Influence of Exercise on Inflammation in Cancer
The evidence to support a benefit of exercise on cancer risk is convincing, especially for breast cancer and colon cancer, both of which heavily are influenced by lifestyle factors. What is less clear are the mechanisms that are responsible for these effects. Based on the animal literature, we are limited to conclude that the current evidence merely supports a link between physical activity, reduced tumor burden, and decreased inflammation. The human literature is less obvious, with some studies reporting reduced inflammation, whereas others convey no change. Future investigations using knockout mice and/or antibodies are necessary to examine a mechanistic link between physical activity, inflammation, and cancer. What will be more challenging will be the determination of whether physical activity is influencing tumorigenesis via a direct effect on inflammatory pathways as opposed to indirect effects as discussed earlier. Given that many of the interrelated factors that are affected by exercise can, in turn, influence inflammatory processes and tumorigenesis, it will be difficult to attribute these potential mechanisms independently to the findings on inflammation and carcinogenesis. The likely scenario is that exercise is affecting several, if not all, of these interrelated pathways including inflammatory pathways, adiposity, energy balance, adipokines, insulin, estrogen, and immune function, leading to a decrease in inflammation and subsequent tumorigenesis.
Conclusions
The evidence to support a benefit of exercise on cancer risk is convincing, especially for breast cancer and colon cancer, both of which heavily are influenced by lifestyle factors. What is less clear are the mechanisms that are responsible for these effects. Based on the animal literature, we are limited to conclude that the current evidence merely supports a link between physical activity, reduced tumor burden, and decreased inflammation. The human literature is less obvious, with some studies reporting reduced inflammation, whereas others convey no change. Future investigations using knockout mice and/or antibodies are necessary to examine a mechanistic link between physical activity, inflammation, and cancer. What will be more challenging will be the determination of whether physical activity is influencing tumorigenesis via a direct effect on inflammatory pathways as opposed to indirect effects as discussed earlier. Given that many of the interrelated factors that are affected by exercise can, in turn, influence inflammatory processes and tumorigenesis, it will be difficult to attribute these potential mechanisms independently to the findings on inflammation and carcinogenesis. The likely scenario is that exercise is affecting several, if not all, of these interrelated pathways including inflammatory pathways, adiposity, energy balance, adipokines, insulin, estrogen, and immune function, leading to a decrease in inflammation and subsequent tumorigenesis.
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