Dietary cholesterol intake suppresses endogenous cholesterol synthesis.

The claim is qualitative (dietary cholesterol suppresses endogenous synthesis) and is supported directly. Feedback inhibition of cholesterol synthesis is described as well-established across sources. Direct human measurements support it: a study measuring synthesis by deuterium incorporation and urinary mevalonic acid found "modestly reduced cholesterogenesis with increasing dietary cholesterol levels" by two independent techniques; classic sterol-balance studies (e.g. work in patients fed up to 3 g/day) found increased absorption evoking compensatory decrease in total-body synthesis plus increased re-excretion; reviews tie the reduced synthesis mechanistically to reduced HMG-CoA reductase activity.

The material subclaim is the biochemical mechanism: increased intracellular cholesterol downregulates HMG-CoA reductase via the SREBP-2 pathway. This is settled textbook cell biology (kept as a low-importance embedded stub) and provides the causal basis. It weighs strongly in favor.

The one qualification in the literature is magnitude, not direction: a British Journal of Nutrition review states dietary cholesterol has "only a slight effect on cholesterol synthesis, because adaptation mainly takes place through intestinal absorption." That bears on how much synthesis falls and on the neighboring claim that dietary cholesterol weakly affects blood cholesterol, but it still affirms that synthesis is suppressed. There is marked inter-individual variability, also consistent with the claim.

Verdict verified rather than supported because the directional effect is confirmed by multiple direct human measurement techniques and an uncontested mechanism. Confidence 0.9 and credence 0.95 reflect strong, convergent evidence with the only live question being magnitude. What would change the verdict: credible direct-measurement evidence that synthesis does not fall (or rises) with increased intake, which the literature does not show.