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sirsar | 2 years ago
> Fatal atherosclerotic events were more common in the control group (70 v. 48; p<0.05). However, total mortality was similar in the two groups: 178 controls v. 174 experimentals, demonstrating an excess of non-atherosclerotic deaths in the experimental group. This was accounted for by a greater incidence of fatal carcinomas in the experimental group [the vegetable oils group].
Modified3019|2 years ago
When things like polyunsaturated fatty acids degrade, they release free radicals, lipid peroxides and other toxic compounds like aldehydes (which are known to be cytotoxic and genotoxic), and it seems very plausible that these things could be outright carcinogenic, or force cells to spend their resources cleaning up this additional load instead of repairing or protecting DNA after damaging sun exposure.
hombre_fatal|2 years ago
Here's Layne Norton making this point yesterday in response to Huberman in a Twitter thread you should read: https://twitter.com/BioLayne/status/1704477570417254530. He lists some of these interesting RCTs as well, but here's the summary:
> If you only look at epidemiology & in vitro/mechanistic data you can hack together a horror story for almost any nutrient
> In RCTs where n-6 PUFAs (aka seed oils) are used in place of SFA there are neutral/positive effects on health
You can speculate all day about how bad certain mechanisms like oxidation or compounds like phytates might be for us. But why would that be convincing to you when these foods, whether it be seed oils or legumes (which have phytates for example), improve human health outcomes in the highest tier of evidence?
There's a reason why "seed oil disrespecters" on social media hang around the lowest tier of evidence like Ray Peat'ian narratives and mechanistic speculation rather than stick to RCTs and metaanalyses.
hombre_fatal|2 years ago
> Many of the cancer deaths in the experimental group were among those who did not adhere closely to the diet. This reduces the possibility that the feeding of polyunsaturated oils was responsible for the excess carcinoma mortality observed in the experi- mental group. However, there were significantly more low adherers in the entire experimental group than in the controls (table vI). In both groups, the numbers of cancer deaths among the various adherence strata are compatible with random distribution (table V). A high incidence among high adherers would be expected if some constituent of the experi-mental diet were contributing to cancer fatality.