Fermentation Ecology Disruption and South Asian Cardiovascular Risk: A Vitamin K2 Hypothesis

This is a hypothesis paper. South Asian populations carry approximately two-fold higher coronary heart disease risk than European comparators after adjustment for conventional risk factors, a disparity that standard cardiovascular frameworks do not fully explain. I propose that the mid-twentieth century disruption of fermentation-based food ecologies — produced by convergent but structurally independent forces including colonial extraction, cattle crossbreeding programs, and industrial food standardization — may have reduced dietary menaquinone (vitamin K2, particularly MK-7) across populations with traditional pastoral food systems. K2 is required to activate Matrix Gla protein (MGP), the most potent known inhibitor of arterial calcification; without adequate K2, MGP accumulates in its inactive dephosphorylated-uncarboxylated form (dp-ucMGP). The central evidence gap motivating this framework is that I could not identify published dp-ucMGP measurement in any South Asian population, in any country, in any clinical or research context — a gap that may mask a mechanistically informative signal. A five-link evidence chain connects this proposed disruption to the South Asian cardiovascular anomaly; four links rest on published literature, and the fifth — direct dp-ucMGP measurement in South Asian populations — remains untested. The framework generates three falsifiable predictions testable within existing cohort infrastructure. The primary prediction is that dp-ucMGP will be elevated in South Asian adults relative to the MESA reference population, with a gradient across South Asian subregions corresponding to depth of fermentation ecology disruption — a prediction achievable in MASALA stored plasma at zero marginal data collection cost. This framework is presented as a testable hypothesis, not an established causal claim.