Food Cues and Obesity: Overpowering Hormones and Energy Balance Regulation
Purpose of Review
In the modern obesogenic environment, food cues play a crucial role in the development of obesity by disrupting hormone and energy balance mechanisms. Thus, it is critical to understand the neurobiology of feeding behaviors and obesity in the context of ubiquitous food cues. The current paper reviews the physiology of feeding, hormonal regulation of energy balance, and food cue responses and discusses their contributions to obesity.
Food cues have strong impact on human physiology. Obese individuals have altered food cue-elicited responses in the brain and periphery, overpowering hormone and energy balance regulation. Disrupted homeostasis during food cue exposure leads to continued food intake, unsuccessful weight management, and poor treatment outcomes, which further contributes to obesity epidemic.
Findings from the review emphasize the crucial role of food cues in obesity epidemic, which necessitates multidimensional approaches to the prevention and treatment of obesity, including psychosocial interventions to reduce food cue reactivity, along with conventional treatment.
KeywordsObesity Food cues Brain activity hormone Energy balance
This work was funded in part by grants from the NIH (K23 DK098286-02 to R Belfort-DeAguiar from the NIDDK), (K08-AA023545 to D Seo from the NIAAA), and a Young Investigator Grant (Seo) from the Brain and Behavior Research Foundation. This publication was made possible by CTSA Grant Number UL1 TR00142 from the National Center for Advancing Translational Science (NCATS), a component of the National Institutes of Health (NIH). Its contents are solely the responsibility of the authors and do not necessarily represent the official view of NIH.
Compliance with Ethical Standards
Conflict of Interest
Renata Belfort-DeAguiar and Dongju Seo declare they have no conflict of interest.
Human and Animal Rights and Informed Consent
All reported studies/experiments with human subjects performed by the authors have been previously published and complied with all applicable ethical standards (including the Helsinki declaration and its amendments, institutional/national research committee standards, and international/national/institutional guidelines).
Papers of particular interest, published recently, have been highlighted as: • Of importance •• Of major importance
- 1.C D Fryar, M D Carroll and C L Ogden. Prevalence of overweight, obesity, and extreme obesity among adults: United States, trends 1960–1962 through 2009–2010. NCHS Health E-Stat. 2014.Google Scholar
- 11.Westerterp-Plantenga MS, Wijckmans-Duijsens NE, Verboeket-van de Venne WP, de Graaf K, van het Hof KH, Weststrate JA. Energy intake and body weight effects of six months reduced or full fat diets, as a function of dietary restraint. Int J Obes Relat Metab Disord. 1998;22(1):14–22.PubMedCrossRefGoogle Scholar
- 13.• Gittelsohn J, Trude A. Diabetes and obesity prevention: changing the food environment in low-income settings. Nutr Rev. 2017;75(suppl 1):62–9. A review of 10 community trials evaluating the impact of changes in the food environment in low-income minority settings. PubMedPubMedCentralCrossRefGoogle Scholar
- 16.• Louzada ML, Baraldi LG, Steele EM, Martins AP, Canella DS, Moubarac JC, et al. Consumption of ultra-processed foods and obesity in Brazilian adolescents and adults. Prev Med. 2015;81:9–15. A dietary survey from 30,243 individuals in Brazil demonstrated that ultra-processed food is associated with obesity and weight gain. PubMedCrossRefGoogle Scholar
- 17.Putnam J, Allshouse J, Kantor LS. U.S. per capita food supply trends: more calories, refined carbohydrates, and fats. Food Rev: Mag Food Econ. 2002;25(3):2–15.Google Scholar
- 20.• Fardet A. Minimally processed foods are more satiating and less hyperglycemic than ultra-processed foods: a preliminary study with 98 ready-to-eat foods. Food Funct. 2016;7(5):2338–46. Evaluation of the glycemic glucose equivalent (GGE) of ultraprocessed food on satiety and blood glucose levels. Ultraprocessed food was associated with higher glycemic response and decreased satiety. PubMedCrossRefGoogle Scholar
- 23.Volkow ND, Wang GJ, Fowler JS, Tomasi D, Baler R. Food and drug reward: overlapping circuits in human obesity and addiction. In: Carter CS, Dalley JW, editors. Brain imaging in behavioral neuroscience. Berlin, Heidelberg: Springer Berlin Heidelberg; 2012. p. 1–24.Google Scholar
- 34.•• Timper K, Bruning JC. Hypothalamic circuits regulating appetite and energy homeostasis: pathways to obesity. Dis Model Mech. 2017;10(6):679–89. A review with the latest information about the role of the hypothalamus on feeding and the pathogenesis of obesity. PubMedPubMedCentralCrossRefGoogle Scholar
- 57.Willms B, Werner J, Holst JJ, Orskov C, Creutzfeldt W, Nauck MA. Gastric emptying, glucose responses, and insulin secretion after a liquid test meal: effects of exogenous glucagon-like peptide-1 (GLP-1)-(7-36) amide in type 2 (noninsulin-dependent) diabetic patients. J Clin Endocrinol Metab. 1996;81(1):327–32.PubMedGoogle Scholar
- 82.• Boswell RG, Kober H. Food cue reactivity and craving predict eating and weight gain: a meta-analytic review. Obes Rev. 2016;17(2):159–77. Meta-analyses of 45 studies evaluating the effect of food cues on eating behavior identified that visual food cues were as effective as real food (and more that olfactory cues) in affecting eating behavior and weight gain. PubMedCrossRefGoogle Scholar
- 92.Berthoud H-R, Lenard NR, Shin AC. Food reward, hyperphagia, and obesity. Am J Phys Regul Integr Comp Phys. 2011;300(6):R1266–R77.Google Scholar
- 100.McCaffery JM, Haley AP, Sweet LH, Phelan S, Raynor HA, Del Parigi A, et al. Differential functional magnetic resonance imaging response to food pictures in successful weight-loss maintainers relative to normal-weight and obese controls. Am J Clin Nutr. 2009;90(4):928–34.PubMedPubMedCentralCrossRefGoogle Scholar
- 103.• Belfort-De Aguiar R, Seo D, Naik S, Hwang J, Lacadie C, Schmidt C, et al. Food image-induced brain activation is not diminished by insulin infusion. Int J Obes (Lond). 2016;40(11):1679–86. In this study, brain responses to food cues were not affected by an intravenous insulin infusion, in comparison to a saline infusion. CrossRefGoogle Scholar
- 106.•• Sun X, Kroemer NB, Veldhuizen MG, Babbs AE, de Araujo IE, Gitelman DR, et al. Basolateral amygdala response to food cues in the absence of hunger is associated with weight gain susceptibility. J Neurosci. 2015;35(20):7964–76. Activity in the amygdala in response to tasting a milkshake in the sated, but not in the hungry state, predicted weight gain in susceptible individuals. PubMedPubMedCentralCrossRefGoogle Scholar
- 107.McCaffery JM, Haley AP, Sweet LH, Phelan S, Raynor HA, Del Parigi A, et al. Differential functional magnetic resonance imaging response to food pictures in successful weight-loss maintainers relative to normal-weight and obese controls. Am J Clin Nutr. 2009;90:928–34.PubMedPubMedCentralCrossRefGoogle Scholar
- 108.• Maciejewski ML, Arterburn DE, Van Scoyoc L, Smith VA, Yancy WS Jr, Weidenbacher HJ, et al. Bariatric surgery and long-term durability of weight loss. JAMA Surg. 2016;151(11):1046–55. Study showing the 10-year sustained effect of bariatric surgery on weight loss. PubMedPubMedCentralCrossRefGoogle Scholar
- 109.Garvey WT, Mechanick JI, Brett EM, Garber AJ, Hurley DL, Jastreboff AM, et al. American Association of Clinical Endocrinologists and American College of Endocrinology comprehensive clinical practice guidelines for medical care of patients with obesity. Endocr Pract. 2016;22(Suppl 3):1–203.PubMedCrossRefGoogle Scholar