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Stress, Food, and Inflammation: Psychoneuroimmunology and Nutrition at the Cutting Edge

From the Department of Psychiatry, The Ohio State Institute for Behavioral Medicine Research, The Ohio State University College of Medicine, Columbus, Ohio.

Address correspondence and reprint requests to Janice K. Kiecolt-Glaser, PhD, Institute for Behavioral Medicine Research, The Ohio State University College of Medicine, IBMR Building, 460 Medical Center Drive, Room 130C, Columbus, OH 43210-1228. E-mail: Janice.Kiecolt-Glaser{at}osumc.edu

Inflammation is the common link among the leading causes of death. Mechanistic studies have shown how various dietary components can modulate key pathways to inflammation, including sympathetic activity, oxidative stress, transcription factor nuclear factor-B activation, and proinflammatory cytokine production. Behavioral studies have demonstrated that stressful events and depression can also influence inflammation through these same processes. If the joint contributions of diet and behavior to inflammation were simply additive, they would be important. However, several far more intriguing interactive possibilities are discussed: stress influences food choices; stress can enhance maladaptive metabolic responses to unhealthy meals; and diet can affect mood as well as proinflammatory responses to stressors. Furthermore, because the vagus nerve innervates tissues involved in the digestion, absorption, and metabolism of nutrients, vagal activation can directly and profoundly influence metabolic responses to food, as well as inflammation; in turn, both depression and stress have well-documented negative effects on vagal activation, contributing to the lively interplay between the brain and the gut. As one example, omega-3 fatty acid intake can boost mood and vagal tone, dampen nuclear factor-B activation and responses to endotoxin, and modulate the magnitude of inflammatory responses to stressors. A better understanding of how stressors, negative emotions, and unhealthy meals work together to enhance inflammation will benefit behavioral and nutritional research, as well as the broader biomedical community.

Key Words: interleukin-6 • C-reactive protein • proinflammatory cytokines • depression • omega-3 • polyunsaturated fatty acid

Abbreviations: CRP = C-reactive protein; EPA = eicosapentaenoic acid; IL = interleukin; TNF = tumor necrosis factor; LPS = lipopolysaccharide; n-3 = omega-3; n-6 = omega-6; NF = nuclear factor; PUFA = polyunsaturated fatty acid.