Introduction
OK folks, into the wayback machine.
In 2010 I stopped eating seed oils, and saw a chronic inflammatory bowel disease resolve in days:
“So a few months ago, I stopped eating industrial seed oils (veggie oils). In two days the diarrhea stopped. Eat the oils, it started again. I no longer craved starch or sugar, so I didn't eat any wheat for a week, without meaning to…. So now I could turn the symptoms of the last 16 years on or off, based on eating veggie oils or wheat. Wow!” (Goodrich, 2010)
I remember following Guyanet when he was studying seed oils as possible culprits and then switching to straight to palatability which just seemed like a red herring. "People eat more because it tastes good!" I'm like, yea, the food I'm eating tastes great but I actually feel full at some point and stop eating. So his palatability hypothesis didn't jive with me. I also limit or avoid my seed oil consumption. Too many folks think anything plant based is holy and healthy.
ReplyDelete"dietary LA appears to be the primary mechanism behind the process of food reward and hyperpalatibility."
ReplyDeleteYou'd almost think big food industry had already been conveniently aware of this for many decades ...
same thoughts here.
Delete"Hall, in his apparent quest to touch all the dietary third rails, did another paper with a bearing on this question (Hall et al., 2021). This paper looked at an Animal-Based, Low-Carb diet (LC) vs. a Plant-Based, Low-Fat diet (LF). Here they found a much greater reduction in fattiness on the LF diet — which was a surprise to many, myself included."
DeleteThe reason why you are surprised by this is because you are not paying attention to the reduction in the arachidonic acid content of the LF diet as compared to an animal-based low-carb diet. That alone would reduce the pool of arachidonic acid available for insertion into cell membranes. I suggest you read this paper. https://pubmed.ncbi.nlm.nih.gov/20398309/
David, that doesn't show that the AA level impacts obesity. If it were to, it would have to be against a background of an already very low n-6 level, as other papers I cite in this post demonstrate, particularly (Garg et al., 1992).
DeleteTucker, you are correct. The article I cited does not address obesity. However, it does say, "...a reduction in AA intake dampens prostanoid signaling,..." This https://pubmed.ncbi.nlm.nih.gov/30360467/ article says, "Arachidonic acid (AA) and its derivatives link nutrient metabolism to immunity and inflammation, thus holding a key role in the emergence and progression of frequent diseases such as obesity, diabetes, non-alcoholic fatty liver disease, and cardiovascular disease."
DeleteThis https://pubmed.ncbi.nlm.nih.gov/28403941/ article title reads, Obesity is positively associated with arachidonic acid-derived 5- and 11-hydroxyeicosatetraenoic acid (HETE).
Rather than go on about this I suggest you Google arachidonic acid in conjunction with adiposity, metabolic syndrome, and obesity. If you Google arachidonic acid in conjunction with diabetes, you will find articles that seem to refute my assertion that excess dietary arachidonic acid intake is problematic. What Undurti Das and others don't seem to realize is that the research they cite compares saturation levels of arachidonic acid intake to supersaturation levels of intake, which is an oxymoron. Is there such a thing as supersaturated saturated fatty acids?