The purpose of this review was to describe the historical development of each epidemiology, experimental pathology, endocrinology (including vitaminology), and thermodynamics surrounding the genesis of
gastric cancer in humans and non-human mammals. Epidemiological studies from other and our laboratories were unanimous in counting the intake of
carbohydrate-rich and salty diet with
vitamin C deficiency as the risk factor of key importance. Information from experimental pathology suggested the possible implication of some
nitroso compounds in a subject with
atrophic gastritis and/or in a state of
vitamin C deficiency of which the establishment should have led to a perturbation of the
steroid milieu of the host. In endocrinology, the association of a specific
steroid disorder (depression of
androgen and
progestin combined with
glucocorticoid excess in urine) with
gastric cancer, as noted in the case-control study of this
neoplasia, was reproduced in mice maintained under biased nutritional conditions. The use of
scurvy-prone ODS rats was found useful in elucidating the interrelation between
vitamin C and
steroid metabolism. Finally, thermodynamic analysis of the data distribution of
gastric cancer risk parameter of both sexes revealed the presence of an interaction between oncogene activation and tumor suppressor gene inactivation in the course of the maintenance of the positive correlation with male predominance between male
gastric cancer and female
gastric cancer as regards the changes of age-adjusted incidence rate (AAIR) in space. In conclusion, all of the information available in the field of
gastric cancer etiology is in support of the pertinence of the
steroid criminal hypothesis of
gastric cancer in humans and in non-human mammals.