#hyperlipid

View On WordPress

https://www.blogger.com/comment.g?blogID=36840063&postID=2170604129686813777

“The conclusion seems to be that there is something nasty in fruit and vegetables, something pro-oxidant. You just have to ask yourself why a plant should manufacture an antioxidant in the first place. You can bet your bottom dollar that it was not for the benefit of herbivores! No, plants hate herbivores and negotiate with substances like strychnine rather than antioxidants. The most likely candidate for a generic pro-oxidant toxin, produced by plants, is fructose. Plants outside of domestication contain relatively little fructose and appear to use it as a lure, to get their seeds eaten, then use the fruit eater as a transport method. They protect themselves from the fructose with antioxidants. Plants in domestication have been selected, by ourselves, to produce quite unreasonable amounts of fructose (plus glucose and sucrose). Just compare the average Granny Smith to a wild crab apple. A bag of sugar.”

“Away from the coast we have to get our DHA from animals (or buy algae derived supplements). They get it from grass. There is DHA present in adipose tissue of herbivores just as much as it is present in lipid membranes of their cells. My suspicion is that DHA is a signal to your metabolism that you have just eaten animal fat, from an animal who's food chain starts with grass [or algae]. The more fat you eat, the stronger the signal. We do not need much DHA overall for our brains as it is well protected in this site, but we might well be using it at low levels as a [G-protein coupled receptor sensed] signal to target metabolic adaptation to process fat. So is McDougall correct that veg*n "brain" tissue is OK, despite their periphery being depleted? Shrug. Fish oil supplements? Well, using our "dietary fat is here" marker to pharmacologically modify some perceived CVD risk factor, without the appropriate change in source of metabolic fuel supply, looks to me to be of very limited value. Large intervention trials do show some benefit from omega 3s provided you do your stats well enough, you have a large enough population to pick up a very small effect and you give a high enough dose. But they do not seem to be any sort of panacea. Especially of you are avoiding dietary fat while "faking" the signal that you have eaten dietary fat... This is not exactly surprising when you try to pick the likely physiology apart. I like the concept of DHA as an animal fat signal. Peter Final thought: Do we need omega 3 PUFA at anything above the most minimal levels if we are in saturated fat based ketosis? Of course I don't know. But the signal to cope with starvation is palmitic acid (physiological insulin resistance), not DHA. I live in starvation mode, not on a mixed diet with only intermittent access to healthy ruminant fat. “

http://high-fat-nutrition.blogspot.com/2007/12/fruit-and-vegetables-re-post.html