Navy Beans Impact the Stool Metabolome and Metabolic Pathways for Colon Health in Cancer Survivors

Abstract

Colorectal cancer (CRC) is the third leading cause of cancer-related death in the United States and emerging evidence supports that increased consumption of legumes, such as navy beans, can reduce risk. Navy bean consumption was previously shown to modulate host and microbiome metabolism, and this investigation was performed to assess the impact on the human stool metabolome, which includes the presence of navy bean metabolites. This 4-week, randomized-controlled trial with overweight and obese CRC survivors involved consumption of 1 meal and 1 snack daily. The intervention contained 35 g of cooked navy bean or macronutrient matched meals and snacks with 0 g of navy beans for the control group (n = 18). There were 30 statistically significant metabolite differences in the stool of participants that consumed navy bean at day 28 compared to the participants’ baseline (p ≤ 0.05) and 26 significantly different metabolites when compared to the control group. Of the 560 total metabolites identified from the cooked navy beans, there were 237 possible navy bean-derived metabolites that were identified in the stool of participants consuming navy beans, such as N-methylpipecolate, 2-aminoadipate, piperidine, and vanillate. The microbial metabolism of amino acids and fatty acids were also identified in stool after 4 weeks of navy bean intake including cadaverine, hydantoin-5 propionic acid, 4-hydroxyphenylacetate, and caprylate. The stool relative abundance of ophthalmate increased 5.25-fold for navy bean consumers that can indicate glutathione regulation, and involving cancer control mechanisms such as detoxification of xenobiotics, antioxidant defense, proliferation, and apoptosis. Metabolic pathways involving lysine, and phytochemicals were also modulated by navy bean intake in CRC survivors. These metabolites and metabolic pathways represent an acute response to increased navy bean intake, which merit further investigation for improving colonic health after long-term consumption.

KRT84 is a potential tumor suppressor and good prognosis signature of oral squamous cell carcinoma

“…Linoleic acid metabolism and arachidonic acid metabolism are two acid metabolism-related pathways that were also significantly activated in KRT High OSCC tumor groups. Acid metabolism have been extensively proved to be associated with cancer initiation and progression [28][29][30] by previously studies. Linoleic acid and arachidonic acid were the two acids that specifically identified in the present study, whose metabolism might be dysregulated by aberrant KRT84 expression, so this should also be potential pathways by which KRT84 could regulate OSCC progression.…”

Phytochemicals and Gastrointestinal Cancer: Cellular Mechanisms and Effects to Change Cancer Progression

“…Navy beans and their metabolites (Table 1) have been implicated in the protection of CRC through the modulation of major metabolic pathways like lysine, sterol, amino and inositol, and fatty acid metabolism. Dietary intake of navy beans (35 g/day) has been found to increase the abundance of several amino acids in stools, showing a protective effect against CRC through the inhibition of cellular progression, reduction of oxidative stress, and induction of cellular apoptosis [192,193]. A study performed on 16 people (seven non-cancer subjects and nine CRC survivors) has shown that the addition of 35 g cooked navy bean powder in meals for 28 days is able to provide chemoprevention effects against CRC [194].…”

Alternative Treatments for Cancer Prevention and Cure [Part 1]

“…(Navy bean) Beans Anacardic acid ( Figure 8e) and nobiletin Imparts glutathione regulation, and involved cancer control mechanisms such as detoxification of xenobiotics, antioxidant defense, proliferation, and apoptosis. Metabolic pathways involving lysine, and phytochemicals were also modulated by navy bean intake in CRC survivors [465]. Anacardic acid efficiently repressed expression of CD44 and MMP14 in HCT116 colon cancer cells, with repression of the SUMOconjugated TFAP2A isoform and elimination of CD44+/hi/ALDH+/hi cells [466].…”