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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.

Author information

1
aSidney Kimmel Medical College at Thomas Jefferson University bDepartment of Radiation Oncology, Sidney Kimmel Cancer Center at Thomas Jefferson University, Philadelphia, Pennsylvania, USA.

Abstract

PURPOSE OF REVIEW:

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

RECENT FINDINGS:

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.

SUMMARY:

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.

PMID:
27168354
DOI:
10.1097/MCO.0000000000000286
[Indexed for MEDLINE]

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