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

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 ep...

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Bibliographic Details
Published inCurrent opinion in clinical nutrition and metabolic care Vol. 19; no. 4; p. 294
Main Authors Wright, Christopher, Simone, Nicole L
Format Journal Article
LanguageEnglish
Published England 01.07.2016
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Summary: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.
ISSN:1473-6519
DOI:10.1097/MCO.0000000000000286