@nostr:npub14am887cf6kvwkce89nt7dsw3v9qrrn0uppxyvr6a2jd7xdwuwccqwnudp2

Cool hypothesis.

Hypotheses need testing. They should also be reasonable. Here are some thoughts:

Excess #linoleicacid linoleic acid (cis,cis-9,12-octadecadienoic acid) (LA), an Omega-6 FA, has indeed been correlated with reduced mitochondrial recycling (e.g. #mitophagy), and subsequent dysfunction in human CELLS through various mechanisms.

1) Elevated levels of LA can impair mitochondrial function, as evidenced by studies showing that high concentrations of LA decrease mitochondrial respiration and cell viability in trophoblast-like cells, leading to increased reactive oxygen species (#ROS) generation and altered inflammatory responses(Shrestha et al., 2018).

2) Chronic exposure to LA in insulinoma cells has been shown to induce apoptosis and reduce mitochondrial membrane potential, further compromising insulin secretion and cellular function(Tuo et al., 2011). But...insulinoma cells are already sick cells.

Overall, reduced mitophagy is a contributor to chronic disease, or at least a harbinger. For example, an early feature in the pathogenesis of nonalcoholic fatty liver disease (NAFLD) is mitochondrial dysfunction and metabolic disturbance (Undamatla et al., 2023).

HOWEVER

LA is a **context-dependent** and minor contributor to mitochondrial membrane health, with effects varying by cell type and age (Marei et al., 2012; Moran et al., 2001; Jeng et al., 2009).

The fatty acid composition of animal products, **including red meat**, is indeed significantly influenced by diet. Animals consuming corn and soy, particularly as soybean oil or roasted soybeans, exhibit increased LA levels in their muscle and fat (Alencar et al., 2021; Fang et al., 2009). For instance, pigs *and beef cattle* fed these diets show higher polyunsaturated fatty acids, including LA, while pasture-raised or wild animals have higher omega-3 levels and a more favorable omega-6 to omega-3 ratio (Zhao et al., 2012; Sergin et al., 2022).

While increased vegetable oil consumption has elevated LA in human diets, probably more so than increased LA in meatstuffs, its specific impact on human mitochondrial LA levels remains underexplored (Jandacek, 2017; Taha, 2020). Further research is necessary to understand the nuanced effects of LA on mitochondrial dynamics in humans (Pepe, 2005; Chen et al., 2023; Choque et al., 2013).

Threw in the 2005 reference because #Pepe.

So yeah, excess dietary LA may disrupt mitochondrial dynamics and exacerbate metabolic disorders in humans. This much is not particularly new. But elevating it to THE cause of metabolic dysfunction / chronic disease is silly and short-sighted. I agree that a low-fat #diet will likely reduce your LA intake (unless all your fat comes from crisco lol) but "red meat" isn't any better than #eggs or #pork. And what are the trade-offs of a low- (or no-) fat diet? They're not nothing. Fat is crucial to health.