Gastric H. pylori–diet synergy

Helicobacter pylori infection and dietary N-nitroso act synergistically on gastric-cancer risk: infection lowers the R19 barrier scale while diet adds bias, and their joint relative risk (≈4.4) exceeds the additive-null (3.3). The same exact-barrier kernel reproduces this super-additivity and additionally predicts sub-multiplicativity near the spinodal. The interaction is verified [V]; absolute incidence open [O].

H. pylori chronic inflammation lowers the cell-fate barrier scale; dietary N-nitroso adds bias. Their joint RR≈4.4 exceeds the additive-null 3.3 (super-additive) yet falls below the multiplicative-null 4.5 (a sub-multiplicative prediction near the spinodal). The interaction is [V]; absolute incidence [O].

Helicobacter pylori infection and dietary N-nitroso act synergistically on gastric-cancer risk: their joint relative risk ≈ 4.388 exceeds the additive-null 3.3, a super-additive interaction. Infection lowers the R19 barrier scale (chronic inflammation reduces cell-fate stability) while diet adds bias on the same switch.

The single exact-barrier kernel reproduces this departure from additivity and, on the same kernel, predicts the joint risk is sub-multiplicative near the spinodal (it falls below the multiplicative-null 4.5). That sub-multiplicativity — diminishing returns at extreme dual exposure — is a concrete, falsifiable prediction.

The infection-by-diet interaction is verified [V] against the cited synergy [L]; absolute incidence is open [O]. The dose-response fans out on an infected background versus an uninfected one, which is the operational signature of the synergy and the part a cohort study can test directly.