Food reward system: current perspectives and future research needs

Abstract

This article reviews current research and cross-disciplinary perspectives on the neuroscience of food reward in animals and humans, examines the scientific hypothesis of food addiction, discusses methodological and terminology challenges, and identifies knowledge gaps and future research needs. Topics addressed herein include the role of reward and hedonic aspects in the regulation of food intake, neuroanatomy and neurobiology of the reward system in animals and humans, responsivity of the brain reward system to palatable foods and drugs, translation of craving versus addiction, and cognitive control of food reward. The content is based on a workshop held in 2013 by the North American Branch of the International Life Sciences Institute.

Keywords: addiction; craving; definitions; food reward system; palatable food; translational science.

Figure 1

Substances of abuse? Science has yet to determine all of the mechanisms of action that may differentiate foods from drugs with regard to craving, dependence, tolerance, and abuse.

Figure 2

Homeostatic and nonhomeostatic influences in regulation of food intake. Food intake is determined by interplay between complex homeostatic and nonhomeostatic controls. Abbreviation: CCK, cholecystokinin.

Figure 3

DSM-5 criteria for substance use disorder. Diagnosis is graded as mild (2–3 items), moderate (4–5 items), or severe (6 or more items).

Figure 4

Dynamic vulnerability model of obesity. TaqIA refers to the single-nucleotide polymorphism of the ANKK1 gene (rs1800497), which has 3 allelic variants: A1/A1, A1/A2, and A2/A2.

Figure 5

Mutations in the leptin-melanocortin pathway in humans. Abbreviations: ACTH, adrenocorticotropic hormone; AgRP, Agouti-related peptide; BDNF, brain-derived neurotrophic factor; CB1, cannabinoid type 1 receptor; incr., increased; LEP, leptin; LEPR, leptin receptor; MCH, melanin-concentrating hormone; MC4R, melanocortin 4 receptor gene; α-MSH, alpha-melanocyte-stimulating hormone; NPY, neuropeptide Y; Ob-Rb, leptin receptor, Ob-Rb isoform; PC1/3, prohormone convertase 1/3; POMC, pro-opiomelanocortin; RQ, respiratory quotient; SIM1, single-minded 1; TRKB, tyrosine kinase B.

Figure 6

Cognitive control of food reward and environmental influences. Regulation of food intake, particularly the modulatory effect of cognitive control over food reward, occurs within the context of multiple levels of environmental influences. According to Gidding et al. (2009), there are 4 levels of influence: the individual level (level 1) is nested within the family environment (level 2) and is influenced by elements such as role modeling, feeding style, provision, and availability of foods, and so forth; the microenvironmental level (level 3) refers to the local environment or community and includes local schools, playgrounds, walking areas, and shopping markets that enable or impede healthful eating behaviors; and the macroenvironmental level (level 4) refers to broader regional, state, national, and international economic and industry policies and laws, which can affect individual choices. Gidding et al. (2009) state that this model “recognizes the importance of both the nesting of levels within one another and reciprocal influences among levels.”