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

Current opinion in clinical nutrition and metabolic care
July 1, 2016
Christopher Wright et al. (2 authors)
Journal ArticleReviewHuman Study
Study Details

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

Extracted Claims (10)
InterventionDirectionEndpointPopulationDosageImpactClaim #
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
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.

Medical Subject Headings (MeSH)
Adaptive ImmunityAdiposityAnimalsCarcinogenesisCombined Modality TherapyDiet, KetogenicDiet, ReducingEndocrine System DiseasesExerciseHumansImmune System DiseasesImmunity, InnateInflammation MediatorsIntra-Abdominal FatNeoplasmsObesityTumor Burden
Study Links
Quality Scores
SafetyNot Assessed
Efficacy75/10
Quality80/10
Citation Metrics
Total Citations36
Citations/Year4.0
Relative Citation Ratio1.29
NIH Percentile59.8%
Research Impact Scores
APT Score0.50
Weight Score0.97
Normalized Score0.66
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