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More testosterone, less aggression…at least in the stomach.

Chronic inflammation contributes to the development of several types of cancer, including gastric cancer. Gastric cancer is the fifth most common neoplasm and fourth leading cause of cancer-associated deaths. 1 While many people develop chronic gastritis as a result of infection with Helicobacter pylori and autoimmune gastritis, only a subset of those affected will develop gastric cancer. 2 Individuals that develop atrophy and metaplasia have a much higher risk of developing gastric cancer than those with mild gastritis. In the stomach, at least two types of metaplasia develop, spasmolytic polypeptide-expressing metaplasia (SPEM) and intestinal metaplasia, and both may be precursors of gastric cancer. 3, 4 There are many risk factors that influence the progression from gastritis to gastric cancer, including infection with pathogenic strains of Helicobacter pylori, genetics, environment, and chronic inflammation. 5, 6 The article by Busada et al. featured in this issue of Gastroenterology investigates the role of androgens and glucocorticoids in the development of gastritis and gastric metaplasia. 7 9 To investigate whether testosterone was responsible for protecting male mice from disease, male mice were adrenalectomized and a subset were castrated to remove sex hormones. Adrenalectomized and castrated males developed gastritis that appeared identical to the ADX female mice. Additionally, gastric metaplasia developed in both ADX female mice and ADX/castrated male mice, but not ADX male mice that were not castrated. Finally, treating female mice with testosterone protected them from gastritis and gastric metaplasia. These data demonstrate that male sex hormones play a role in suppressing pathogenic gastric inflammation and metaplasia in this model of ADX-induced disease. of gastritis and gastric metaplasia. The data demonstrate that androgens likely provide males with additional protection by suppressing immune cell activity. While it remains to be determined whether androgens regulate inflammation and gastric metaplasia in other models (H. pylori infection, autoimmune gastritis) and in human with gastritis, these findings provide evidence that glucocorticoids and sex hormones can contribute to inflammatory disease and differences in disease incidence between males and females. For example, this could help explain why men have lower rates of inflammatory and autoimmune diseases than women. However, men are nearly two times more likely than women to develop gastric cancer, indicating that there are other factors that contribute to disease risk. 17 Furthermore, aberrant expression and activation of androgen receptors has been associated with carcinogenesis, cell proliferation, and angiogenesis facilitated by dysregulation of cell-cycle inhibitors and angiogenic factors. 18 This suggests that androgens may function as both protecting from inflammation and autoimmune diseases under normal conditions and promoting carcinogenesis when dysregulated. These findings suggest that attention should be given to differences in the cytokines and immune cells in males and females and offer additional insight into the complex mechanisms that regulate gastric carcinogenesis.