Bioelectric networks, as established by Levin and colleagues, encode morphogenetic information through voltage gradients and ion fluxes, guiding development and regeneration. However, the upstream regulation of these networks remains underexplored. This paper proposes the Bioelectric-Methylation Interface Hypothesis (BMIH): that epigenetic modifications via one-carbon metabolism (methylation) regulate ion channel expression and function, thereby determining bioelectric capacity. We present evidence for a bidirectional feedback loop in which mitochondrial membrane potential (ΔΨm) regulates nuclear methylation through a novel phospholipid-mediated mechanism—not through canonical metabolites or redox changes, but through altered phosphatidylcholine/phosphatidylethanolamine (PC/PE) ratios that reroute methyl groups from SAM to nuclear DNA. Drawing on recent findings from Mori et al. (2025), we demonstrate that this loop involves: (1) mtDNA methylation affecting ETC expression; (2) ETC function driving ΔΨm; (3) chronic ΔΨm elevation triggering phospholipid remodeling; (4) decreased PC synthesis rerouting methyl groups to nuclear 5mC; and (5) nuclear hypermethylation regulating ion channel genes. Environmental disruptors—including synthetic folic acid, cyanocobalamin, linoleic acid-rich seed oils, fluoride, glyphosate, and certain pharmaceuticals—converge on this interface through NADPH depletion, glutathione (GSH) reduction, and S-adenosylmethionine (SAM) dysregulation, leading to bioelectric instability. Novel contributions include: (1) methylation as a modulator of bioelectric bandwidth; (2) phospholipid remodeling as the mechanistic link between ΔΨm and nuclear epigenetics (per Mori et al.); (3) integration with the author's companion hypotheses on cobalt redox preservation and carbon geometry as perceptual filter (see Related Works); (4) transgenerational inheritance of disrupted interfaces via germline epigenetics; and (5) testable predictions for functional medicine interventions. This framework bridges Levin’s bioelectrics with epigenetic causation, revealing modifiable constraints under environmental attack. Keywords: bioelectrics, methylation, epigenetics, ion channels, mitochondrial membrane potential, phospholipids, PC/PE ratio, NADPH, cobalt, linoleic acid, cardiolipin, morphogenesis, mitochondrial dysfunction, transgenerational inheritance, hypothesis.