Influence of dietary lipid upon ultraviolet light-carcinogenesis | Hacker News Reader

Influence of dietary lipid upon ultraviolet light-carcinogenesis

pubmed.ncbi.nlm.nih.gov

18 pointsoldschoolib10 comments

Please note this is from 1984. This paper has made the meme rounds. There is a reason why a more recent publication is not cited, the strongest evidence for the implicit hypothesis is 40 years old.

The only double blind RCT (lasting 10 years) to ever investigate the differential effects of seed oils and animal fats on skin cancer in humans found that the seed oil group (unsaturated fats) had their risk of skin cancer cut in half.

https://pubmed.ncbi.nlm.nih.gov/4100347/

Wait, doesn’t that say that carcinomas were doubled in the experimental group? The vegetable oil group had 31 deaths vs 17 in the control group.

That is... not what your link says at all. Rather the opposite:

> 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].

This makes perfect sense, given that fatty acids become more susceptible to oxidation (accelerated by heat, light and air exposure) the more unsaturated they are. One can very, very roughly think of the increase in susceptibility as increasing an order of magnitude moving from saturated->monounsaturated->polyunsaturated, though the exact amount will vary depending on the particular fatty acid. Rustic survival foods with long ambient temperature "shelf" life such as pemmican was generally made with fat from ruminants, which is generally very saturated (compared to monogastric animals like pigs and chickens, who tend to bioaccumulate polyunsaturated fats from their feed). The best fat to use was basically the saturated hard wax found near the kidneys of bison, which could last many months before going rancid (oxidized)

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.

If all of that is true, then you have to answer for why "seed oils" improve human health outcomes in RCTs.

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.

The increased carcinoma in the experimental group was an anomaly. It was pretty much all accounted for by non-adherers, which cuts against the notion that PUFA increased the risk. There were no significant differences in the higher adherence strata.

> 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.

I always thought that the basic fact that unsaturated fats oxidize easier points to them not being ideal for protecting from UVs.

Alternatively oxidizing is the act of taking on the oxidative damage for you

Kind of like putting iron filings in ration packets to scavenge any residual oxygen... makes sense I guess.

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