disease..

Am I reading it wrong?

answered Sep 29 at 14:04

Jamie
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I'm not positive how to interpret it myself... lol. I apologize but I don't completely follow your thoughts (it's probably me). What i got out of it: foam cells = malfunctioning macrophages unable to 'digest' cholesterol and other debris. foam cell formation -> suppresses inflammatory gene expression = anti- inflammatory. Desmosterol = final stage before cholesterol is formed . Desmosterol -> signals more cholesterol uptake and less cholesterol formation/release. Desmosterol -> helps macrophages better digest cholesterol, (reducing foam cell formation?) – cbucker Sep 29 at 14:57

Well yes, the foam cells are unable to digest cholesterol, but they are anti-inflammatory. Desmosterol is a precursor, meaning its what the cholesterol is made from. That implies that if you eat cholesterol raising foods, youd also have more cholesterol lowering precursors, no? And more importantly, where does the inflammation really come from, if it has no connection to cholesterol? And what causes the desmosterol to become crippled? All I am getting at, as this raises more questions than it answers...and it kinda mystrifies the actual process esp compared to standard lipid hypothesis.. – Jamie Sep 29 at 15:58

Desmosterol is the cholesterol precursor, not a cholesterol lowering precursor. Its ability to reduce the # of foam cells by making macrophages more adept at clearing cholesterol(s) would have a relative inflammatory effect since foam cells are anti inflammatory according to the study. Seems to me that by upping Desmosterol by eating non esterified cholesterol (I'm not sure how to up per-se Desmosterol) the macrophages would clear Debris stuck in the endothelial wall much better but our inflammation would have a relative bump up compared to having anti-inflammatory foam cell formation. – cbucker Oct 1 at 13:45

Imani Burrell · Answer 2 · 2012-09-29 18:15:06Z UTC

From my research into cholesterol, the investigators have made an error in their baseline assumption. Cholesterol is formed in r(x)n to an acid/alkaline imbalance. It is the stuff that protects our vein and arteries from corrosion. The higher the acid state, the more cholesterol will be produced. Inflamation is the cause of acid/alkaline imbalance or acid/alkaline imbalance causes inflamation, this is the important distinction the investigators have missed.

Verrry interesting article: Thoughts? interpretations?

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