Possible Nutrition-Related Mechanisms of Metabolic Management in Cancer Treatment

Abstract

Context: Somatic mutation theory has been considered as a potential cause for cancer. However, major inconsistencies with the gene theory have necessitated serious reconsideration of this assumption. According to these inconsistencies, cancer may be considered as a metabolic disorder. According to the mitochondrial metabolic theory, substrate-level phosphorylation has been suggested to be superior to oxidative phosphorylation in cancer cells. Cancer metabolic therapies such as ketogenic diets (KD) and limitation in glutamine and calorie can be beneficial and are in line with this theory. In this study, we have reviewed the potential effects of KD as well as glutamine and calorie restriction in various types/stages of cancer with a focus on possible mechanisms. Evidence Acquisition: A comprehensive electronic search of different databases was performed using “cancer”, “ketogenic diet”, and “metabolic” as the main keywords. A comprehensive electronic search of different databases was performed using “cancer”, “ketogenic diet”, and “metabolic” as the main keywords. Results: Emerging evidence has indicated that KD can affect tumor cells by reducing glucose availability and simultaneous elevation of ketone bodies as non-fermentable metabolic fuels. KD has been suggested to be more effective as a non-toxic therapeutic measure in combination with glutamine targeting agents, chloroquine for lysosomal targeting, hyperbaric oxygen therapy, and calorie restriction. Conclusions: This metabolic approach can be considered as a promising non-toxic strategy for cancer management.

Is There any Possible Association Between Trimethylamine N-Oxide (TMAO) and Cancer? A Review Study

“…In previous articles, we discussed about glucose and glutamine restrictions along with the increase in non-fermentable ketones for cancer treatment [50][51][52][53]. It is suggested that TMAO Should be considered in dietary interventions for cancer prevention and treatment purposes.…”

Nutritional Metabolomics in Diet–Breast Cancer Relations: Current Research, Challenges, and Future Directions—A Review

“…Lysophosphatidylcholine acyltransferase 1 (LPCAT1) converts LPC to PC, and it is overexpressed in breast cancer with poor prognosis [143], which demonstrates that a higher level of PC is associated with a high risk of breast cancer. In addition, a study conducted a metabolomics analysis in a large cohort of women and identified several metabolites that were positively associated with breast cancer risk, including sphingomyelin (d18:1/18:0), phosphatidylcholine (16:0/18:1), and lysophosphatidylcholine (C17:0) [13,144]. Another study reported that high levels of circulating SFA, particularly myristic acid (14:0), are correlated with an increased risk of breast cancer [135].…”