Title : Artificial radionuclides and evolutionary mismatch: Vulnerability of the colon, pancreas, diabetes, and arteries
Abstract:
The global dissemination of artificial radionuclides since 1945 represents a novel environmental condition in evolutionary terms. Isotopes such as Cesium-137 (Cs-137) and Iodine-131 (I-131), generated through nuclear weapons testing, reactor accidents, and nuclear energy production, were not present during the evolutionary history of terrestrial life. The new radio-iodine decays into inert Xenon, while carbon-14 decays into nitrogen-14 via beta emission; this transformation occurs at the atomic level and does not directly disrupt established macromolecular carbon frameworks, although local molecular damage may occur during decay events. This paper suggests an evolutionary hypothesis that chronic internal exposure to such radionuclides may constitute an underexplored factor in long-term metabolic, pancreatic, colon and arterial disorders. The framework integrates evolutionary biology, ion mimicry theory, oxidative stress mechanisms, and internal dosimetry. It further addresses an ongoing scientific disagreement regarding the adequacy of prevailing low-dose radiation risk models, particularly with respect to non-cancer metabolic endpoints. While no causal association between environmental Cs-137 exposure and arteries, diabetes, pancreatic or colorectal cancer is currently recognized by major international health authorities, this position paper of CCPDA-hypothesis, supports that targeted interdisciplinary investigation is warranted.
