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Curr Opin Clin Nutr Metab Care. 2016 Jul;19(4):294-9. doi: 10.1097/MCO.0000000000000286.

Obesity and tumor growth: inflammation, immunity, and the role of a ketogenic diet.

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aSidney Kimmel Medical College at Thomas Jefferson University bDepartment of Radiation Oncology, Sidney Kimmel Cancer Center at Thomas Jefferson University, Philadelphia, Pennsylvania, USA.



This article reviews the impact the obese state has on malignancy through inflammation and immune dysregulation using recent excerpts from the medical literature.


The obese state creates a proinflammatory endocrinologic milieu altering cellular signaling between adipocytes, immunologic cells, and epithelial cells, leading to the over-activation of adipose tissue macrophages and the upregulation of compounds associated with carcinogenesis. Obesity correlates with a deficiency in numerous immunologic cells, including dendritic cells, natural killer cells, and T cells. In part, this can be attributed to a recent finding of leptin receptor expression on these immune cells and the upregulation of leptin signaling in the obese state. A number of clinical trials have demonstrated the feasibility of a high-fat, low-carbohydrate diet as an adjuvant treatment for cancer, and current trials are investigating the impact of this intervention on disease outcomes. In preclinical trials, a ketogenic diet has been shown to impede tumor growth in a variety of cancers through anti-angiogenic, anti-inflammatory, and proapoptotic mechanisms.


Obesity is becoming more prevalent and its link to cancer is clearly established providing a rationale for the implementation of dietary interventions as an adjuvant therapeutic strategy for malignancy.

[Indexed for MEDLINE]

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