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Cited by 211Regulation of Appetite and ObesityEating Disorders and BehaviorsNeurotransmitter Receptor Influence on Behavior

Role of addiction and stress neurobiology on food intake and obesity

Open access
Sinha, Rajita·2018·Biological Psychology
DOI 10.1016/j.biopsycho.2017.05.001PMC PMC6784832
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Abstract

The US remains at the forefront of a global obesity epidemic with a significant negative impact on public health. While it is well known that a balance between energy intake and expenditure is homeostatically regulated to control weight, growing evidence points to multifactorial social, neurobehavioral and metabolic determinants of food intake that influence obesity risk. This review presents factors such as the ubiquitous presence of rewarding foods in the environment and increased salience of such foods that stimulate brain reward motivation and stress circuits to influence eating behaviors. These rewarding foods via conditioned and reinforcing effects stimulate not only metabolic, but also stress hormones, that, in turn, hijack the brain emotional (limbic) and motivational (striatal) pathways, to promote food craving and excessive food intake. Furthermore, the impact of high levels of stress and trauma and altered metabolic environment (e.g. higher weight, altered insulin sensitivity) on prefrontal cortical self-control processes that regulate emotional, motivational and visceral homeostatic mechanisms of food intake and obesity risk are also discussed. A heuristic framework is presented in which the interactive dynamic effects of neurobehavioral adaptations in metabolic, motivation and stress neurobiology may further support food craving, excessive food intake and weight gain in a complex feed-forward manner. Implications of such adaptations in brain addictive-motivational and stress pathways and their effects on excessive food intake and weight gain are discussed to highlight key questions that requires future research attention in order to better understand and address the growing obesity epidemic.

AI snapshot

Written from the paper’s full text.

TL;DR

This narrative review proposes that highly palatable foods and food cues, via reward/motivation and stress neurobiology, promote food craving, excessive intake, and weight gain in a feed-forward manner. It integrates human and animal evidence on metabolic hormones, glucocorticoids, stress/trauma, and prefrontal self-control to frame obesity risk as overlapping with addiction neurobiology.

Key findings

  • More than 500 million people worldwide are classified as obese (BMI ≥ 30 kg/m²), and two-thirds of the US population is overweight or obese (BMI ≥ 25 kg/m²).
  • Highly palatable foods and related cues are conditioned/reinforcing and activate brain reward and motivation pathways; in a large community sample, higher food craving was associated with greater intake of these foods, and higher BMI was associated with greater food craving. Fast foods such as potato chips, processed meats, and sugar-sweetened beverages predicted long-term weight gain in large prospective US cohorts.
  • Metabolic and stress signals interact with reward circuits: insulin resistance/high insulin may promote rather than suppress food craving and intake and increase activation in dopamine-rich regions (VTA, nucleus accumbens, dorsal striatum); higher leptin predicted blunted VmPFC/rACC activation to high-fat food images and glucose/fructose in adolescents; higher ghrelin was associated with greater food cravings; and higher chronic stress, insulin, and cortisol responses predicted greater weight gain at 6-month follow-up.
  • Stress, trauma, and adversity are positively associated with adiposity, BMI, and weight gain, with stronger associations among overweight and binge-eating individuals; stress can increase fast food, snacks, calorie-dense highly palatable foods, and binge eating, and overweight/obese individuals may be more vulnerable to stress-driven eating.

Methods

  • Narrative review, not a primary empirical study; it synthesizes human and animal research on addiction, stress neurobiology, metabolic hormones, and food intake.
  • No new sample or dataset is analyzed; the paper cites prior studies, including the author’s own cross-sectional, longitudinal, and neuroimaging work.
  • Main analysis is conceptual integration, culminating in a heuristic feed-forward framework (Fig. 1) modified from Sinha & Jastreboff (2013).

Limitations

  • The paper states that the link between glucocorticoids, ghrelin, insulin, and leptin on food motivation and intake in humans is not clear; the influence of specific food types on peripheral and central glucocorticoids and food craving/intake is not known; whether adaptations differ for sweets, fats, and carbohydrates versus proteins is unclear; and the role of additives/preservatives is not well studied.
  • The paper states that longitudinal studies measuring metabolic and stress hormone adaptations and their impact on food intake and weight gain in community samples are needed, as are experimental studies assessing neural and biobehavioral changes relating to food cues, stress, and food intake.
  • Evident from the text: as a narrative review, it does not use a systematic search or meta-analytic synthesis, and many cited findings come from animal models, cross-sectional studies, or observational cohorts; the proposed heuristic framework is presented rather than empirically tested in the paper.

Model-written summary. Check it against the paper before relying on it.

Integrity signals

Registry

Crossref · 10.1016/j.biopsycho.2017.05.001

Cites

152 of 152 references verified0 citation errors · 0 not checkable

Statistics

Nothing to recompute.

Claims the paper makes

0 of 167 cited sources checked · 0 supported · 0 flagged

  • Findingcitation

    Higher food craving was significantly associated with greater intake of highly palatable foods.

    “higher food craving was significantly associated with greater intake of these foods”
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    • cites Chao, Grilo, White, & Sinha, 2014

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  • Findingcitation

    In a cross-sectional study with a large community sample, higher food craving for highly palatable foods was found.

    “in a cross sectional study with a large community sample, we found higher food craving for these HP foods”
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    • cites Chao, Grilo, White, & Sinha, 2014

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  • Findingcitation

    Individuals with higher body mass index reported greater levels of food craving.

    “those with higher body mass index (BMI) reported greater levels of food craving”
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    • cites Chao, Grilo, White, & Sinha, 2014

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  • Findingcitation

    Higher leptin levels associated with obesity predicted blunted ventromedial prefrontal cortex and rostral anterior cingulate activation to high-fat food images and to glucose and fructose intake in adolescents.

    “higher leptin levels (associated with obesity) predicted blunted ventromedial prefrontal cortex and rostral anterior cingulate (VmPFC/rACC) activation to high fat food images and to glucose and fructose intake in adolescents”
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    • cites Jastreboff et al., 2014 source

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    • cites Jastreboff et al., 2016 source

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  • Findingcitation

    Higher activity in the insula and dorsal striatum correlated with higher insulin levels, insulin resistance, and food craving when participants were placed in their favorite food contexts via imagined exposure.

    “higher activity in the insula and dorsal striatum correlated with higher insulin levels, insulin resistance and with food craving when participants were placed in their favorite food contexts via imagined exposure”
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    Findingcitation

    Acute stress increases amygdala and blunts medial orbitofrontal cortex response to milkshake versus tasteless receipt, but this effect was moderated by high cortisol levels and by high body mass index respectively.

    “acute stress increases amygdala and blunts medial orbito-frontal cortex response to milkshake vs tasteless receipt, but this effect was moderated by high cortisol levels and by high BMI respectively”
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    Findingcitation

    Experimentally reducing blood glucose to mild hypoglycemic levels relative to normal euglycemic levels increases plasma cortisol and increases wanting of highly palatable foods and brain activation of reward-motivational and emotion-stress regions in response to high-fat, high-sugar highly palatable versus low-fat and non-food pictures.

    “experimentally reducing blood glucose to mild hypoglycemic levels relative to normal euglycemic levels, not only increases plasma cortisol but also increases wanting of HP foods and brain activation of reward-motivational (striatal) and emotion-stress (limbic) regions in response to high fat, high sugar HP versus low fat and non-food pictures”
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    • cites Page et al., 2011 source

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    Premisecitation

    Social factors including easy availability and low cost of high-calorie highly palatable foods, marketing, increased use of sugars, sugar substitutes, preservatives and sugar-sweetened beverages, altered eating patterns, and sedentary lifestyles contribute to the obesity pandemic.

    “a number of social factors such as the easy availability and relatively low cost of high calorie foods that are highly palatable (HP), widespread marketing of such HP foods, increased use of sugars, sugar substitutes, preservatives and sugar sweetened beverages, altered eating patterns as well as the promotion of sedentary lifestyles all contribute to this pandemic”
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    Premisecitation

    Body weight was previously thought to be regulated by hypothalamic homeostatic and physiologic metabolic processes that maintain energy balance.

    “previously believed notions that body weight is regulated by the hypothalamus with homeostatic and physiologic metabolic processes that maintain a balance between energy intake and energy expenditure”
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    Premisecitation

    Animal and human research has documented activation of brain reward regions and increased dopaminergic transmission with highly palatable food cue exposure, along with increases in food craving and motivation.

    “Research with animals and humans has documented activation of brain reward regions and increased dopaminergic transmission with HP food cue exposure, along with concomitant increases in food craving and motivation”
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    Interpretationreasoning

    Sensory and autobiographical associations with highly palatable foods serve as conditioned cues that may increase liking, preference, seeking, and facilitate craving and intake.

    “their related sensory (including both discrete and context related) and autobiographical associations such as sights, smells, tastes, place where eaten, with whom, when and time and other context factors serve as conditioned cues that may increase liking and preference for such foods, tendency towards seeking them, thereby resulting in facilitating food craving and intake of these foods”
    Quote in the paperSubstantial claim
    • Rests on an assumption: Highly palatable foods are more liked, preferred, and found rewarding in taste.
    • Rests on an assumption: Highly palatable foods are ubiquitous in the current obesogenic environment.

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    Premisecitation

    Highly palatable and processed foods and their cues stimulate brain reward and motivation pathways similarly to reinforcing drugs of abuse and, via conditioning, increase the likelihood of highly palatable food seeking and consumption.

    “Such highly palatable and processed foods and their related associations or ‘cues’ stimulate the brain reward and motivation pathways just as reinforcing drugs of abuse and via learning/conditioning mechanisms increase the likelihood of HP food seeking and consumption”
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    Premisecitation

    Conditioned properties of highly palatable foods and increased intake promote heightened salience, leading to greater wanting and seeking, similar to incentive salience with alcohol and drug intake.

    “The conditioned properties of these HP foods and related increases in their intake promotes their heightened salience, and, in turn, results in greater ‘wanting’ and seeking of HP foods, similar to the incentive salience processes that occur with increasing alcohol and drug intake”
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    • cites Robinson & Berridge, 2008 source

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    • cites Sinha & Jastreboff, 2013

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    Premisecitation

    Exposure to high-fat diets, yo-yo dieting, and withdrawal from such diets may alter extrahypothalamic CRF pathways involved in stress regulation and disrupt brain reward motivation responses to increase compulsive food seeking and stress-induced highly palatable food seeking.

    “exposure to high fats diets, yo–yo dieting and withdrawal from such diets, may alter extrahypothalamic CRF pathways involved in the regulation of stress responses and also disrupt brain reward motivation responses to increase compulsive food seeking and stress-induced HP food seeking”
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    Premisecitation

    Chronic high peripheral insulin and insulin resistance, as observed in many individuals with obesity, may promote rather than suppress food craving and intake and increase brain activation in dopamine-rich reward regions such as the ventral tegmental area, nucleus accumbens, and dorsal striatum.

    “chronic high levels of peripheral insulin and insulin resistance, as is observed in many individuals with obesity, may promote rather than suppress food craving and intake as well as increase brain activation in dopamine-rich reward regions such as the ventral tegmental area (VTA), nucleus accumbens and dorsal striatum”
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    Premisecitation

    Overconsumption of highly palatable food reduces reward thresholds and upregulates extrahypothalamic CRF in the amygdala and related limbic striatal pathways, which may promote food craving and greater neural reactivity to food cues in these brain regions, increasing risk of overeating highly palatable foods.

    “Overconsumption of HP food intake is also known to reduce reward thresholds along with an upregulation of the extrahypothalamic Corticotrophin Releasing Factor (CRF) in the amygdala and related limbic striatal pathways, which, in turn, may promote food craving and associated greater neural reactivity to food cues in these brain regions thereby increasing risk of overeating of HP foods”
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    • cites Cifani, Polidori, Melotto, Ciccocioppo, & Massi, 2009

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    Interpretationreasoning

    Cortisol rise with macronutrient intake may serve to promote gluconeogenesis, underscoring the critical role of glucocorticoids in energy homeostasis.

    “cortisol rise with macronutrient intake may serve to promote gluconeogenesis underscoring the critical role of glucocorticoids in energy homeostasis”
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    Premisecitation

    With greater consumption of highly palatable foods, changes in carbohydrate and fat metabolism, insulin sensitivity, and appetite hormones may influence neural reward regions involved in increasing salience and motivation for food intake, which may alter energy homeostasis.

    “with greater consumption of HP foods, the concomitant changes in carbohydrate and fat metabolism, insulin sensitivity and appetite hormones may influence neural reward regions involved in increasing salience and motivation for food intake, that, in turn, may alter energy homeostasis”
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    Interpretationreasoning

    Specific types of foods may significantly affect both hypothalamic and extrahypothalamic peripheral sources of cortisol and may modulate stress responses to promote food motivation and intake.

    “specific types of foods may significantly affect both hypothalamic and extrahypothalamic peripheral sources of cortisol and may modulate stress responses to promote food motivation and intake”
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    Premisecitation

    Binge and heavy alcohol use, high nicotine use, and other psychostimulant use reduce the increased cortisol responses observed with acute alcohol or drug intake.

    “binge and heavy alcohol use, but also high nicotine and other psychostimulant use, reduces the well-known increased cortisol responses observed with acute alcohol/drug intake”
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    Interpretationreasoning

    It is possible that higher intake of highly palatable comfort foods may alter cortisol responses to such food intake, with glucocorticoid-related alterations influencing homeostatic functions of glucocorticoids in energy balance and hypothalamic and extrahypothalamic regulation of food intake.

    “it is possible that higher intake of HP comfort foods may alter cortisol responses to such food intake, with glucocorticoid-related alterations that not only influence homeostatic functions of glucocorticoids in energy balance, but also affect hypothalamic and extrahypothalamic regulation of food intake”
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    Premisecitation

    Leptin and ghrelin influence dopaminergic transmission in brain reward regions and food seeking behavior in animals, and activate brain reward regions in humans.

    “leptin and ghrelin influence dopaminergic transmission in brain reward regions and food seeking behavior in animals, and activate brain reward regions in humans”
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    Premisecitation

    Stress affects glucose levels and increases glucose variability in patients with type 1 and type 2 diabetes.

    “stress affects glucose levels and increased glucose variability in both patients with type 1 and 2 diabetes”
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    Premisecitation

    Chronic high levels of insulin downregulate HPA axis responses and increase basal sympathetic tone.

    “chronic high levels of insulin have been shown to downregulate HPA axis responses and increase basal sympathetic tone”
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    Premisenone given

    High levels of stress and glucocorticoids increase glucose and insulin levels and promote insulin resistance.

    “high levels of stress and glucocorticoids increase glucose and insulin levels and also promote insulin resistance”
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    Premisecitation

    Growing evidence from animal and human research indicates that increased weight, insulin resistance, and high-fat diets are associated with blunted glucocorticoid responses and altered autonomic and peripheral catecholamine responses to stress challenge.

    “growing evidence from animal and human research indicates that increased weight, insulin resistance and high fat diets are associated with blunted glucocorticoid responses, and also altered autonomic and peripheral catecholamine responses to stress challenge”
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    Premisecitation

    Ghrelin, via signaling of reward pathways, promotes appetite and feeding, and is involved in stress-induced food reward and food seeking.

    “ghrelin, which, via signaling of reward pathways promotes appetite and feeding (Malik et al., 2008), is also involved in stress-induced food reward and food seeking”
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    Premisecitation

    Considerable evidence from population-based and clinical studies indicates a significant positive association of high uncontrollable stressful events and chronic stress states with both substance addiction and with adiposity, body mass index, and weight gain.

    “Considerable evidence from population-based and clinical studies indicates a significant and positive association of high uncontrollable stressful events and chronic stress states with both substance addiction (Sinha, 2008) and with adiposity, BMI and weight gain”
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    Premisecitation

    Stress-driven eating is exacerbated in obese women, whereas stress-driven eating appears to have an inconsistent effect on food consumption in lean individuals.

    “Stress-driven eating has been found to be exacerbated in obese women (Laitinen et al., 2002) whereas stress-driven eating appears to have an inconsistent effect on food consumption in lean individuals”
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    Premisecitation

    Stress and adversity can increase consumption of fast food, snacks, calorie-dense and highly palatable foods, and stress is associated with increased binge eating.

    “stress and adversity can increase consumption of fast food (Steptoe, Lipsey, & Wardle, 1998), snacks (Oliver & Wardle, 1999), calorie-dense and highly-palatable foods (Epel et al., 2001), and stress has been associated with increased binge eating”
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    Premisecitation

    Alterations in metabolic state may influence both responses of brain reward regions to impact motivation and hypothalamic circuits that interact with overlapping stress and energy regulation circuitry.

    “such alterations in metabolic state may influence both responses of brain reward regions to impact motivation, but also affect hypothalamic circuits that interact with overlapping stress and energy regulation circuitry”
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    • cites Sinha & Jastreboff, 2013

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    Premisecitation

    Glucocorticoids increase plasma leptin and ghrelin levels, while ghrelin, which also increases with stress, appears to contribute to regulating anxiety and mood.

    “Glucocorticoids increase plasma leptin and ghrelin levels, while ghrelin which also increases with stress, appears to contribute to regulating anxiety and mood”
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    Premisecitation

    Bilateral adrenalectomy reduces food intake, and glucocorticoid administration increases food intake by stimulating NPY release and inhibiting CRF release.

    “bilateral adrenalecomy reduces food intake, and GC administration increases food intake by stimulating the release of NPY and inhibiting CRF release”
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    • cites Cavagnini, Croci, Putignano, Petroni, & Invitti, 2000

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    Premisecitation

    Following exposure to psychological stress, satiated overweight people have greater craving for desserts and snacks and higher caloric intake compared to lean individuals.

    “Following exposure to psychological stress, satiated overweight people have been shown to have greater craving for desserts and snacks and have higher caloric intake as compared to lean individuals”
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    Premisecitation

    The hypothalamus is responsive to glucocorticoids via negative feedback, to insulin, and to hormones like leptin, which inhibits appetite, and ghrelin, which promotes appetite.

    “In addition to the hypothalamus being responsive to GCs via negative feedback, it is also responsive to insulin, secreted from the pancreas and integral to glucose metabolism and energy storage (Dallman et al., 2005; Schwartz, Figlewicz, Baskin, Woods, & Porte, 1992), and to hormones like leptin, which inhibits appetite, and ghrelin, which promotes appetite”
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    Interpretationreasoning

    Stress, trauma, and adversity may promote obesity risk, irregular eating patterns, and alter food preference, but overweight and obese individuals may be more vulnerable to such effects, possibly via weight-related adaptations in energy regulation and homeostasis.

    “This research suggests that stress, trauma and adversity may promote obesity risk, irregular eating patterns and alter food preference, but that overweight and obese individuals may be more vulnerable to such effects, possibly via weight-related adaptations in energy regulation and homeostasis”
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    Premisecitation

    Chronic activation of the HPA axis alters glucose metabolism, promotes insulin resistance, and changes appetite-related hormones and feeding neuropeptides.

    “Chronic activation of the HPA axis is known to alter glucose metabolism, promote insulin resistance, with changes in a number of appetite-related hormones (e.g. leptin, ghrelin) and feeding neuropeptides (e.g. NPY)”
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    Premisecitation

    Food restriction and high-fat diets alter HPA axis responses to stress and glucocorticoid gene expression in brain regions involved in energy homeostasis and stress.

    “Food restriction and high fat diets not only alter HPA axis responses to stress (Appelhans et al., 2010; Dallman, 2010; Hillman et al., 2012; Tyrka et al., 2012), but also alter GC gene expression in a number of brain regions involved in energy homeostasis and stress”
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    • cites Appelhans et al., 2010

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    Premisecitation

    The autonomic nervous system stress response is coordinated by the sympathoadrenal medullary and parasympathetic pathways.

    “The second is the autonomic nervous system, which is coordinated by the sympathoadrenal medullary (SAM) and the parasympathetic pathways”
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    Premisecitation

    Chronic and high levels of repeated and uncontrollable stress result in dysregulation of the HPA axis, with changes in glucocorticoid gene expression.

    “Chronic and high levels of repeated and uncontrollable stress results in dysregulation of the HPA axis, with changes in GC gene expression”
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    Premisecitation

    In the HPA axis, CRF is released from the paraventricular nucleus of the hypothalamus, stimulating ACTH secretion from the anterior pituitary, which stimulates glucocorticoid secretion from the adrenal glands.

    “The first is the HPA axis, in which CRF is released from the paraventricular nucleus (PVN) of the hypothalamus, stimulating secretion of adrenocorticotrophin hormone (ACTH) from the anterior pituitary, which subsequently stimulates the secretion of glucocorticoids (GC) (cortisol or corticosterone) from the adrenal glands”
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    Premisecitation

    Adrenal steroids increase glucose and insulin levels as well as selection and intake of high-caloric foods.

    “adrenal steroids increase glucose and insulin levels as well as selection and intake of high caloric foods”
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    Premisecitation

    Chronic stress persistently increases glucocorticoids and promotes abdominal fat, which in the presence of insulin decreases HPA axis activity.

    “Chronic stress persistently increases GCs and promotes abdominal fat, which in the presence of insulin, decreases HPA axis activity”
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    • cites Benson et al., 2009

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    • cites Tyrka et al., 2012

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    Premisecitation

    In healthy lean women, binge eating increases fasting glucose, insulin response, and alters the diurnal pattern of leptin secretion.

    “In healthy lean women, binge eating increases fasting glucose, insulin response, and alters the diurnal pattern of leptin secretion”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites Taylor, Hubbard, & Anderson, 1999

      Not checked in the free run.

  • May combine two claims.

    Premisecitation

    Medial and lateral components of the prefrontal cortex are involved in higher cognitive and executive control functions and in regulating emotions, visceral and physiological responses, impulses, desires, and craving.

    “the medial and lateral components of the prefrontal cortex (PFC) are involved in higher cognitive and executive control functions and also in regulating emotions, visceral and physiological responses, impulses, desires and craving”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites Arnsten, Mazure, & Sinha, 2012

      Not checked in the free run.

  • May combine two claims.

    Premisecitation

    Release of orexigenic NPY during stress and increased NPY mRNA in the arcuate nucleus of the hypothalamus, amygdala, and hippocampus increase feeding but also decrease anxiety and stress.

    “release of orexigenic NPY during stress and increased NPY mRNA in the arcuate nucleus of the hypothalamus, amygdala and hippocampus, increase feeding, but also decrease anxiety and stress”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites Maniam & Morris, 2012

      Not checked in the free run.

  • May combine two claims.

    Premisecitation

    High levels of repeated stress result in sympathetic overactivity, and stress-related increases in autonomic responses are related to insulin levels and insulin resistance in adolescents and adults.

    “High levels of repeated stress also result in sympathetic overactivity, and stress-related increases in autonomic responses are related to insulin levels and insulin resistance in adolescents and adults”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites Keltikangas-Jarvinen et al., 1996 source

      Not checked in the free run.

  • May combine two claims.

    Premisecitation

    Increased drug taking and high-fat diets alter CRF, glucocorticoid, and noradrenergic activity to increase sensitization of reward pathways including the ventral tegmental area, nucleus accumbens, dorsal striatum, and medial prefrontal cortex, influencing preference for addictive substances and highly palatable foods and increasing drug or food craving and intake.

    “Increased drug taking and high fat diets alter CRF, GC and noradrenergic activity to increase sensitization of reward pathways (including the ventral tegmental area [VTA], nucleus accumbens [NAc], dorsal striatum and the mPFC regions) which influences preference for addictive substances and HP foods and increases drug/food craving and intake”
    Quote in the paperSubstantial claim0 of 3 sources checked
    • cites Aston-Jones & Kalivas, 2008

      Not checked in the free run.

    • cites Cottone et al., 2009 source

      Not checked in the free run.

    • cites Shaham & Hope, 2005

      Not checked in the free run.

  • May combine two claims.

    Premisecitation

    Amygdala, hippocampus, and insula play an important role in encoding reward, reward cue-based learning and memory for high emotional and reward cues, and potentiating emotion and reward cue-based feeding.

    “amygdala, hippocampus and insula play an important role in encoding of reward, reward cue-based learning and memory for high emotional and reward cues and potentiating emotion and reward cue-based feeding”
    Quote in the paperSubstantial claim0 of 3 sources checked
    • cites Berthoud, 2012

      Not checked in the free run.

    • cites Holland, Petrovich, & Gallagher, 2002

      Not checked in the free run.

    • cites Small, 2002

      Not checked in the free run.

  • May combine two claims.

    Premisecitation

    Stress and glucocorticoids potentiate dopaminergic transmission and impact reward seeking and intake in laboratory animals.

    “Stress and GCs potentiate dopaminergic transmission and impact reward seeking and intake in laboratory animals”
    Quote in the paperSubstantial claim0 of 3 sources checked
    • cites Dallman, 2010 source

      Not checked in the free run.

    • cites Dallman et al., 2003

      Not checked in the free run.

    • cites Piazza, 1991

      Not checked in the free run.

  • May combine two claims.

    Premisecitation

    The motivational circuit overlaps with limbic and emotional regions such as the amygdala, hippocampus, and insula that play a role in experiencing emotions and stress, and in learning and memory processes contributing to behavioral and cognitive responses critical for adaptation and homeostasis.

    “this motivational circuit overlaps with limbic/emotional regions (eg. the amygdala, hippocampus, and insula) that play a role in experiencing emotions and stress, and in learning and memory processes that contribute to negotiating behavioral and cognitive responses critical for adaptation and homeostasis”
    Quote in the paperSubstantial claim0 of 3 sources checked
    • cites Arnsten, 2009 source

      Not checked in the free run.

    • cites Paulus, 2007

      Not checked in the free run.

    • cites Phan et al., 2005 source

      Not checked in the free run.

  • May combine two claims.

    Premisecitation

    Acute stress increases acquisition of food reward, intake of high-fat diets, and compulsive food seeking of highly palatable foods, and promotes reward-dependent habits.

    “Acute stress increases acquisition of food reward, intake of high fat diets (Adam & Epel, 2007; Wilson et al., 2008), and compulsive food seeking of HP foods (Lemmens et al., 2011), and promotes reward dependent habits”
    Quote in the paperSubstantial claim0 of 3 sources checked
    • cites Adam & Epel, 2007 source

      Not checked in the free run.

    • cites Wilson et al., 2008

      Not checked in the free run.

    • cites Lemmens et al., 2011 source

      Not checked in the free run.

  • May combine two claims.

    Premisecitation

    The stress response is initiated via the amygdala, and stress regulation occurs partially via glucocorticoid negative feedback to the hippocampus and medial prefrontal cortical regions.

    “The stress response is initiated via the amygdala and stress regulation occurs partially via GC negative feedback to the hippocampus and medial prefrontal cortical (mPFC) regions”
    Quote in the paperNot a substantial claim0 of 2 sources checked
    • cites Heinrichs, 2005

      Not checked in the free run.

    • cites McEwen, 2007 source

      Not checked in the free run.

  • May combine two claims.

    Interpretationreasoning

    Prefrontal circuits involved in self-control, emotion regulation, and decision making, as well as emotional and motivational brain pathways, are key targets for stress chemicals, which influence addiction vulnerability and obesity risk.

    “Therefore, prefrontal circuits involved in self-control, emotion regulation and decision making as well as the emotional and motivational brain pathways are key targets for the brain and body’s stress chemicals, that, in turn, influence addiction vulnerability and also obesity risk”
    Quote in the paperSubstantial claim

  • Probably not a substantial claim: may not pass S3 (load-bearing), S4 (based).

    Premisenone given

    Chronic stress downregulates HPA axis responses.

    “it is known that chronic stress downregulates the HPA axis responses”
    Quote in the paperNot a substantial claim

  • Probably not a substantial claim: may not pass S4 (based).

    Interpretationnone given

    Whether addictive motivation and stress-relevant adaptations differ for sweets, fats, and carbohydrates versus proteins and their impact on excessive intake of certain foods and nutrients to promote obesity risk is not clear.

    “Whether these addictive motivation and stress-relevant adaptations are different for sweets, fats and carbohydrates versus proteins and their impact on excessive intake of certain foods and nutrients to promote obesity risk is also not clear”
    Quote in the paperNot a substantial claim

  • Probably not a substantial claim: may not pass S3 (load-bearing), S4 (based). May combine two claims.

    Premisenone given

    With increases in weight there is increasing insulin insensitivity and alterations in leptin and ghrelin signaling.

    “with increases in weight there is increasing insulin insensitivity and alterations in leptin and ghrelin signaling”
    Quote in the paperNot a substantial claim

  • Classified as probably not a substantial claim.

    Interpretationnone given

    The link between glucocorticoids, ghrelin, insulin, and leptin on food motivation and intake in humans is not clear.

    “the link between glucocorticoids, ghrelin, insulin and leptin on food motivation and intake in humans is not clear”
    Quote in the paperSubstantial claim

  • Probably not a substantial claim: may not pass S3 (load-bearing), S4 (based).

    Interpretationnone given

    The role of food-related products such as additives and preservatives on stress and metabolic changes is not well studied.

    “the role of food related products such as additives and preservatives on stress and metabolic changes are not well studied”
    Quote in the paperNot a substantial claim

  • May combine two claims.

    Premisecitation

    High and repeated stress alters structural and functional responses in prefrontal and limbic brain regions, providing some basis for the effects of chronic stress on cortico-limbic regions that modulate food reward and craving.

    “High and repeated stress alters structural and functional responses in these prefrontal and limbic brain regions, providing some basis for the effects of chronic stress on cortico-limbic regions that modulate food reward and craving”
    Quote in the paperSubstantial claim0 of 3 sources checked
    • cites Arnsten, 2009 source

      Not checked in the free run.

    • cites Arnsten et al., 2012

      Not checked in the free run.

    • cites Dias-Ferreira et al., 2009 source

      Not checked in the free run.

  • Probably not a substantial claim: may not pass S2 (checkable).

    Interpretationnone given

    The influence of these changes on reward and food motivation and intake is not well understood.

    “their influence on reward and food motivation and intake is not well understood”
    Quote in the paperNot a substantial claim

  • Probably not a substantial claim: may not pass S4 (based).

    Interpretationnone given

    The influence of specific food types on related peripheral and central glucocorticoids and their effects on food craving and intake is not known.

    “the influence of specific food types on related peripheral and central glucocorticoids and their effects on food craving and intake is not known”
    Quote in the paperNot a substantial claim

  • May combine two claims.

    Interpretationreasoning

    Converging lines of evidence suggest that ubiquitous highly palatable food cues and their intake may alter eating behaviors, which may result in metabolic changes and affect brain reward and motivation pathways to increase craving and motivation for highly palatable foods.

    “On the basis of the converging lines of evidence suggesting that ubiquitous HP food cues and their intake may alter eating behaviors (e.g., restraint and skipping meals, bingeing and overeating of HP foods), which, in turn, may result in metabolic changes and also affect the brain reward and motivation pathways to increase craving and motivation for HP foods”
    Quote in the paperSubstantial claim
    • Rests on an assumption: Highly palatable foods are more liked, preferred, and found rewarding in taste.
    • Rests on an assumption: Highly palatable foods are ubiquitous in the current obesogenic environment.
58 of 58

  • The paper relies on this without support.

    Highly palatable foods are more liked, preferred, and found rewarding in taste.

    “Highly palatable (HP) foods are more liked, preferred and found to be rewarding in taste”

  • The paper relies on this without support.

    Highly palatable foods are ubiquitous in the current obesogenic environment.

    “These foods are ubiquitous in our current obesogenic environment”

  • The paper relies on this without support.

    Genetic and other social and biological variables alone do not explain pandemic levels of obesity.

    “but these alone do not explain the pandemic levels of obesity”
3 of 3

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

Cites

Flagged first, then by citations

Research works printed but not linked: 2

  1. Heinrichs, 2005, Behavioral consequences of altered corticotropin-relaeasing factor activation in brian; a functionalist view of affective neuroscience, Vol. 15, 155
  2. Klein, 1996, Gender differences in eating after exposure to noise stressor, Annals of Behavioural Medicine, 18, S103

Cited by

Sorted by citations

Related

Authors
Sinha, R.
Affiliations
Yale University (US)
Corresponding author
Sinha, Rajita
ORCID
Sinha, Rajita
Venue
Biological Psychology
Publisher
Elsevier BV
Published
2018-01
Volume
131
Pages
5-13
ISSN
0301-0511 (ISSN-L)
DOI
10.1016/j.biopsycho.2017.05.001
PMC
PMC6784832
OpenAlex
W2610477874
Semantic Scholar
a05a1d3853b5ad3626a6ca31b1b6ee871bcf15ed
Cited by
211
References
152
Citations by year
2026: 18 · 2025: 20 · 2024: 42 · 2023: 25 · 2022: 19 · 2021: 35 · 2020: 29 · 2019: 15 · 2018: 4 · 2017: 4
FWCI
8.70
Type
journal article
Language
en
Open access
Licence
www.elsevier.com/tdm/userlicense/1.0/ (tdm)
Locations
  • Biological Psychology (publishedVersion)
  • PubMed (publishedVersion)
  • Europe PMC (PubMed Central) (acceptedVersion)
  • PubMed Central (acceptedVersion)
Funders
  • National Institute of Diabetes and Digestive and Kidney Diseases/National Institutes of Health (R01-DK099039)
  • National Institutes of Health Roadmap for Medical Research Common Fund (UL1-DE019586, UL1-RR024139)
Topics
  • Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Regulation of Appetite and Obesity
  • Social Sciences › Psychology › Clinical Psychology › Eating Disorders and Behaviors
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neurotransmitter Receptor Influence on Behavior
Keywords
obesity, dietary intake, food addiction, food reward, food cravings, stress hormones, insulin resistance, trauma, energy homeostasis, obesity epidemic
MeSH terms
Food Addiction, Eating, Emotions, Feeding Behavior, Humans, Motivation, Obesity, Reward, Stress, Psychological, Weight Gain, Craving

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Claims read by deepseek-v4.1-flash under definition version 3 (extract-v3) on 2026-10-09.

Classified by jev-1.13-20260917 (gold-guideline-v0.2) on 2026-10-09.

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