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Sources and notes Saturated and Trans Fatty Acids Were Not Associated with All-Cause or Cause-Specific Mortality in a Japanese Population with Relatively Low Intakes: The Japan Public Health Center-Based Prospective Study. The Journal of Nutrition. Published journal paper, not a preprint. DOI: 10.1016/j.tjnut.2026.101922 agingresearch.news/s/3zyuiv This prospective observational study included 90,807 Japanese adults aged 45–74 without a history of cancer or cardiovascular disease. A validated food questionnaire assessed diets. Models compared mortality across five intake groups for total, saturated, monounsaturated and polyunsaturated fats—the latter two being types of unsaturated fat—and trans fats. Trans fats were also examined by industrial and ruminant sources, meaning cud-chewing animals. Average follow-up was 18.9 years. There were 22,618 deaths. Higher intake of none of the fat categories went with higher all-cause mortality across the five intake groups, including industrial trans fats. For women, comparing the highest with the lowest intake group, polyunsaturated fat had a hazard ratio of 0.92 (95% confidence interval 0.84–0.997) for all-cause mortality. Monounsaturated fat had a hazard ratio of 0.84 (0.73–0.97) for cancer mortality. A hazard ratio compares death rates over time; values below one indicate a lower rate. Both findings were described as tentative. Women also had higher respiratory disease mortality with higher total fat and monounsaturated fat intake. Saturated fat showed a suggestive pattern in the same direction; P for trend <0.05. - Diets were self-reported. - The observational design cannot establish cause and effect or prove an absence of risk. - The findings do not necessarily apply to populations with higher fat intakes. - The findings do not necessarily apply to people with prior cancer or cardiovascular disease.

So he read it wrong the first time, or he's reading it wrong now. I think it's the latter. The paper he cites first: “Ference et al., 2017 — “Low-density lipoproteins cause atherosclerotic cardiovascular disease” About which he says: “This is probably the single best paper for the intellectual foundation of my reversal.” I've called this paper a fraud in the past. I still think it's the case. I'm not the only one. @zoeharcombe wrote a nice analysis of the problems with this paper here: zoeharcombe.com/2026/06/does… With part 2 here: zoeharcombe.com/2026/06/does… Next he mentions: “Borén et al., 2020” One of my favorites. It makes the case that ApoB is not causal, but only if you spend a lot of time going through and understanding the references. My favorite example is their discussion of ‘aggregated’ LDL, which they claim, correctly, is dangerous. They don't mention it in the paper, but one of their references shows that LDL only aggregates when it contains linoleic acid. Remove that, LDL is protected from aggregation. I don't think carnivore is enough to protect people from CVD or chronic disease. You're not necessarily removing the cause, if you're eating industrially-fed animals like chicken and pork. This is not a compelling post for me.

Assuming they died less of ASCVD @drpablocorral, what did they die of more to result in no all-cause mortality benefit?

If everybody had low LDL cholesterol (between 35-50 mg/dL) for their whole life, there may be no more heart attacks. Dr. Sek Kathiresan (@skathire), CEO at Verve Therapeutics and head of obesity research at Eli Lilly, explains:

Restoring mortality data in the FOURIER cardiovascular outcomes trial of evolocumab in patients with cardiovascular disease: a reanalysis based on regulatory data - bmjopen.bmj.com/content/12/1… "In the meantime, clinicians should be sceptical about prescribing evolocumab . . ."

Yes. Often overlooked when people focus on the pooled diamond rather than what produced it. FOURIER showed no all-cause mortality benefit. ODYSSEY was only nominally significant and VESALIUS mortality was exploratory after the testing hierarchy failed at CHD death.

Your veins and arteries carry the same blood. Same LDL. Same ApoB. Same everything. Yet veins almost never get plaque. Arteries constantly do. Maybe you've seen the recent discussions about this. It's an interesting question that provides clues in cardiovascular science, and could challenge how we think about LDL and ApoB. 🧵

The absolute difference was 6.6% vs 9.7%. The harder composite was 2.3% vs 3.6%. So yes, benefit in this specific secondary-prevention trial, but “the lower the LDL, the better” is still a slogan, not the full conclusion.