Obesity and tumor growth: inflammation, immunity, and the role of a ketogenic diet.
Study Goal
The researchers aimed to review the impact of obesity on malignancy and explore the feasibility of a high-fat, low-carbohydrate diet as an adjuvant treatment for cancer.
Results Summary
The study found that a ketogenic diet impeded tumor growth in preclinical trials through anti-angiogenic, anti-inflammatory, and proapoptotic mechanisms. Clinical trials demonstrated its feasibility as an adjuvant treatment, though disease outcome impacts are still under investigation.
Population
Preclinical trials (animal models) and clinical trials involving cancer patients (specifics not detailed).
Effective Dosage
Not specified
Duration
Not specified
Interactions
None mentioned
| Intervention | Direction | Endpoint | Population | Dosage | Impact | Claim # |
|---|---|---|---|---|---|---|
obese state | increase | proinflammatory endocrinologic milieu | - | - | creates | #1 |
obese state | increase | cellular signaling between adipocytes, immunologic cells, and epithelial cells | - | - | alters | #2 |
obese state | increase | adipose tissue macrophages | - | - | leads to the over-activation of | #3 |
obese state | increase | compounds associated with carcinogenesis | - | - | leads to the upregulation of | #4 |
obesity | decrease | numerous immunologic cells, including dendritic cells, natural killer cells, and T cells | - | - | correlates with a deficiency in | #5 |
leptin signaling | increase | leptin signaling | in the obese state | - | upregulation of | #6 |
high-fat, low-carbohydrate diet | neutral | adjuvant treatment for cancer | clinical trials | - | demonstrated the feasibility of | #7 |
ketogenic diet | decrease | tumor growth | preclinical trials | - | has been shown to impede | #8 |
ketogenic diet | neutral | anti-angiogenic, anti-inflammatory, and proapoptotic mechanisms | a variety of cancers | - | impedes tumor growth through | #9 |
dietary interventions | neutral | adjuvant therapeutic strategy for malignancy | - | - | implementation of | #10 |
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.