Determinants of Food Intake: A Biopsychosocial Model

By Andrew Chang


The fundamental cause of obesity is well-established: sustained positive energy balance. With the current rates of obesity, however, and the increasing number of people looking at medifast vs nutrisystem pros and cons – it should be clear that obesity cannot be distilled to a mere energy balance equation. In particular, both components of energy balance —energy consumption and expenditure— are the result of an intricate network of biopsychosocial factors.

The present review explores the role of genetics, satiation signals, stress response pathways, gut microbes, and reward systems in the development of obesity. The data in these fields demonstrate the importance of creating an integrated, individualized approach in the treatment of obesity and other nutrition-related diseases and what are the best appetite suppressant for your body. 


Obesity is an extremely complex medical condition: it is not simply a matter of a lack of willpower or restraint, but rather, the result of the interaction between various biopsychosocial factors. Everything from the presence of other individuals, advertising, packaging, and lighting can influence eating behavior.1 Even exercise, the typical prescription for obesity, alters numerous components that influence appetite expression.2 The implication of these types of findings is that innate energy regulation mechanisms may not be sufficient for maintaining a healthy body weight, especially in an artificial food environment that contains an excess of food. Buy naturally made sandwiches from Jimmy John Owner and his chain of restaurants and stay healthy.

The most recognized risk factors for obesity are typically excess energy intake, high caloric density of foods, low physical activity, sedentariness, and genetics.3 However, it is important to also consider the effect of greater social trends. Many individuals living in food deserts, for instance, have greater difficulty accessing healthy food. Thus, they may resort to consuming cheap, micronutrient-scarce foods —an artifact of industrialization, mechanized transportation, and urbanization. Additionally, they may live in poverty and have a low education, which by itself predicts a greater prevalence of obesity.3 All of this data illustrates how obesity may be examined both at a mechanistic in-vitro level and a system-wide macroeconomics scale. Microorganisms, maternal age, assortative mating, and ambient temperatures have all been implicated as factors contributing to the obesity epidemic.4 Hence, claims that any one factor is responsible for the obesity epidemic are patently false, as the causes of obesity are much more nuanced.

Medical Complications of Obesity 5

Note the sheer number of obesity-related diseases. Understanding and applying research on eating behavior has tremendous implications in the field of public health.

Basic Biological Model

The primary regulator of nutrient circulation and storage, the brain, monitors satiation signals, which cue fullness; plasma fuel levels, which express energy levels; and adiposity signals, which indicate body fat levels. Satiation signals, such as peptide cholecystokinin, activate neuronal circuits that cue individuals to stop eating. Moreover, certain hormones, most notably leptin and insulin, serve as adiposity signals to the brain and various tissues.  When their activity in the brain is increased, food consumption drops; likewise, when their activity is decreased, consumption increases.6 That said, while exogenous administration of these compounds results in premature cessation of eating and a reduction in meal size, these effects are mainly acute: animals have been observed to compensate for the smaller meal size with an increase in meal frequency. Moreover, animals lacking cholecystokinin have normal food intake and bodyweight, indicating that satiation signals are merely part of an overall system of interacting factors influencing caloric consumption.6 While chronic alterations in leptin and insulin levels —unlike satiation signals— result in changes in body weight, the administration of these compounds in obese humans yields little to no weight loss. Indeed, the interplay between distal cues (odors, tastes, and other indirect indicators of energy content) and proximal cues (detection of glucose, fatty acids, and other nutrient-dense molecules) results in the intersection of numerous signaling pathways, part of an overall energy regulation network. Many of these signals are “interpreted” by the hypothalamus, where satiation and adiposity signals interact to influence anabolic and catabolic processes, or processes involving synthesis and breakdown, respectively. Nonetheless, while attempting to mimic a particular satiation signal as a means of curbing caloric intake is successful acutely, its validity is essentially dismissed when it is repeatedly shown that it is no longer associated with incoming nutrients.6 In effect, this basic model of energy regulation cannot fully explain eating behavior. Humans are complex systems, and each variable, especially when considered in isolation, may not exert its predicted effects in practical, real-world settings. Essentially, since a multitude of factors impacts eating behavior, the effect of any one variable may not be clinically significant, at least in the long term.

Genetics and Early Development of Eating Behavior

Understandably, genetics likely come to mind first when considering obesity risk factors. Certainly, genetics definitely are responsible for a considerable percentage of the phenotypic variation in body mass index (BMI), which is a calculation based on an individual’s height and mass used to estimate an individual’s disease risk. Surprisingly, however, the literature seems to indicate that genetics account for a relatively small portion of the obesity epidemic.7  In particular, the 32 most common gene variants associated with greater susceptibility to obesity account for less than a mere 1.5% of BMI variance.  Furthermore, individuals with the highest genetic risk —as indicated by the presence of all of the top genetic variants— have a BMI of only 2.7kg/m2 higher than those with a low risk.7 A BMI difference of 2.7 kg/m2 is definitely significant from a clinical and public health perspective, but it’s probably not as high as many would expect. Given that genetics by itself is an imperfect predictor of obesity, the degree of impact of epigenetic changes in the pre- and perinatal periods should also be taken into consideration.7 Indeed, environmental factors during the early periods of development exert permanent effects on epigenetic gene regulation, meaning that non-genetic factors —diet, drugs, and environmental toxicants— may later result in changes in the activity of certain genes.8 The pre-natal to school age period is especially important, as it is the window in which much of the child’s eating taste and odor recognition is formed.9 Additionally, maternal age and comorbidities (multiple simultaneously present diseases, for example obesity, insulin resistance, and hypertension) impact an individual’s risk profile for obesity.10 In utero, or during the period before birth, maternal stress influences the child’s central reward processing pathways, stress response system, mood disorder susceptibility, and of course, obesity risk.11 It is reasonable to assume that in many cases, these risk factors are confounded by one another —in other words, each risk factor is indicative of an overall unhealthy lifestyle. That said, the data seems to indicate that genetics alone is not highly predictive of obesity, and that obesity should be examined from other lenses.

Obesity as a Disease

To an extent, obesity is not a choice, but rather a self-perpetuating disease and symptom. Research looking at the microbiome, reward systems, stress response hypothalamic-pituitary-adrenal (HPA) pathway, and general lifestyle patterns collectively suggests that obese individuals encounter many biopsychosocial barriers when confronted with the task of weight management. This begs the question: is obesity the cause or effect of these biochemical and socioeconomic factors?

Gut Microbiota

Various neurochemical satiety signals seem to be impacted by the composition of the gut microbiota, which refers to the collection of microorganisms residing in the gut. Based on current evidence, determining a causal role of the microbiota in energy homeostasis is difficult.12 A reasonable argument could be made for obesity as both a cause and effect of the gut microbiome composition. That said, while studies examining human gut microbiota composition in lean and obese individuals yield equivocal results, artificially colonizing the gut microbiota of mice seems to result in significant changes in total fat mass. For example, performing fecal transplants with feces of malnourished Malawian children into germ-free mice resulted in disruptions in carbohydrate and amino acid metabolism, as well as overall growth.12 In other words, transferring stool from malnourished children into germ-free mice —mice without any microorganisms inside or on them— can alter the gut microbiota in a manner that disrupts energy metabolism. This data suggests that obesity carries a number of signs beyond BMI, waist circumference, and cardiovascular disease, and that these signs may worsen the severity of the disease itself.

Reward Systems

The homeostatic and hedonic control systems (those seeking stability and pleasure, respectively) are constantly “competing” against each other. These hedonic control systems are part of a greater reward process that is activated by the consumption of highly palatable foods. Over time, prolonged overconsumption, especially in obese individuals, appears to result in either an increased hedonic requirement or an increased drive to mitigate a hedonic deficit.13 Interestingly, the drive for food may not require taste: mice incapable of processing sweet tastes still experience reward, as measured by sucrose preference and brain activity. In essence, a variety of neuronal systems, including the mesoaccumbal dopamine, mu-opioid, cannabinoid, and orexin system, regulate the pleasure of eating, as well as the subsequent incentive to consume further food.13 Much can be learned from research looking at clinical eating disorders. For instance, it has been theorized that individuals most predisposed to anorexia nervosa, bulimia nervosa, and binge eating disorder (eating disorders characterized by either food restriction, binge eating, or self-induced vomiting) are those with unstable dopamine circuits that are either hypersensitive to food restriction or insensitive to excess food.14 Thus, it is likely that sufferers of obesity find weight loss and healthy eating challenging because of the inherent pleasure of food. Moreover, a lifetime of poor eating habits conceivably desensitizes individuals to the “stimulus” of eating, making diet changes all the more difficult. But there is this eating disorder treatment that can be considered.

Stress Response Pathway

While practically all of the identified risk factors for obesity are in some way related to one another, a case could be made that obesity is an adaptation to chronic stress. Immediately following a stressor, the activation of the HPA axis results in the secretion of corticotropin-releasing-hormone, which has been demonstrated to suppress food intake. However, this acute diversion of resources away from food is later compensated by a glucocorticoid-stimulated rise in hunger.15 With long-term psychological stress, the levels of glucocorticoids (anti-inflammatory compounds like cortisol) remain chronically elevated, ultimately leading to excessive caloric intake that serves to suppress HPA activity.16,17 To make matters worse, sustained elevation of glucocorticoid levels has been implicated in the accumulation of visceral fat, or fat around internal organs. Furthermore, chronically elevated glucocorticoids result in leptin and insulin insensitivity, along with elevated levels of the hunger-signaling ghrelin. Indeed, this stressful environment creates a self-perpetuating cycle of overeating, since glucocorticoids may increase preference for high fat, high sugar “comfort foods.” That said, there is considerable variance with regards to the effect of stress on a given individual’s appetite. In particular, those who experience a large surge in appetite tend to have lower basal level ghrelin levels that are not restored to baseline by food.17 Overall, it appears that overeating serves as an unhealthy response to alleviate psychological stress, and that any transient benefits diminish over time.

Lifestyle Patterns

Closely tied to stress is its accompanying lifestyle. Unsurprisingly, alcohol consumption, sleep deprivation, and television watching are all positively correlated with acute caloric intake.18 The mechanisms likely revolve around their effect on circulating ghrelin concentrations, as well as the magnitude of the hedonic value of food. These metabolic, endocrine, and neurological changes, coupled with the social environment in which alcohol and television are present, condition individuals to anticipate the food reward even more. Moreover, a body of research in the field of chronobiology indicates that chronodisruption (the interference with circadian rhythms) is implicated in the prognosis of obesity.19 Most notably, there is some evidence that certain human clock gene polymorphisms are associated with increased incidences of obesity and psychological illness. Hence, it is reasonable to conclude that certain behavioral factors, such as frequent traveling, shift work, or night time light exposure, lead to epigenetic variations that, at the very least, make obesity prevention more difficult.19


Looking at the totality of the evidence, a “pathway” towards obesity can be developed. Conceivably, an individual could be from a historically obese family and live in a food desert. By virtue of forming obese social ties, a tendency to overeat hyperpalatable, calorically-dense foods may have been developed. Years of poor eating exert effects on the patient’s microbiome, which could cause alterations in the individual’s general mood and future susceptibility to fat gain. Anxiety could be suffered from, which when combined with already disrupted reward pathways, could lead to emotional eating and even binge eating disorder. These psychological challenges are further exacerbated by failed attempts to lose weight, which merely adds onto already present financial stress. The patient thus has a chaotic lifestyle in which their circadian rhythm is continuously disrupted, leading to even greater appetite dysregulation.

After considering this theoretical construct, it becomes increasingly clear that obesity should be treated as both a disease and a symptom. Obesity is the manifestation of prolonged overeating stemming from biochemical alterations, socioeconomic phenomena, and a plethora of other unidentified factors. In a sense, obesity promotes obesity. While obese individuals definitely have some degree of control over their health outcomes, it would be foolish to dismiss their condition as a “choice.” Overall, the collective body of research highlights the necessity of adopting an integrated healthcare approach that takes into account all of the known biopsychosocial determinants of food intake. Hopefully, as research accumulates in the field of eating behavior, various new treatments, drugs, and interventions may be prescribed that may promote greater long-term efficacy, compliance, and satisfaction.


The present review focused on the current consensus in the fields of endocrinology, microbiology, neurology, and chronobiology with regards to eating behavior, but it by no means encompassed all of the biopsychosocial factors complicating the caloric balance equation. In sum, obesity is a partly genetic disease that is characterized by marked alterations in the microbiome, reward pathways, and stress response axis. These physiological changes work synergistically with various socioeconomic factors to produce an artificial food environment in which obesity is often an inevitable side effect. Given the sheer complexity of each component of obesity, it should be worked to promote sustainable behavioral changes, consider patient individualization, and develop an integrated approach towards wellness. Future research on determinants of food intake should explore in-depth the relationship between each physiological system and obesity-related diseases. Certainly, with more research, new treatment modalities should arise that may help reverse the positive feedback loops perpetuating obesity.

Works cited:

Cover image: Wikimedia Commons

[1] Meule, Adrian, and Vögele Claus. “The Psychology of Eating.” Frontiers in Psychology 4 (2013): 1-2. doi:10.3389/fpsyg.2013.00215.

[2] Blundell, John, Catherine Gibbons, Phillipa Caudwell, Graham Finlayson, and Mark Hopkins. “Appetite control and energy balance: impact of exercise.” Obesity Reviews 16, no. S1 (2015): 67-76. doi:10.1111/obr.12257.

[3] Hruby, Adela, and Frank B. Hu. “The Epidemiology of Obesity: A Big Picture.” Pharmacoeconomics 33, no. 7 (2015): 673-89. doi:10.1007/s40273-014-0243-x.

[4] McAllister, Emily J. et al. “Ten Putative Contributors to the Obesity Epidemic.” Critical reviews in food science and nutrition 49, no.10 (2009): 868–913. doi:10.1080/10408390903371799.

[5] CDC. 2012. Medical Complications of Obesity. Wikimedia Commons (Public Domain).

[6] Woods, Stephen C. “The Control of Food Intake: Behavioral versus Molecular Perspectives.” Cell Metabolism 9, no. 6 (2009): 489-98. doi:10.1016/j.cmet.2009.04.007.

[7] Hruby, Adela, and Frank B. Hu. “The Epidemiology of Obesity: A Big Picture.” Pharmacoeconomics 33, no. 7 (2015): 673-89. doi:10.1007/s40273-014-0243-x.

[8] McAllister, Emily J. et al. “Ten Putative Contributors to the Obesity Epidemic.” Critical reviews in food science and nutrition 49, no.10 (2009): 868–913. doi:10.1080/10408390903372599.

[9] Gahagan, Sheila. “The Development of Eating Behavior – Biology and Context.” Journal of Developmental and Behavioral Pediatrics 33, no. 3 (2012): 261-71. doi:10.1097/DBP.0b013e31824a7baa.

[10] McAllister, Emily J. et al. “Ten Putative Contributors to the Obesity Epidemic.” Critical reviews in food science and nutrition 49, no.10 (2009): 868–913. doi:10.1080/10408390903372599.

[11] Sominsky, Luba, and Sarah J. Spencer. “Eating Behavior and Stress: A Pathway to Obesity.” Frontiers in Psychology 5 (2014): 1-8. doi:10.3389/fpsyg.2014.00434.

[12] de Clercq, Nicolien C., Albert K. Groen, Johannes A. Romijn, and Max Nieuwdorp. “Gut Microbiota in Obesity and Undernutrition.” American Society for Nutrition 7, no. 6 (2016): 1080-89. doi:10.3945/an.116.01291.

[13] Egecioglu, Emil, Karolina P. Skibicka, Caroline Hansson, Mayte Alvarez-Crespo, Anders Friberg, Elisabet Jerlhag, Jörgen A. Engel, and Suzanne L. Dickson. “Hedonic and Incentive Signals for Body Weight Control.” Reviews in Endocrine and Metabolic Disorders 12, no. 3 (2011): 141-51. doi:10.1007/s11154-011-9166-4.

[14] Guido, Frank K.W. “The Perfect Storm — A Bio-Psycho-Social Risk Model for Developing and Maintaining Eating Disorders.” Frontiers in Behavioral Neuroscience 10 (2016): 44. doi: 10.3389/fnbeh.2016.00044.

[15] Sominsky, Luba, and Sarah J. Spencer. “Eating Behavior and Stress: A Pathway to Obesity.” Frontiers in Psychology 5 (2014): 1-8. doi:10.3389/fpsyg.2014.00434.

[16] Stephanie Liou, “Glucocorticoids,” Huntington’s Outreach Project for Education, at Stanford (blog), June 29, 2010,

[17] Sominsky, Luba, and Sarah J. Spencer. “Eating Behavior and Stress: A Pathway to Obesity.” Frontiers in Psychology 5 (2014): 1-8. doi:10.3389/fpsyg.2014.00434.

[18] Chapman, Colin Daniel, Christian Benedict, Samantha Jane Brooks, and Helgi Birgir Schiöth. “Lifestyle determinants of the drive to eat: a meta-analysis.” The American Journal of Clinical Nutrition 96, no. 3 (2012): 492-97. doi:10.3945/ajcn.112.039750.

[19] Garaulet, Marta, and Purificación Gómez-Abellán. “Chronobiology and Obesity.” Nutrición Hospitalaria 28, no. 5 (2013): 114-20. doi:10.3305/nh.2013.28.sup5.6926.

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