The DOI matches its Crossref record; 151 of the 152 references it cites were found in a registry or an index; 1 of the 167 sources its claims cite were checked for support.
Role of addiction and stress neurobiology on food intake and obesity
Open accessAbstract
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.
Overview
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.
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Claims the paper makes
80 Not checked yet · 22 Own interpretation · 3 No basis given · 1 Supported so far
In the paper
“higher food craving was significantly associated with greater intake of these foods”
§ Role of addiction and stress neurobiology on food intake and obesity > Highly palatable (HP) foods and related cues, food seeking and intake
What the sources say
- Not checked yetcites Chao, Grilo, White, & Sinha, 2014
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
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In the paper
“in a cross sectional study with a large community sample, we found higher food craving for these HP foods”
§ Role of addiction and stress neurobiology on food intake and obesity > Highly palatable (HP) foods and related cues, food seeking and intake
What the sources say
- Not checked yetcites Chao, Grilo, White, & Sinha, 2014
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“those with higher body mass index (BMI) reported greater levels of food craving”
§ Role of addiction and stress neurobiology on food intake and obesity > Highly palatable (HP) foods and related cues, food seeking and intake
What the sources say
- Not checked yetcites Chao, Grilo, White, & Sinha, 2014
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
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None of the sources cited for this claim have been checked yet.
In the paper
“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”
§ Role of addiction and stress neurobiology on food intake and obesity > Overeating of HP foods and metabolic and stress hormone responses
What the sources say
plaincorrelational- Asserted: passes — The authors put it forward as true.
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In the paper
“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”
§ Role of addiction and stress neurobiology on food intake and obesity > Overeating of HP foods and metabolic and stress hormone responses
What the sources say
- Not checked yetcites Jastreboff et al., 2013 source
plaincorrelational- Asserted: passes — The authors put it forward as true.
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In the paper
“higher chronic stress, insulin and cortisol responses predicted greater weight gain at a future 6-month follow-up assessment”
§ Role of addiction and stress neurobiology on food intake and obesity > Overeating of HP foods and metabolic and stress hormone responses
What the sources say
- Not checked yetcites Chao, Grilo, White, & Sinha, in press
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“we found in a recent longitudinal study of community volunteers that higher ghrelin was associated with greater food cravings”
§ Role of addiction and stress neurobiology on food intake and obesity > Overeating of HP foods and metabolic and stress hormone responses
What the sources say
- Not checked yetcites Chao, Grilo, White, & Sinha, in press
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
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In the paper
“higher cortisol responses in the hypoglycemic state was associated with higher striatal-limbic brain activation during concurrent assessment of these responses”
§ Role of addiction and stress neurobiology on food intake and obesity > Overeating of HP foods and metabolic and stress hormone responses
What the sources say
- Not checked yetcites Page et al., 2011 source
plaincorrelational- Asserted: passes — The authors put it forward as true.
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In the paper
“in response to a standard glucose drink, healthy lean individuals showed increased connectivity between the hypothalamus and dopamine-rich regions of the ventral and dorsal striatum as well as the insula”
§ Role of addiction and stress neurobiology on food intake and obesity > Overeating of HP foods and metabolic and stress hormone responses
What the sources say
- Not checked yetcites Page, Sinha, & Sherwin, 2013
plaindirect- Asserted: passes — The authors put it forward as true.
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None of the sources cited for this claim have been checked yet.
In the paper
“genetic and other social and biological variables may also contribute towards vulnerability to obesity and weight gain”
§ Role of addiction and stress neurobiology on food intake and obesity > Multifactorial determinants of body weight and food intake
What the sources say
hedgedconditional- Asserted: passes — The authors put it forward as true.
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- It may state two separate claims as one. 50
- Probably not a substantial claim. 10
The sources with a verdict support this claim; the rest weren’t checked yet, have no full text we could read, or their verdicts aren’t rated yet.
In the paper
“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”
§ Role of addiction and stress neurobiology on food intake and obesity > Stress, trauma, adversity and obesity risk
What the sources say
- Supportedcites Sinha, 2008 source
Split into 2 atoms — 2 confirmed, 0 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.
- Not checked yetcites Block, He, Zaslavsky, Ding, & Ayanian, 2009
- Not checked yetcites Epel, Lapidus, McEwen, & Brownell, 2001
hedgedcorrelational- Asserted: passes — The authors put it forward as true.
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- Supported
In the paper
“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”
§ Role of addiction and stress neurobiology on food intake and obesity > Metabolic and stress adaptations with increased body weight
What the sources say
- Not checked yetcites Rudenga, Sinha, & Small, 2013 source
plaindirect- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
In the paper
“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”
§ Role of addiction and stress neurobiology on food intake and obesity > Overeating of HP foods and metabolic and stress hormone responses
What the sources say
- Not checked yetcites Page et al., 2011 source
plaindirect- Asserted: passes — The authors put it forward as true.
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None of the sources cited for this claim have been checked yet.
In the paper
“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”
§ Role of addiction and stress neurobiology on food intake and obesity > Multifactorial determinants of body weight and food intake
What the sources say
- Not checked yetcites Hill & Peters, 1998
- Not checked yetcites Ogden et al., 2007
- Not checked yetcites Wang, Volkow, Thanos, & Fowler, 2004
plaindirect- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“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”
§ Role of addiction and stress neurobiology on food intake and obesity > Multifactorial determinants of body weight and food intake
What the sources say
- Not checked yetcites Berthoud, 2012
- Not checked yetcites Yeo&Heisler, 2012
plain- Asserted: passes — The authors put it forward as true.
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Probably not a substantial claim.
None of the sources cited for this claim have been checked yet.
In the paper
“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”
§ Role of addiction and stress neurobiology on food intake and obesity > Highly palatable (HP) foods and related cues, food seeking and intake
What the sources say
- Not checked yetcites Kelley, Schiltz, & Landry, 2005
- Not checked yetcites Small, Zatorre, Dagher, Evans, & Jones-Gotman, 2001
- Not checked yetcites Wang et al., 2001 source
plaindirect- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“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”
§ Role of addiction and stress neurobiology on food intake and obesity > Highly palatable (HP) foods and related cues, food seeking and intake
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- 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.
None of the sources cited for this claim have been checked yet.
In the paper
“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”
§ Role of addiction and stress neurobiology on food intake and obesity > Highly palatable (HP) foods and related cues, food seeking and intake
What the sources say
- Not checked yetcites Alsio, Olszewski, Levine, & Schioth, 2012
- Not checked yetcites Avena, Rada, & Hoebel, 2009 source
- Not checked yetcites Berthoud, 2012
plaindirect- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“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”
§ Role of addiction and stress neurobiology on food intake and obesity > Highly palatable (HP) foods and related cues, food seeking and intake
What the sources say
- Not checked yetcites Robinson & Berridge, 2008 source
- Not checked yetcites Sinha & Jastreboff, 2013
plaindirect- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“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”
§ Role of addiction and stress neurobiology on food intake and obesity > Overeating of HP foods and metabolic and stress hormone responses
What the sources say
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
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It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“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”
§ Role of addiction and stress neurobiology on food intake and obesity > Overeating of HP foods and metabolic and stress hormone responses
What the sources say
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“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”
§ Role of addiction and stress neurobiology on food intake and obesity > Overeating of HP foods and metabolic and stress hormone responses
What the sources say
- Not checked yetcites Cifani, Polidori, Melotto, Ciccocioppo, & Massi, 2009
- Not checked yetcites Cottone et al., 2009 source
- Not checked yetcites Ghitza, Gray, Epstein, Rice, & Shaham, 2006
hedgedconditional- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“cortisol rise with macronutrient intake may serve to promote gluconeogenesis underscoring the critical role of glucocorticoids in energy homeostasis”
§ Role of addiction and stress neurobiology on food intake and obesity > Overeating of HP foods and metabolic and stress hormone responses
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
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It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“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”
§ Role of addiction and stress neurobiology on food intake and obesity > Overeating of HP foods and metabolic and stress hormone responses
What the sources say
- Not checked yetcites Alsio et al., 2012
- Not checked yetcites Chuang et al., 2011
- Not checked yetcites DiLeone, 2009
hedgedconditional- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“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”
§ Role of addiction and stress neurobiology on food intake and obesity > Overeating of HP foods and metabolic and stress hormone responses
hedgedconditional- Asserted: passes — The authors put it forward as true.
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In the paper
“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”
§ Role of addiction and stress neurobiology on food intake and obesity > Overeating of HP foods and metabolic and stress hormone responses
What the sources say
- Not checked yetcites Koob & Kreek, 2007
- Not checked yetcites Lee & Rivier, 1997
- Not checked yetcites Richardson, Lee, O'Dell, Koob, & Rivier, 2008 source
boosteddirect- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“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”
§ Role of addiction and stress neurobiology on food intake and obesity > Overeating of HP foods and metabolic and stress hormone responses
hedgedconditional- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“leptin and ghrelin influence dopaminergic transmission in brain reward regions and food seeking behavior in animals, and activate brain reward regions in humans”
§ Role of addiction and stress neurobiology on food intake and obesity > Overeating of HP foods and metabolic and stress hormone responses
What the sources say
- Not checked yetcites Chuang et al., 2011
- Not checked yetcites DiLeone, 2009
- Not checked yetcites Farooqui, 2009
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“stress affects glucose levels and increased glucose variability in both patients with type 1 and 2 diabetes”
§ Role of addiction and stress neurobiology on food intake and obesity > Metabolic and stress adaptations with increased body weight
What the sources say
plaindirect- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
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In the paper
“chronic high levels of insulin have been shown to downregulate HPA axis responses and increase basal sympathetic tone”
§ Role of addiction and stress neurobiology on food intake and obesity > Metabolic and stress adaptations with increased body weight
What the sources say
boosteddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
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It may state two separate claims as one.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“high levels of stress and glucocorticoids increase glucose and insulin levels and also promote insulin resistance”
§ Role of addiction and stress neurobiology on food intake and obesity > Metabolic and stress adaptations with increased body weight
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
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It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“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”
§ Role of addiction and stress neurobiology on food intake and obesity > Metabolic and stress adaptations with increased body weight
What the sources say
- Not checked yetcites Appelhans, Pagoto, Peters, & Spring, 2010
- Not checked yetcites Benson et al., 2009
- Not checked yetcites Hillman et al., 2012
hedgedcorrelational- Asserted: passes — The authors put it forward as true.
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None of the sources cited for this claim have been checked yet.
In the paper
“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”
§ Role of addiction and stress neurobiology on food intake and obesity > Metabolic and stress adaptations with increased body weight
What the sources say
- Not checked yetcites Malik et al., 2008
- Not checked yetcites Chuang & Zigman, 2010
plaindirect- Asserted: passes — The authors put it forward as true.
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None of the sources cited for this claim have been checked yet.
In the paper
“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”
§ Role of addiction and stress neurobiology on food intake and obesity > Stress, trauma, adversity and obesity risk
What the sources say
- Not checked yetcites Laitinen et al., 2002
- Not checked yetcites Greeno & Wing, 1994
hedgedcorrelational- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“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”
§ Role of addiction and stress neurobiology on food intake and obesity > Stress, trauma, adversity and obesity risk
What the sources say
- Not checked yetcites Steptoe, Lipsey, & Wardle, 1998
- Not checked yetcites Oliver & Wardle, 1999
- Not checked yetcites Epel et al., 2001 source
plaindirect- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“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”
§ Role of addiction and stress neurobiology on food intake and obesity > Metabolic and stress adaptations with increased body weight
What the sources say
- Not checked yetcites Sinha & Jastreboff, 2013
- Not checked yetcites Ulrich-Lai & Ryan, 2014
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Glucocorticoids increase plasma leptin and ghrelin levels, while ghrelin which also increases with stress, appears to contribute to regulating anxiety and mood”
§ Role of addiction and stress neurobiology on food intake and obesity > The overlapping neurobiology of stress, reward and energy homeostasis > Peripheral and central stress biology, energy homeostasis and food intake
What the sources say
hedgeddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“bilateral adrenalecomy reduces food intake, and GC administration increases food intake by stimulating the release of NPY and inhibiting CRF release”
§ Role of addiction and stress neurobiology on food intake and obesity > The overlapping neurobiology of stress, reward and energy homeostasis > Peripheral and central stress biology, energy homeostasis and food intake
What the sources say
- Not checked yetcites Cavagnini, Croci, Putignano, Petroni, & Invitti, 2000
plaindirect- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
In the paper
“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”
§ Role of addiction and stress neurobiology on food intake and obesity > Stress, trauma, adversity and obesity risk
What the sources say
- Not checked yetcites Lemmens et al., 2011 source
plaindirect- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“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”
§ Role of addiction and stress neurobiology on food intake and obesity > The overlapping neurobiology of stress, reward and energy homeostasis > Peripheral and central stress biology, energy homeostasis and food intake
What the sources say
- Not checked yetcites Dallman et al., 2005 source
- Not checked yetcites Schwartz, Figlewicz, Baskin, Woods, & Porte, 1992
- Not checked yetcites Currie, Mirza, Fuld, Park, & Vasselli, 2005
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
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It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“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”
§ Role of addiction and stress neurobiology on food intake and obesity > Stress, trauma, adversity and obesity risk
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
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- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“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)”
§ Role of addiction and stress neurobiology on food intake and obesity > The overlapping neurobiology of stress, reward and energy homeostasis > Peripheral and central stress biology, energy homeostasis and food intake
What the sources say
- Not checked yetcites Bjorntorp, 1992 source
- Not checked yetcites Kaplan, Adams, Clarkson, & Koritnik, 1984
- Not checked yetcites Kuo et al., 2007
boosteddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“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”
§ Role of addiction and stress neurobiology on food intake and obesity > The overlapping neurobiology of stress, reward and energy homeostasis > Peripheral and central stress biology, energy homeostasis and food intake
What the sources say
- Not checked yetcites Appelhans et al., 2010
- Not checked yetcites Dallman, 2010 source
- Not checked yetcites Hillman et al., 2012
plaindirect- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
In the paper
“The second is the autonomic nervous system, which is coordinated by the sympathoadrenal medullary (SAM) and the parasympathetic pathways”
§ Role of addiction and stress neurobiology on food intake and obesity > The overlapping neurobiology of stress, reward and energy homeostasis > Peripheral and central stress biology, energy homeostasis and food intake
What the sources say
- Not checked yetcites Kyrou & Tsigos, 2007
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
None of the sources cited for this claim have been checked yet.
In the paper
“Chronic and high levels of repeated and uncontrollable stress results in dysregulation of the HPA axis, with changes in GC gene expression”
§ Role of addiction and stress neurobiology on food intake and obesity > The overlapping neurobiology of stress, reward and energy homeostasis > Peripheral and central stress biology, energy homeostasis and food intake
What the sources say
plaindirect- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
In the paper
“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”
§ Role of addiction and stress neurobiology on food intake and obesity > The overlapping neurobiology of stress, reward and energy homeostasis > Peripheral and central stress biology, energy homeostasis and food intake
What the sources say
- Not checked yetcites Kyrou & Tsigos, 2007
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“adrenal steroids increase glucose and insulin levels as well as selection and intake of high caloric foods”
§ Role of addiction and stress neurobiology on food intake and obesity > The overlapping neurobiology of stress, reward and energy homeostasis > Peripheral and central stress biology, energy homeostasis and food intake
What the sources say
- Not checked yetcites Chrousos, 2000
- Not checked yetcites Dallman et al., 2003
- Not checked yetcites Tataranni et al., 1996
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
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It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Chronic stress persistently increases GCs and promotes abdominal fat, which in the presence of insulin, decreases HPA axis activity”
§ Role of addiction and stress neurobiology on food intake and obesity > The overlapping neurobiology of stress, reward and energy homeostasis > Peripheral and central stress biology, energy homeostasis and food intake
What the sources say
- Not checked yetcites Benson et al., 2009
- Not checked yetcites Dallman et al., 2005 source
- Not checked yetcites Tyrka et al., 2012
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
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It may state two separate claims as one.
In the paper
“In healthy lean women, binge eating increases fasting glucose, insulin response, and alters the diurnal pattern of leptin secretion”
§ Role of addiction and stress neurobiology on food intake and obesity > Stress, trauma, adversity and obesity risk
What the sources say
- Not checked yetcites Taylor, Hubbard, & Anderson, 1999
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“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”
§ Role of addiction and stress neurobiology on food intake and obesity > The overlapping neurobiology of stress, reward and energy homeostasis > Extrahypothalamic neural regulation of food reward, motivation and intake
What the sources say
- Not checked yetcites Arnsten, Mazure, & Sinha, 2012
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
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It may state two separate claims as one.
In the paper
“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”
§ Role of addiction and stress neurobiology on food intake and obesity > The overlapping neurobiology of stress, reward and energy homeostasis > Extrahypothalamic neural regulation of food reward, motivation and intake
What the sources say
- Not checked yetcites Maniam & Morris, 2012
plaindirect- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
In the paper
“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”
§ Role of addiction and stress neurobiology on food intake and obesity > The overlapping neurobiology of stress, reward and energy homeostasis > Peripheral and central stress biology, energy homeostasis and food intake
What the sources say
- Not checked yetcites Keltikangas-Jarvinen et al., 1996 source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“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”
§ Role of addiction and stress neurobiology on food intake and obesity > The overlapping neurobiology of stress, reward and energy homeostasis > Extrahypothalamic neural regulation of food reward, motivation and intake
What the sources say
- Not checked yetcites Aston-Jones & Kalivas, 2008
- Not checked yetcites Cottone et al., 2009 source
- Not checked yetcites Shaham & Hope, 2005
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
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It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“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”
§ Role of addiction and stress neurobiology on food intake and obesity > The overlapping neurobiology of stress, reward and energy homeostasis > Extrahypothalamic neural regulation of food reward, motivation and intake
What the sources say
- Not checked yetcites Berthoud, 2012
- Not checked yetcites Holland, Petrovich, & Gallagher, 2002
- Not checked yetcites Small, 2002
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
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It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Stress and GCs potentiate dopaminergic transmission and impact reward seeking and intake in laboratory animals”
§ Role of addiction and stress neurobiology on food intake and obesity > The overlapping neurobiology of stress, reward and energy homeostasis > Extrahypothalamic neural regulation of food reward, motivation and intake
What the sources say
- Not checked yetcites Dallman, 2010 source
- Not checked yetcites Dallman et al., 2003
- Not checked yetcites Piazza, 1991
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“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”
§ Role of addiction and stress neurobiology on food intake and obesity > The overlapping neurobiology of stress, reward and energy homeostasis > Extrahypothalamic neural regulation of food reward, motivation and intake
What the sources say
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“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”
§ Role of addiction and stress neurobiology on food intake and obesity > The overlapping neurobiology of stress, reward and energy homeostasis > Extrahypothalamic neural regulation of food reward, motivation and intake
What the sources say
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“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”
§ Role of addiction and stress neurobiology on food intake and obesity > The overlapping neurobiology of stress, reward and energy homeostasis > Extrahypothalamic neural regulation of food reward, motivation and intake
What the sources say
- Not checked yetcites Heinrichs, 2005
- Not checked yetcites McEwen, 2007 source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“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”
§ Role of addiction and stress neurobiology on food intake and obesity > The overlapping neurobiology of stress, reward and energy homeostasis > Extrahypothalamic neural regulation of food reward, motivation and intake
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
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It may state two separate claims as one.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“it is known that chronic stress downregulates the HPA axis responses”
§ Role of addiction and stress neurobiology on food intake and obesity > Summary and future directions
boosteddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
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Probably not a substantial claim. The paper’s conclusions may not depend on it. The paper may give no reason why it holds.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“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”
§ Role of addiction and stress neurobiology on food intake and obesity > Summary and future directions
plain- Asserted: passes — The authors put it forward as true.
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Probably not a substantial claim. The paper may give no reason why it holds.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“with increases in weight there is increasing insulin insensitivity and alterations in leptin and ghrelin signaling”
§ Role of addiction and stress neurobiology on food intake and obesity > Summary and future directions
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
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Probably not a substantial claim. The paper’s conclusions may not depend on it. The paper may give no reason why it holds. It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“the link between glucocorticoids, ghrelin, insulin and leptin on food motivation and intake in humans is not clear”
§ Role of addiction and stress neurobiology on food intake and obesity > Summary and future directions
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
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Probably not a substantial claim.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“the role of food related products such as additives and preservatives on stress and metabolic changes are not well studied”
§ Role of addiction and stress neurobiology on food intake and obesity > Summary and future directions
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: fails — The paper may give no reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. The paper may give no reason why it holds.
None of the sources cited for this claim have been checked yet.
In the paper
“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”
§ Role of addiction and stress neurobiology on food intake and obesity > The overlapping neurobiology of stress, reward and energy homeostasis > Extrahypothalamic neural regulation of food reward, motivation and intake
What the sources say
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“their influence on reward and food motivation and intake is not well understood”
§ Role of addiction and stress neurobiology on food intake and obesity > Summary and future directions
plain- Asserted: passes — The authors put it forward as true.
- Checkable: fails — It may be too vague to check against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. It may be too vague to check against evidence.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“the influence of specific food types on related peripheral and central glucocorticoids and their effects on food craving and intake is not known”
§ Role of addiction and stress neurobiology on food intake and obesity > Summary and future directions
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: fails — The paper may give no reason why it holds.
Probably not a substantial claim. The paper may give no reason why it holds.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“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”
§ Role of addiction and stress neurobiology on food intake and obesity > The overlapping neurobiology of stress, reward and energy homeostasis > Extrahypothalamic neural regulation of food reward, motivation and intake
hedgedconditional- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
- 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.
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”
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?
In the citing paper
“Highly palatable foods stimulate stress hormones that alter the limbic system (emotions) and striatal (motivational) pathways, promoting further food craving and excessive intake [169].”
From Food Addiction and Psychosocial Adversity: Biological Embedding, Contextual Factors, and Public Health Implications (2020) · cites this paper as [169]
Citations
Cites
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Metadata
- 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)
- 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
- FWCI
- 8.70
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- 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.
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