Summary: A new study reveals a link between elevates microbiome levels of indole and hedonic eating. Researchers report those with higher levels of indole are more likely to have food addiction and overeating disorders.
A study of 63 healthy people showed that those with elevated microbiome levels of the metabolite indole — produced when gut bacteria break down the amino acid tryptophan — had stronger function and connectivity in specific areas of the brain’s reward network. Such activity in the brain indicates that a person is more prone to “hedonic eating,” or eating for pleasure rather than for hunger. Those with higher levels of indole also were more likely to have food addiction, as determined by questionnaires they completed.
Certain areas of the brain’s reward network have long been known to drive eating behaviors. In particular, the nucleus accumbens — which processes reward stimuli such as food — and the amygdala — which helps regulate emotions — are activated when people are hungry or eating. In this study, people with higher indole levels showed stronger function and connectivity in these two areas.
Higher function and connectivity in the brain’s reward system could indicate an overactive reward system that promotes and reinforces overeating. Such overactivity of the reward system in obese individuals with food addiction has been reported in previous research.
The researchers obtained functional MRI brain imaging from the healthy participants. They collected and analyzed fecal samples in order to determine the presence of particular gut metabolites. The subjects completed questionnaires that measured their propensity for food addiction.
The study — the first in humans to show the association between specific metabolites produced by gut bacteria and overeating behaviors — suggests that indole, or gut bacteria’s ability to produce it, could contribute to such behaviors. It opens the door to future study about whether specific interventions, such as changes to diet, could affect brain function and thus affect the desire to overeat or to eat when not hungry.
The senior author is Dr. Emeran Mayer, director of the G. Oppenheimer Center for Neurobiology of Stress and Resilience and co-director of the CURE: Digestive Diseases Research Center at UCLA. Vadim Osadchiy, a student at the David Geffen School of Medicine at UCLA, is the first author. The other authors are Jennifer Labus, Arpana Gupta, Dr. Jonathan Jacobs, Cody Ashe-McNalley and Elaine Hsiao, all of the UCLA Vatche and Tamar Manoukian Division of Digestive Diseases.
Funding: The study was supported by grants from the National Institutes of Health.
Source: Ryan Hatoum – UCLA
Publisher: Organized by NeuroscienceNews.com.
Image Source: NeuroscienceNews.com image is in the public domain.
Original Research: Open access research for “Correlation of tryptophan metabolites with connectivity of extended central reward network in healthy subjects” by Y. Vadim Osadchiy, Jennifer S. Labus, Arpana Gupta, Jonathan Jacobs, Cody Ashe-McNalley, Elaine Y. Hsiao, and Emeran A. Mayer in PLOS ONE. Published August 6 2018.
Correlation of tryptophan metabolites with connectivity of extended central reward network in healthy subjects
A growing body of preclinical and clinical literature suggests that brain-gut-microbiota interactions play an important role in human health and disease, including hedonic food intake and obesity. We performed a tripartite network analysis based on graph theory to test the hypothesis that microbiota-derived fecal metabolites are associated with connectivity of key regions of the brain’s extended reward network and clinical measures related to obesity.
DTI and resting state fMRI imaging was obtained from 63 healthy subjects with and without elevated body mass index (BMI) (29 males and 34 females). Subjects submitted fecal samples, completed questionnaires to assess anxiety and food addiction, and BMI was recorded.
The study results demonstrate associations between fecal microbiota-derived indole metabolites (indole, indoleacetic acid, and skatole) with measures of functional and anatomical connectivity of the amygdala, nucleus accumbens, and anterior insula, in addition to BMI, food addiction scores (YFAS) and anxiety symptom scores (HAD Anxiety).
The findings support the hypothesis that gut microbiota-derived indole metabolites may influence hedonic food intake and obesity by acting on the extended reward network, specifically the amygdala-nucleus accumbens circuit and the amygdala-anterior insula circuit. These cross sectional, data-driven results provide valuable information for future mechanistic studies.