Eating Dinner Earlier May Help Reduce Prostate, Breast Cancer Risk, Study Suggests

Eating Dinner Earlier May Help Reduce Prostate, Breast Cancer Risk, Study Suggests
Eating dinner earlier and allowing more time between the last meal and sleep may help reduce the risk of prostate and breast cancer, a new study in Spain found. The study, “Effect of mistimed eating patterns on breast and prostate cancer risk (MCC‐Spain Study),” appeared in the International Journal of Cancer. Disruption of the body’s internal clock, or circadian rhythm, has been associated with diseases such as cancer, obesity, and type 2 diabetes. Working nights has been linked to prostate and breast cancer, although not all studies support this correlation. Experimental studies have shown that changes in meal timing affect inflammation, glucose levels, and cancer growth. However, unlike the type and the quantity of food intake, less evidence has been published about the relationship between cancer and the timing of eating. Data on the influence of diet and other factors on prostate cancer risk is particularly limited. To assess if the timing of eating and sleep patterns are associated with prostate and breast cancer risk, the research team conducted a large population-based study. They also evaluated whether the timing of meals alters the effect of factors associated with cancer risk, such as adherence to cancer prevention recommendations, age, educational level, body mass index, family history of cancer, and smoking status. The research included 621 patients with prostate cancer and 1,205 with breast cancer who were assessed from 2008 to 2013. A total of 2,1
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José is a science news writer with a PhD in Neuroscience from Universidade of Porto, in Portugal. He has also studied Biochemistry at Universidade do Porto and was a postdoctoral associate at Weill Cornell Medicine, in New York, and at The University of Western Ontario in London, Ontario, Canada. His work has ranged from the association of central cardiovascular and pain control to the neurobiological basis of hypertension, and the molecular pathways driving Alzheimer’s disease.

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