The Pathway Between “you Are” and “what You Eat”

Significant connections between the brain and gut that influence mood and cognitive processes have long been hypothesized. In the 19th century, Ireland’s psychiatrists described “the insanity of malnutrition,” a concerning correlation between rising asylum admissions and patients’ inability to acquire healthy food ( 1 Miller I. The gut-brain axis: Historical reflections. Microb Ecol Health Dis. 2018; 291542921 Google Scholar ). Earlier still, Shakespeare’s Julius Caesar proclaimed, “Yond Cassius has a lean and hungry look, He thinks too much.” These rudimentary observations alluded to what is now widely recognized as the gut-brain axis, the intricate system of neural and endocrine cells in the gut that reciprocally communicate with the brain. More intriguingly, these early inferred relationships subtly imply that the gut, rather than the brain, perhaps caused the negative behavioral state. SEE CORRESPONDING ARTICLE ON PAGE 609 SEE CORRESPONDING ARTICLE ON PAGE 609 Role of PPAR-Allopregnanolone Signaling in Behavioral and Inflammatory Gut-Brain Axis CommunicationsBiological PsychiatryVol. 94Issue 8PreviewThe gut microbiome regulates emotional behavior, stress responses, and inflammatory processes by communicating with the brain. How and which neurobiological mediators underlie this communication remain poorly understood. PPAR-α (peroxisome proliferator-activated receptor α), a transcription factor susceptible to epigenetic modifications, regulates pathophysiological functions, including metabolic syndrome, inflammation, and behavior. Mood disorders, inflammatory processes, and obesity are intertwined phenomena that are associated with low blood concentrations of the anti-inflammatory and “endogenous tranquilizer” neurosteroid allopregnanolone and poor PPAR-α function. Full-Text PDF