Food reward, hyperphagia, and obesity
Open accessAbstract
Given the unabated obesity problem, there is increasing appreciation of expressions like “my eyes are bigger than my stomach,” and recent studies in rodents and humans suggest that dysregulated brain reward pathways may be contributing not only to drug addiction but also to increased intake of palatable foods and ultimately obesity. After describing recent progress in revealing the neural pathways and mechanisms underlying food reward and the attribution of incentive salience by internal state signals, we analyze the potentially circular relationship between palatable food intake, hyperphagia, and obesity. Are there preexisting individual differences in reward functions at an early age, and could they be responsible for development of obesity later in life? Does repeated exposure to palatable foods set off a cascade of sensitization as in drug and alcohol addiction? Are reward functions altered by secondary effects of the obese state, such as increased signaling through inflammatory, oxidative, and mitochondrial stress pathways? Answering these questions will significantly impact prevention and treatment of obesity and its ensuing comorbidities as well as eating disorders and drug and alcohol addiction.
AI snapshot
Written from the paper’s full text.
TL;DR
This review argues that food reward (“liking,” “wanting,” and learning) interacts with homeostatic metabolic signals and may contribute to hyperphagia and obesity through preexisting reward differences, addiction-like neuroadaptation to palatable foods, and secondary effects of the obese state. It concludes that evidence remains largely indirect/correlative, with mesolimbic dopamine implicated in “wanting” but still unclear whether over- or under-activity drives hyperphagia.
Key findings
- Food reward is a composite of “liking” (hedonic impact), “wanting” (incentive salience), and learning, with separable brain systems: μ-opioid-mediated “liking” hotspots in nucleus accumbens shell/ventral pallidum, and mesolimbic dopamine for “wanting”; leptin, ghrelin, and insulin modulate these processes.
- Three non-exclusive mechanisms may link reward to obesity: preexisting differences in reward function, repeated palatable-food intake as an escalating addictive process, and obesity-induced changes in reward circuitry; among ~20 major obesity genes, none are directly implicated in reward, and combined effects account for less than ∼5% of human obesity.
- In Wistar rats, a palatable cafeteria diet produced sustained hyperphagia over 40 days and increased lateral hypothalamic self-stimulation threshold in parallel with weight gain; after 14 days of abstinence, reward threshold did not normalize despite hypophagia and ∼10% body weight loss, unlike the relatively rapid ∼48 h normalization seen after cocaine abstinence.
- Obesity/high-fat diet can alter reward: obesity-prone rats on chow or high-fat diet without extra weight gain showed reduced progressive ratio break point for sucrose, amphetamine-induced conditioned place preference, and nucleus accumbens dopamine turnover; leptin-deficient humans showed exaggerated nucleus accumbens activation to food images that was abolished by leptin.
Methods
- Narrative review, not a primary empirical study; it synthesizes rodent, nonhuman primate, and human literature on food reward, hyperphagia, and obesity.
- Data/sample: cited animal models (rats, mice, primates) and human neuroimaging/clinical studies; no new sample or original dataset.
- Main analysis: conceptual synthesis of neural pathways and three hypothesized reward–obesity mechanisms; no meta-analysis or statistical pooling.
Limitations
- The paper states there is “no smoking gun” for a single specific neural pathway or molecule, and it is not yet clear whether over- or under-activity of dopamine signaling is at the origin of hyperphagia or which mesolimbic dopamine projections are specifically involved.
- The paper notes that few studies dissociate preexisting reward differences from secondary effects of the obese state, and that only longitudinal studies in genetically defined populations will provide more conclusive answers; controlled human studies showing long-term effects of palatability on energy balance are few.
- Evident from the text: as a narrative review, conclusions rely heavily on indirect and correlative evidence from heterogeneous animal models and methodologies, without systematic review or meta-analytic quantification.
Model-written summary. Check it against the paper before relying on it.
Integrity signals
Registry
Cites
Statistics
Claims the paper makes
0 of 153 cited sources checked · 0 supported · 0 flagged
- Premisecitation
Nutrient sensors in the gastrointestinal tract and elsewhere in the body contribute to the generation of food reward during and after a meal.
“nutrient sensors in the gastrointestinal tract and elsewhere in the body appear to also contribute to the generation of food reward during and after a meal ([153](#B153)).”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites [153] source
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- Interpretationreasoning
In the preparatory phase, before any oral contact is made with food, reward expectancy plays a pivotal role.
“In the preparatory phase, before any oral contact is made with food, reward expectancy plays a pivotal role.”
Quote in the paperNot a substantial claim - Interpretationreasoning
These reward-related neural systems likely evolved to engage powerful motivations and drives for guaranteed supply and ingestion of beneficial foods from a sparse and often hostile environment.
“By forming representations and reward expectancies through processes of learning and memory, these systems likely evolved to engage powerful motivations and drives for guaranteed supply with and ingestion of beneficial foods from a sparse and often hostile environment.”
Quote in the paperNot a substantial claim - Premisecitation
The current obesity epidemic is best explained as a mismatch between the modern environment/lifestyle and biological response patterns that evolved in a scarce environment.
“the current obesity epidemic is best explained as a mismatch between the modern environment/lifestyle and biological response patterns that evolved in a scarce environment.”
Quote in the paperSubstantial claim0 of 2 sources checked - Interpretationreasoning
Reward expectancy appears to be the main driver to keep focused during the procurement phase.
“Reward expectancy appears to be the main driver to keep focused during this journey.”
Quote in the paperNot a substantial claim
- Interpretationreasoning
These reward-related systems are directly and primarily involved in the interactions of the modern environment and lifestyle with the human body.
“These systems are directly and primarily involved in the interactions of the modern environment and lifestyle with the human body.”
Quote in the paperSubstantial claim - Interpretationreasoning
Reward expectancy is perhaps the main factor determining the outcome of the decision-making process responsible for switching attention.
“reward expectancy is perhaps the main factor determining the outcome of this process.”
Quote in the paperNot a substantial claim - Interpretationreasoning
The decision to pursue a new goal largely depends on expecting but not actually consuming the reward.
“Thus, the decision to pursue this new goal largely depends on expecting but not actually consuming the reward.”
Quote in the paperNot a substantial claim - Premisecitation
To make a choice, the brain uses representations of reward-expectancy and effort/risk requirement from prior experiences to optimize cost/benefit.
“Research suggests that to make this choice, the brain uses representations of reward-expectancy and effort/risk requirement from prior experiences to optimize cost/benefit”
Quote in the paperNot a substantial claim0 of 3 sources checked - Premisecitation
Even when all taste processing is eliminated by genetic manipulation, mice still learn to prefer sugar over water.
“But even when all taste processing is eliminated by genetic manipulation, mice still learn to prefer sugar over water, suggesting the generation of food reward by processes of glucose utilization ([44](#B44)).”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [44] source
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- Interpretationnone given
Hedonic evaluation and reward processing is carried out in each of the three phases of ingestive behavior and critically determines their outcome.
“Hedonic evaluation and reward processing is carried out in each of these three phases of ingestive behavior and critically determines their outcome.”
Quote in the paperNot a substantial claim - Premisecitation
Some genes involved in the homeostatic regulator are crucial for energy balance, as manifested in monogenic obesity models such as leptin deficiency.
“Some of the genes involved in this homeostatic regulator are crucial for energy balance as manifested in the well-known monogenic obesity models such as leptin-deficiency”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites [58] source
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- Premisecitation
The same taste receptors found in the oral cavity are also expressed in gut epithelial cells.
“The same taste receptors found in the oral cavity are also expressed in gut epithelial cells ([144](#B144))”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites [144] source
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- Premisecitation
The same taste receptors found in the oral cavity are also expressed in the hypothalamus.
“and in the hypothalamus ([131](#B131))”
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- Premisecitation
These systems are now overwhelmed with an abundance of food and food cues that are no longer contested by predators and interrupted by famines.
“Now these systems are simply overwhelmed with an abundance of food and food cues that are no longer contested by predators and interrupted by famines”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [168] source
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- Premisecitation
Berridge and colleagues demonstrated narrowly circumscribed, μ-opioid receptor-mediated pleasure ("liking") hotspots in the nucleus accumbens shell and ventral pallidum.
“Using this method, Berridge and colleagues ([12](#B12), [122](#B122)) have demonstrated narrowly circumscribed, μ-opioid receptor-mediated pleasure (“liking”) hotspots in the nucleus accumbens shell and ventral pallidum.”
Quote in the paperSubstantial claim0 of 2 sources checked - Premisecitation
One of the few specific test paradigms for core liking/aversion in animals is measurement of positive and negative orofacial expressions when tasting pleasurable or aversive stimuli.
“In animals, only the subconscious components of pleasure (Berridge's core “liking”) and aversion are experimentally accessible, and one of the few specific test paradigms is measurement of positive and negative orofacial expressions when tasting pleasurable (typically sweet) or aversive stimuli ([11](#B11)).”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [11] source
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- Premisecitation
Neuroimaging studies in humans suggest that pleasure, as measured by subjective ratings, is computed within portions of the orbitofrontal and perhaps insular cortex.
“Neuroimaging studies in humans suggest that pleasure, as measured by subjective ratings, is computed within portions of the orbitofrontal and perhaps insular cortex ([13](#B13), [99](#B99)).”
Quote in the paperNot a substantial claim0 of 2 sources checked - Interpretationreasoning
Multiple neural systems are involved in pleasure and reward in ingestive and other motivated behaviors.
“Given the complex involvement of pleasure and reward in ingestive (and other) motivated behaviors as outlined above, it is clear that multiple neural systems are involved.”
Quote in the paperNot a substantial claim- Rests on an assumption: There is no hunger center and no pleasure center in the brain.
- Interpretationcitation
Endogenous μ-opioid signaling in the nucleus accumbens (ventral striatum) is critically involved in the expression of "liking".
“Together the findings suggest that endogenous μ-opioid signaling in the nucleus accumbens (ventral striatum) is critically involved in the expression of “liking.””
Quote in the paperSubstantial claim - Interpretationreasoning
The ventral striatal "liking" hotspot must somehow communicate with the basic brainstem reflex circuitry.
“Because the measured behavioral output is organized within the brainstem, the ventral striatal “liking” hotspot must somehow communicate with this basic reflex circuitry, but the pathways of communication are unclear.”
Quote in the paperNot a substantial claim - Interpretationreasoning
Dopamine signaling in the nucleus accumbens plays a role in both the preparatory and consummatory phases of an ingestive bout.
“Dopamine signaling in the nucleus accumbens thus appears to play a role in both the preparatory and consummatory phases of an ingestive bout.”
Quote in the paperSubstantial claim - Interpretationcitation
The forebrain is not necessary for expression of the most primitive form of core "liking".
“suggesting that the forebrain is not necessary for expression of this most primitive form of core “liking” ([13](#B13)).”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites [13] source
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- Interpretationreasoning
Brainstem circuits are normally not acting in isolation, but are intimately communicating with the forebrain.
“However, even if some of this primitive taste-guided reflexive behavior is organized within the brainstem, it is clear that the brainstem circuits are normally not acting in isolation, but are intimately communicating with the forebrain.”
Quote in the paperNot a substantial claim - Interpretationcitation
The most primitive form of liking and disliking may already be inherent to components of the peripheral gustatory pathways.
“These findings suggest that the most primitive form of liking and disliking may already be inherent to components of the peripheral gustatory pathways.”
Quote in the paperNot a substantial claim - Premisecitation
In mammals, the caudal brainstem is the equivalent of the subesophageal ganglion, where direct sensory feedback from the tongue and the gut are integrated into basic motor patterns of ingestion.
“In mammals, the caudal brainstem is the equivalent of the subesophageal ganglion, where direct sensory feedback from the tongue and the gut are integrated into basic motor patterns of ingestion ([166](#B166), [179](#B179)).”
Quote in the paperNot a substantial claim0 of 2 sources checked - Premisecitation
Expression of the characteristic happy face when tasting sweets appears to be neurologically organized within the brainstem.
“As demonstrated in the decerebrate rat ([70](#B70)) and anencephalic baby ([171](#B171)), expression of the characteristic happy face when tasting sweets ([11](#B11), [13](#B13)) appears to be neurologically organized within the brainstem”
Quote in the paperSubstantial claim0 of 3 sources checked- cites [70] source
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- cites [171] Steiner JE. The Gustofacial Response: Observations on Normal and Anancephalic Newborn Infants . Bethesda, MD: U.S. Department of Health, Education, and Welfare, 1973, p. 125–167.
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- cites [11] source
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- Interpretationcitation
Taste evolved as a hardwired system telling the animal to either accept or reject certain foods.
“Even in the fruit fly with its primitive nervous system, stimulation of gustatory neurons with sugar activated, while stimulation with a bitter substance inhibited, a pair of motor neurons in the subesophageal ganglion, leading to either vigorous ingestion or rejection ([68](#B68)), adding to the mounting evidence that taste evolved as a hardwired system telling the animal to either accept or rej”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites [68] source
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- Premisecitation
Phasic activity of dopamine neuron projections from the ventral tegmental area to the nucleus accumbens in the ventral striatum are specifically involved in the decision-making process during the preparatory (appetitive) phase of ingestive behavior.
“Phasic activity of dopamine neuron projections from the ventral tegmental area to the nucleus accumbens in the ventral striatum are specifically involved in the decision-making process during the preparatory (appetitive) phase of ingestive behavior ([26](#B26), [148](#B148)).”
Quote in the paperNot a substantial claim0 of 2 sources checked - Premisecitation
For the full sensory impact of palatable food, and the subjective feeling of pleasure in humans, taste is integrated with other sensory modalities such as smell and mouth feel in forebrain areas including the amygdala, as well as primary and higher-order sensory cortical areas, including the insular and orbitofrontal cortex, to form sensory representations of particular foods.
“Clearly, for the full sensory impact of palatable food, and the subjective feeling of pleasure in humans, taste is integrated with other sensory modalities such as smell and mouth feel in forebrain areas including the amygdala, as well as primary and higher-order sensory cortical areas, including the insular and orbitofrontal cortex, to form sensory representations of particular foods ([43](#B43),”
Quote in the paperNot a substantial claim0 of 3 sources checked - Interpretationreasoning
This loop is likely important for the attribution of incentive salience to goal objects by metabolic state signals available to the lateral hypothalamus.
“This loop is likely important for the attribution of incentive salience to goal objects by metabolic state signals available to the lateral hypothalamus, as discussed below.”
Quote in the paperNot a substantial claim - Premisecitation
Nucleus accumbens injection of a μ-opioid receptor antagonist transiently suppressed sucrose-evoked positive hedonic orofacial reactions.
“We have recently demonstrated that nucleus accumbens injection of a μ-opioid receptor antagonist transiently suppressed such sucrose-evoked positive hedonic orofacial reactions ([158](#B158)).”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [158] source
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- Interpretationcitation
Dopamine signaling within the mesolimbic dopamine projection system appears to be a crucial component of the process by which motivation to obtain a reward is translated into action.
“Dopamine signaling within the mesolimbic dopamine projection system appears to be a crucial component of this process.”
Quote in the paperSubstantial claim - Premisecitation
When palatable foods such as sucrose are actually consumed, a sustained and sweetness-dependent increase occurs in nucleus accumbens dopamine levels and turnover.
“In addition, when palatable foods such as sucrose are actually consumed, a sustained and sweetness-dependent increase occurs in nucleus accumbens dopamine levels and turnover ([75](#B75), [80](#B80), [165](#B165)).”
Quote in the paperSubstantial claim0 of 3 sources checked - Premisecitation
Quinine, a cognate bitter ligand, produced strong attraction in mice with expression of a bitter receptor in sweet-sensing taste receptor cells.
“Most remarkably, quinine, a cognate bitter ligand, produced strong attraction in mice with expression of a bitter receptor in sweet-sensing taste receptor cells ([114](#B114)).”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [114] source
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- Interpretationcitation
The generation of food reward can occur by processes of glucose utilization.
“suggesting the generation of food reward by processes of glucose utilization ([44](#B44)).”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites [44] source
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- Premisecitation
Foods considered bland under normal conditions were liked very much in the absence of leptin signaling.
“Even foods considered bland under normal conditions (with leptin in the satiated state) were liked very much in the absence of leptin signaling.”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [57] source
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- Premisecitation
Leptin may modulate sensory processing at higher gustatory and olfactory processing steps, as indicated by the presence of leptin receptors and leptin-induced Fos expression in the nucleus of the solitary tract, parabrachial nucleus, olfactory bulb, and insular and piriform cortices of rodents.
“Leptin may also modulate sensory processing at higher gustatory and olfactory processing steps, as indicated by the presence of leptin receptors and leptin-induced Fos expression in the nucleus of the solitary tract, parabrachial nucleus, olfactory bulb, and insular and piriform cortices of rodents”
Quote in the paperNot a substantial claim0 of 3 sources checked - Premisecitation
In the orbitofrontal cortex and amygdala of monkeys, individual neurons responsive to the taste of specific nutrients such as glucose, amino acids, and fat were modulated by hunger in a sensory-specific manner.
“In the orbitofrontal cortex and amygdala of monkeys, individual neurons responsive to the taste of specific nutrients such as glucose, amino acids, and fat were modulated by hunger in a sensory-specific manner”
Quote in the paperSubstantial claim0 of 3 sources checked - Premisecitation
After diet-induced 10% body weight loss in obese humans, neural changes induced by visual food cues were significantly enhanced in several brain areas dealing with higher-order sensory perception and processing of working memory, including the middle temporal gyrus.
“In a recent study exploring the functional neurological consequences of dieting in obese humans, it was found that after a diet-induced 10% body weight loss, neural changes induced by visual food cues were significantly enhanced in several brain areas dealing with higher-order sensory perception and processing of working memory, including an area in the middle temporal gyrus involved in higher-”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [142] Rosenbaum M, 2008, J Clin Invest
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- Premisecitation
Pictures of food that elicited strong activation of visual and premotor cortex, hippocampus, and hypothalamus under eucaloric conditions elicited much weaker activation after 2 days of overfeeding.
“In another study, pictures of food that elicited strong activation of visual and premotor cortex, hippocampus, and hypothalamus under eucaloric conditions, elicited much weaker activation after 2 days of overfeeding”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [30] source
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- Premisecitation
Metabolic signals modulate the stimulation threshold for lateral hypothalamic-elicited self-stimulation and feeding.
“Metabolic signals modulate the stimulation threshold for lateral hypothalamic elicited self-stimulation and feeding”
Quote in the paperSubstantial claim0 of 3 sources checked - Premisecitation
Taste-induced changes in neuronal activation occur within several areas of the human insular and orbitofrontal cortex and preferentially in the right hemisphere.
“Also by fMRI measurement, it was shown that taste-induced changes in neuronal activation occurred within several areas of the human insular and orbitofrontal cortex and preferentially in the right hemisphere”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites [164] source
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- Premisecitation
Food deprivation increases activation of visual (occipitotemporal cortex) and gustatory (insular cortex) sensory processing areas by the sight and taste of food.
“Comparing the fasted vs. fed state, food deprivation increased activation of visual (occipitotemporal cortex) and gustatory (insular cortex) sensory processing areas by the sight and taste of food”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [181] source
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- Interpretationreasoning
Lateral hypothalamic orexin neurons are in an ideal position to link internal needs with environmental possibilities to make optimal adaptive choices.
“All of these strategic projections put lateral hypothalamic orexin neurons in an ideal position to link internal needs with environmental possibilities to make optimal adaptive choices.”
Quote in the paperNot a substantial claim - Premisecitation
In the leptin-deficient state, nucleus accumbens activation is positively correlated with ratings of liking for the food shown in images in both the fasted and fed state.
“In the leptin-deficient state, nucleus accumbens activation was positively correlated with ratings of liking for the food shown in images in both the fasted and fed state.”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [57] source
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- Premisecitation
Lateral hypothalamic neurons expressing orexin and other transmitters such as neurotensin provide modulatory input to midbrain dopamine neurons.
“Recent investigations show that lateral hypothalamic neurons expressing orexin ([77](#B77), [199](#B199)) and other transmitters such as neurotensin ([101](#B101), [107](#B107)) provide modulatory input to midbrain dopamine neurons”
Quote in the paperSubstantial claim0 of 3 sources checked - Interpretationreasoning
Part of the orexigenic drive of ghrelin and the anorexigenic drive of leptin is achieved by direct modulation of reward-seeking functions mediated by midbrain dopamine neurons.
“Together, these findings suggest that part of the orexigenic drive of ghrelin and the anorexigenic drive of leptin is achieved by direct modulation of reward-seeking functions mediated by midbrain dopamine neurons.”
Quote in the paperSubstantial claim - Premisecitation
After leptin treatment in leptin-deficient patients and in normal subjects, nucleus accumbens activation is only correlated with ratings of liking in the fasted state.
“After leptin treatment in these leptin-deficient patients, and in normal subjects, nucleus accumbens activation was only correlated with ratings of liking in the fasted state”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [57] source
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- Premisecitation
Orexin neurons can integrate metabolic state signals such as leptin, insulin, and glucose.
“Orexin neurons can integrate various metabolic state signals such as leptin, insulin, and glucose”
Quote in the paperSubstantial claim0 of 3 sources checked - Premisecitation
Leptin and insulin injections directly into the midbrain dopamine area suppressed expression of food-conditioned place preference.
“After the initial demonstration that leptin and insulin injections directly into this brain area suppressed expression of food-conditioned place preference ([61](#B61))”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [61] source
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- Interpretationnone given
Few studies have attempted to dissociate whether differences in reward functions are preexisting or secondary to the obese state.
“Such differences could exist before the development of obesity or could be secondary to the obese state, but few studies have attempted to dissociate these two mechanisms.”
Quote in the paperNot a substantial claim - Premisecitation
PET neuroimaging showed reduced dopamine D2-receptor availability mostly in the dorsal and lateral, but not ventral, striatum.
“Furthermore, PET neuroimaging showed reduced dopamine D2-receptor availability mostly in the dorsal and lateral, but not ventral, striatum ([187](#B187)).”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [187] source
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- Interpretationreasoning
Processes of subconscious hedonic evaluation and subjective experience of pleasantness in animals and humans are modulated by internal state.
“Thus, it is quite clear that processes of subconscious hedonic evaluation and subjective experience of pleasantness in animals and humans are modulated by the internal state.”
Quote in the paperSubstantial claim - Interpretationreasoning
It is unlikely that the mechanisms attributing incentive salience to appetitive stimuli exclusively originate from nutrient-sensing areas in the mediobasal hypothalamus.
“It is thus unlikely that the mechanisms attributing incentive salience to appetitive stimuli are exclusively originating from nutrient-sensing areas in the mediobasal hypothalamus.”
Quote in the paperSubstantial claim - Premisecitation
In selectively bred lines of obesity-prone and obesity-resistant rats, several differences in mesolimbic dopamine signaling have been reported.
“In selectively bred lines of obesity-prone and obesity-resistant rats, several differences in mesolimbic dopamine signaling have been reported ([41](#B41), [65](#B65)), but most of these studies used adult, already obese animals.”
Quote in the paperSubstantial claim0 of 2 sources checked - Interpretationreasoning
Metabolic state signals impinge on almost every neural process involved in procuring, consuming, and learning about food.
“In summary, metabolic state signals impinge on almost every neural process involved in procuring, consuming, and learning about food.”
Quote in the paperSubstantial claim - Premisecitation
There is a considerable body of literature demonstrating differences in reward functions between lean and obese animals and humans.
“There is a considerable body of literature demonstrating differences in reward functions between lean and obese animals and humans ([40](#B40), [162](#B162), [173](#B173), [174](#B174)).”
Quote in the paperSubstantial claim0 of 3 sources checked - Interpretationnone given
Preexisting differences in reward functions do not automatically result in obesity later in life.
“It is also important to note that preexisting differences in reward functions do not automatically result in obesity later in life.”
Quote in the paperNot a substantial claim - Interpretationcitation
Most studies of mesolimbic dopamine signaling differences in obesity-prone and obesity-resistant rats used adult, already obese animals.
“In selectively bred lines of obesity-prone and obesity-resistant rats, several differences in mesolimbic dopamine signaling have been reported ([41](#B41), [65](#B65)), but most of these studies used adult, already obese animals.”
Quote in the paperSubstantial claim - Premisecitation
Neural activity in brain areas involved in cognitive processing of food representations, such as the amygdala and hippocampal complex, is modulated by leptin and ghrelin.
“Furthermore, neural activity in brain areas thought to be involved in cognitive processing of representations of food such as the amygdala and hippocampal complex is modulated by leptin ([78](#B78), [79](#B79), [105](#B105)) and ghrelin ([27](#B27), [50](#B50), [92](#B92), [109](#B109), [147](#B147), [189](#B189)).”
Quote in the paperSubstantial claim0 of 3 sources checked - Interpretationreasoning
The life-sustaining process of attributing incentive salience to appetitive stimuli is organized in a redundant and distributed fashion.
“Rather, this life-sustaining process is organized in a redundant and distributed fashion.”
Quote in the paperSubstantial claim - Premisecitation
In only one preliminary study was a difference in mesolimbic dopamine signaling seen at an early age in obesity-prone and obesity-resistant rats.
“In only one preliminary study was a difference seen at an early age ([65](#B65)), so it is not clear whether differences in reward functions are preexisting and genetically determined or acquired by exposure to palatable food stimuli and/or secondary to the obese state.”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [65] source
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- Premisecitation
Repeated exposure to drugs of abuse causes neuroadaptive changes leading to elevations in reward thresholds (decreased reward) that drive accelerated drug intake.
“It is well-known that repeated exposure to drugs of abuse causes neuroadaptive changes leading to elevations in reward thresholds (decreased reward) that drive accelerated drug intake ([4](#B4), [87](#B87), [96](#B96), [97](#B97), [110](#B110), [145](#B145)).”
Quote in the paperSubstantial claim0 of 3 sources checked - Premisecitation
Comparing lean and obese subjects carrying different alleles of either the dopamine D2-receptor or μ-opioid receptor genes reveals differences in behavioral and neural responses to palatable food.
“Comparing lean and obese subjects carrying different alleles of either the dopamine D2-receptor or μ-opioid receptor genes does reveal differences in behavioral and neural responses to palatable food ([39](#B39), [40](#B40), [60](#B60), [172](#B172)).”
Quote in the paperSubstantial claim0 of 3 sources checked - Premisecitation
Among the approximately 20 major genes linked to obesity development, none are directly implicated in known reward function mechanisms.
“Among the 20 or so major genes (clear evidence from at least two independent studies) linked to the development of obesity ([129](#B129)), none are directly implicated in known mechanisms of reward functions.”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [129] source
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- Premisecitation
Unlimited access to palatable food leads to hedonic overeating and eventually obesity (the gluttony hypothesis).
“One fundamental premise here is that unlimited access to palatable food leads to hedonic overeating and eventually obesity, called the gluttony hypothesis for simplicity.”
Quote in the paperSubstantial claim0 of 3 sources checked - Interpretationreasoning
Differences in reward functions are responsible for vulnerability to increased availability of palatable food and food cues.
“Here we argue that differences in reward functions are responsible”
Quote in the paperNot a substantial claim- Rests on an assumption: Not all subjects exposed to the same toxic environment gain weight.
- Interpretationcitation
Besides classical genetic, epigenetic and nongenetic mechanisms could also be potentially responsible for differences in neural reward circuitry and reward behaviors at a young age, predisposing to hyperphagia and obesity later in life.
“Besides classical genetic, epigenetic and nongenetic mechanisms ([23](#B23), [34](#B34), [36](#B36), [37](#B37), [62](#B62), [67](#B67), [126](#B126), [155](#B155), [176](#B176), [184](#B184)) could also be potentially responsible for differences in neural reward circuitry and reward behaviors at a young age, predisposing to hyperphagia and obesity later in life.”
Quote in the paperSubstantial claim0 of 3 sources checked - Premisecitation
The combined effect of the major genes linked to obesity accounts for less than about 5% of human obesity.
“However, because the combined effect of these genes only accounts for less than ∼5% of human obesity, it is very likely that many important genes have not yet been discovered, some of which could operate within the reward system.”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [129] source
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- Interpretationreasoning
Differences in mesolimbic dopamine signaling are most strongly implicated in altered food anticipatory and consummatory behaviors and obesity.
“In summary, differences in mesolimbic dopamine signaling are most strongly implicated in altered food anticipatory and consummatory behaviors and obesity.”
Quote in the paperSubstantial claim - Interpretationreasoning
Preexisting differences make some individuals more vulnerable to the increased availability of palatable food and food cues.
“This suggests that preexisting differences make some individuals more vulnerable to the increased availability of palatable food and food cues”
Quote in the paperSubstantial claim- Rests on an assumption: Not all subjects exposed to the same toxic environment gain weight.
- Interpretationreasoning
Reward circuitry in corticolimbic and other areas is likely to be affected by obesity-induced changes in peripheral signals to the brain and local brain signaling through inflammatory, oxidative, and mitochondrial stress pathways.
“Just like brain areas involved in homeostatic energy balance regulation, such as the hypothalamus, and in cognitive control, such as the hippocampus and neocortex, reward circuitry in corticolimbic and other areas is likely to be affected by obesity-induced changes in peripheral signals to the brain and local brain signaling through inflammatory, oxidative, and mitochondrial stress pathways.”
Quote in the paperNot a substantial claim - Interpretationreasoning
The most convincing evidence exists for a role of the mesolimbic dopamine pathway in the "wanting" aspect of ingestive behavior.
“The most convincing evidence exists for a role of the mesolimbic dopamine pathway in the “wanting” aspect of ingestive behavior, but it is not yet clear whether over- or under-activity of dopamine signaling is at the origin of hyperphagia.”
Quote in the paperSubstantial claim - Premisecitation
High-fat diets disturb the relationship between glial cells and neurons in the hypothalamus through increased endoplasmic reticulum and oxidative stress, leading to stress-response pathways with generally cytotoxic effects.
“A number of recent studies directed attention to the hypothalamus, where high-fat diets disturb the delicate relationship between glial cells and neurons through increased endoplasmic reticulum and oxidative stress, leading to stress-response pathways with generally cytotoxic effects ([48](#B48), [121](#B121), [177](#B177), [198](#B198)).”
Quote in the paperSubstantial claim0 of 3 sources checked - Premisecitation
A similar insensitivity of the reward system was previously seen in addicted rats, self-administering intravenous cocaine or heroin.
“A similar insensitivity of the reward system was previously seen in addicted rats, self-administering intravenous cocaine or heroin ([4](#B4), [110](#B110)).”
Quote in the paperSubstantial claim0 of 2 sources checked- cites [4] source
Not checked in the free run.
- cites [110] Markou A, 1991, Neuropsychopharmacology
Not checked in the free run.
- Premisecitation
The obese, leptin-deficient mouse is much more sensitive to chemically-induced neurodegeneration such as metamphetamine-induced dopamine nerve terminal degeneration as indicated by reduced striatal dopamine levels.
“The obese, leptin-deficient mouse is much more sensitive to chemically-induced neurodegeneration such as metamphetamine-induced dopamine nerve terminal degeneration as indicated by reduced striatal dopamine levels ([170](#B170)).”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [170] source
Not checked in the free run.
- Premisecitation
Dopamine D2-receptor expression in the dorsal striatum was significantly reduced in parallel to worsening of the reward threshold, to levels found in cocaine-addicted rats.
“Furthermore, dopamine D2-receptor expression in the dorsal striatum was significantly reduced in parallel to worsening of the reward threshold ([89](#B89)), to levels found in cocaine-addicted rats ([35](#B35)).”
Quote in the paperSubstantial claim0 of 2 sources checked - Interpretationreasoning
These toxic effects can also affect brain areas involved in reward processing.
“However, these toxic effects do not stop at the level of the hypothalamus, but can also affect brain areas involved in reward processing.”
Quote in the paperSubstantial claim - Interpretationcitation
Given the observation that cocaine addicts and obese human subjects exhibit low D2R availability in the dorsal striatum, dopamine plasticity due to repeated consumption of palatable food is somewhat similar to that due to repeated consumption of drugs of abuse.
“Given the observation that cocaine addicts and obese human subjects exhibit low D2R availability in the dorsal striatum ([190](#B190)), these findings suggest that dopamine plasticity due to repeated consumption of palatable food is somewhat similar to that due to repeated consumption of drugs of abuse.”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [190] source
Not checked in the free run.
- Interpretationreasoning
The lack of normalization of reward threshold after 14 days of abstinence from palatable diet may indicate the presence of irreversible changes caused by the high-fat content of the diet.
“This is in contrast to the relatively rapid (∼48 h) normalization in reward thresholds in rats abstaining from cocaine self-administration ([110](#B110)) and may indicate the presence of irreversible changes caused by the high-fat content of the diet (see next section).”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [110] Markou A, 1991, Neuropsychopharmacology
Not checked in the free run.
- Interpretationcitation
The obesity-induced toxic internal environment does not spare the brain.
“It is becoming clear that the obesity-induced toxic internal environment does not spare the brain ([24](#B24), [46](#B46), [48](#B48), [52](#B52), [59](#B59), [95](#B95), [121](#B121), [127](#B127), [177](#B177), [182](#B182), [198](#B198)).”
Quote in the paperSubstantial claim0 of 3 sources checked - Interpretationreasoning
Early observations in rodents suggest that some palatable foods such as sucrose have addictive potential in certain experimental animal models, as they recapitulate at least some key criteria established for drugs and alcohol.
“In summary, early observations in rodents suggest that some palatable foods such as sucrose have addictive potential in certain experimental animal models, as they recapitulate at least some key criteria established for drugs and alcohol.”
Quote in the paperSubstantial claim
- May combine two claims. 44
- Classified as probably not a substantial claim. 8
May combine two claims.
PremisecitationStrong attraction to food and food cues, slow satiety mechanisms, and high metabolic efficiency were advantageous for survival in a scarce environment.
“Biological traits like strong attraction to food and food cues, slow satiety mechanisms, and high metabolic efficiency, advantageous for survival in a scarce environment, seem now to be our worst enemies when it comes to resisting an abundance of food”
Quote in the paperSubstantial claim0 of 2 sources checkedProbably not a substantial claim: may not pass S3 (load-bearing).
PremisecitationIngestive behavior consists of preparatory, consummatory, and postconsummatory phases.
“Ingestive behavior is not limited to the act of eating, but consists of preparatory, consummatory, and postconsummatory phases”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites [15] source
Not checked in the free run.
May combine two claims.
PremisecitationDuring eating, immediate, direct pleasure is derived mainly from gustatory and olfactory sensations, driving consumption throughout the meal until satiation signals dominate.
“During eating, immediate, direct pleasure is derived from mainly gustatory and olfactory sensations, driving consumption throughout the meal until satiation signals dominate ([166](#B166)).”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites [166] source
Not checked in the free run.
May combine two claims.
PremisecitationFood intake and energy expenditure are controlled by complex, redundant, and distributed neural systems, likely involving thousands of genes and reflecting the fundamental biological importance of adequate nutrient supply and energy balance.
“Food intake and energy expenditure are thought to be controlled by complex, redundant, and distributed neural systems, likely involving thousands of genes and reflecting the fundamental biological importance of adequate nutrient supply and energy balance”
Quote in the paperNot a substantial claim0 of 2 sources checkedMay combine two claims.
InterpretationcitationStrong attraction to food and food cues, slow satiety mechanisms, and high metabolic efficiency now make it difficult to resist an abundance of food.
“Biological traits like strong attraction to food and food cues, slow satiety mechanisms, and high metabolic efficiency, advantageous for survival in a scarce environment, seem now to be our worst enemies when it comes to resisting an abundance of food”
Quote in the paperSubstantial claim0 of 2 sources checkedProbably not a substantial claim: may not pass S3 (load-bearing), S4 (based).
InterpretationreasoningNeural systems activated by thinking about a favorite dish, savoring a candy in the mouth, or leaning back after a satiating meal are likely very different, although they may contain common elements.
“Neural systems activated by thinking about a favorite dish, savoring a candy in the mouth, or leaning back after a satiating meal, are likely very different, although they may contain common elements.”
Quote in the paperNot a substantial claimProbably not a substantial claim: may not pass S3 (load-bearing), S4 (based).
Interpretationnone givenA variety of sensory stimuli and emotional states or feelings with vastly different temporal profiles make up the rewarding experience of eating.
“Thus, a variety of sensory stimuli and emotional states or feelings with vastly different temporal profiles make up the rewarding experience of eating, and the underlying neural functions are only beginning to be understood.”
Quote in the paperNot a substantial claimMay combine two claims.
PremisecitationEven in Drosophila, taste-specific receptor cells do not directly synapse on motor neurons responsible for the taste-guided behavioral output, leaving opportunities for modulatory influences from other areas of the nervous system.
“Even in *Drosophila*, the taste-specific receptor cells do not directly synapse on motor neurons responsible for the taste-guided behavioral output ([68](#B68)), leaving plenty of opportunities for modulatory influences from other areas of the nervous system.”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites [68] source
Not checked in the free run.
May combine two claims.
PremisecitationIn fruit fly, stimulation of gustatory neurons with sugar activated, while bitter inhibited, a pair of motor neurons in the subesophageal ganglion, leading to either vigorous ingestion or rejection.
“Even in the fruit fly with its primitive nervous system, stimulation of gustatory neurons with sugar activated, while stimulation with a bitter substance inhibited, a pair of motor neurons in the subesophageal ganglion, leading to either vigorous ingestion or rejection ([68](#B68))”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [68] source
Not checked in the free run.
May combine two claims.
InterpretationreasoningThe basic brainstem circuitry appears to be able to recognize the usefulness and perhaps pleasantness of a taste stimulus and initiate appropriate behavioral responses.
“Thus, this basic brainstem circuitry appears to be able to recognize the usefulness and perhaps pleasantness of a taste stimulus and initiate appropriate behavioral responses.”
Quote in the paperNot a substantial claimMay combine two claims.
PremisecitationIn mice with transgenic expression of the receptor for an ordinarily tasteless ligand in either sweet or bitter taste receptor cells, stimulation with the ligand produced either strong attraction or avoidance of sweet solutions, respectively.
“In mice with transgenic expression of the receptor for an ordinarily tasteless ligand in either sweet or bitter taste receptor cells, stimulation with the ligand produced either strong attraction or avoidance of sweet solutions, respectively ([197](#B197)).”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [197] source
Not checked in the free run.
May combine two claims.
PremisecitationThe nucleus accumbens shell is part of a neural loop including the lateral hypothalamus and the ventral tegmental area, with orexin neurons playing a key role.
“The nucleus accumbens shell is thereby part of a neural loop including the lateral hypothalamus and the ventral tegmental area, with orexin neurons playing a key role ([7](#B7), [22](#B22), [77](#B77), [98](#B98), [115](#B115), [125](#B125), [175](#B175), [199](#B199)).”
Quote in the paperNot a substantial claim0 of 3 sources checkedProbably not a substantial claim: may not pass S3 (load-bearing), S4 (based).
Interpretationnone givenThe most important processing step in the translation of sensory representations into actions is the attribution of what Berridge calls "incentive salience".
“Perhaps the most important processing step in the translation of such sensory representations into actions is the attribution of what Berridge calls “incentive salience.””
Quote in the paperNot a substantial claimProbably not a substantial claim: may not pass S3 (load-bearing), S4 (based). May combine two claims.
Interpretationnone givenThe mechanism of incentive salience allows a starving animal to know it needs calories or a salt-depleted organism to know it needs salt.
“This mechanism allows a starving animal to know it needs calories or a salt-depleted organism to know it needs salt.”
Quote in the paperNot a substantial claimMay combine two claims.
PremisecitationLeptin receptors are located in hypothalamic areas beyond the arcuate nucleus, including the ventromedial, dorsomedial, premammillary, lateral, and perifornical areas, where they likely contribute to leptin's effects on food intake and energy expenditure.
“But clearly, leptin receptors are located in other hypothalamic areas such as the ventromedial, dorsomedial, and premammillary nuclei, as well as the lateral and perifornical areas where they likely contribute to leptin's effects on food intake and energy expenditure”
Quote in the paperNot a substantial claim0 of 2 sources checkedMay combine two claims.
PremisecitationSubjective pleasantness in humans is coded by neural activity in the medial orbitofrontal cortex as measured by fMRI and is subject to sensory-specific satiety.
“Similarly, subjective pleasantness in humans was coded by neural activity in the medial orbitofrontal cortex as measured by functional MRI (fMRI) and was subject to sensory-specific satiety, a form of reinforcer devaluation”
Quote in the paperSubstantial claim0 of 3 sources checkedMay combine two claims.
PremisecitationLeptin injections into the VTA decreased dopamine neuron activity and acutely suppressed food intake, while adenoviral knockdown of leptin receptors specifically in the VTA resulted in increased sucrose preference and sustained palatable food intake.
“other studies demonstrated that such leptin injections decreased dopamine neuron activity and acutely suppressed food intake, while adenoviral knockdown of leptin receptors specifically in the ventral tegmental area (VTA) resulted in increased sucrose preference and sustained palatable food intake ([84](#B84))”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [84] source
Not checked in the free run.
May combine two claims.
PremisecitationIn normal rats, leptin promotes tyrosine hydroxylase activity and amphetamine-mediated dopamine efflux in the nucleus accumbens.
“Also, in normal rats, leptin promotes tyrosine hydroxylase activity and amphetamine-mediated dopamine efflux in the nucleus accumbens”
Quote in the paperSubstantial claim0 of 2 sources checkedMay combine two claims.
PremisecitationOrexin neurons project widely within both forebrain and hindbrain, including a hypothalamic-thalamic-striatal loop and projections to oromotor and autonomic motor areas in the caudal brainstem.
“In addition to midbrain dopamine neurons, orexin neurons project widely within both forebrain and hindbrain. In particular, a hypothalamic-thalamic-striatal loop involving orexin projections to the paraventricular nucleus of the thalamus and cholinergic striatal interneurons ([93](#B93)), and orexin projections to oromotor and autonomic motor areas in the caudal brainstem ([6](#B6)).”
Quote in the paperSubstantial claim0 of 2 sources checkedMay combine two claims.
PremisecitationLeptin-deficient mice exhibit suppressed rather than increased dopamine neuron activity, and leptin-replacement therapy restored normal dopamine neuron activity as well as amphetamine-induced locomotor sensitization.
“leptin-deficient mice (absence of leptin-receptor signaling) exhibit suppressed rather than increased dopamine neuron activity [as expected from the viral knockdown experiments in rats ([84](#B84))], and leptin-replacement therapy restored normal dopamine neuron activity as well as amphetamine-induced locomotor sensitization ([63](#B63))”
Quote in the paperSubstantial claim0 of 2 sources checkedMay combine two claims.
PremisecitationGhrelin action directly within the VTA activates dopamine neurons, increases accumbens dopamine turnover, and increases food intake.
“In contrast, ghrelin action directly within the VTA appears to activate dopamine neurons, increase accumbens dopamine turnover, and increase food intake”
Quote in the paperSubstantial claim0 of 3 sources checkedMay combine two claims.
InterpretationcitationWeight loss-induced differences in neural responses to food cues are reversed after leptin treatment, suggesting that low leptin sensitizes brain areas responding to food cues.
“Both of these weight loss-induced differences were reversed after leptin treatment, suggesting that low leptin sensitizes brain areas responding to food cues.”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [142] Rosenbaum M, 2008, J Clin Invest
Not checked in the free run.
May combine two claims.
PremisecitationElectrical stimulation of the lateral hypothalamus elicits food intake, and rats learn quickly to self-administer such stimulation.
“It has long been known that electrical stimulation of the lateral hypothalamus elicits food intake and that rats learn quickly to self-administer electrical stimulation”
Quote in the paperNot a substantial claim0 of 2 sources checkedMay combine two claims.
PremisecitationNeural activation in the nucleus accumbens elicited by visual food stimuli is very high in genetically leptin-deficient adolescents and promptly returns to normal levels upon leptin administration.
“Neural activation in the nucleus accumbens elicited by visual food stimuli is very high in genetically leptin-deficient adolescents and promptly returns to normal levels upon leptin administration”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [57] source
Not checked in the free run.
May combine two claims.
PremisecitationIn rodents, absence of leptin increases and addition of leptin dampens peripheral taste and olfactory sensitivity.
“In rodents, absence of leptin has been shown to increase and addition of leptin to dampen peripheral taste and olfactory sensitivity”
Quote in the paperNot a substantial claim0 of 3 sources checkedMay combine two claims.
PremisecitationIn one study, only about half of male C57/BL6J mice became obese on a palatable high-fat diet, but reward functions were not assessed.
“In one such study, only about half of male C57/BL6J mice became obese on a palatable high-fat diet ([55](#B55)), but reward functions were not assessed.”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [55] source
Not checked in the free run.
May combine two claims.
PremisecitationRepeated sucrose access can upregulate dopamine release and dopamine transporter, and change dopamine D1 and D2 receptor availability in the nucleus accumbens.
“The limited information available suggests that repeated sucrose access can upregulate dopamine release ([5](#B5)) and dopamine transporter ([9](#B9)), and change dopamine D1 and D2 receptor availability ([5](#B5), [8](#B8)) in the nucleus accumbens.”
Quote in the paperSubstantial claim0 of 3 sources checkedMay combine two claims.
PremisecitationThere are many human studies showing acute effects of manipulating palatability, variability, and availability of food, although few controlled studies show long-term effects on energy balance.
“There are also plenty of human studies showing acute effects of manipulating palatability, variability, and availability of food ([191](#B191), [192](#B192)), although few controlled studies show long-term effects on energy balance ([120](#B120), [134](#B134)).”
Quote in the paperNot a substantial claim0 of 3 sources checkedMay combine two claims.
PremisecitationNumerous animal studies demonstrate increased intake of palatable foods and development of diet-induced obesity.
“This hypothesis is supported by numerous studies in animals demonstrating increased intake of palatable foods and development of obesity, so called diet-induced obesity”
Quote in the paperSubstantial claim0 of 3 sources checkedMay combine two claims.
PremisecitationMesolimbic dopamine signaling is severely suppressed in leptin-deficient ob/ob mice and rescued by systemic leptin replacement.
“Mesolimbic dopamine signaling is also severely suppressed in leptin-deficient *ob/ob* mice and rescued by systemic leptin replacement ([63](#B63)).”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [63] source
Not checked in the free run.
May combine two claims.
PremisecitationIn genetically leptin-deficient humans, neural activity in the nucleus accumbens elicited by viewing pictures of palatable foods was exaggerated in the absence of leptin and abolished after leptin administration.
“However, in genetically leptin-deficient humans, neural activity in the nucleus accumbens elicited by viewing pictures of palatable foods was exaggerated in the absence of leptin and abolished after leptin administration ([57](#B57)).”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [57] source
Not checked in the free run.
May combine two claims.
Interpretationnone givenPreexisting differences in obesity risk could be determined by genetic and epigenetic alterations and by early life experience through developmental programming.
“Preexisting differences could be determined by genetic and epigenetic alterations, and by early life experience through developmental programming.”
Quote in the paperSubstantial claimMay combine two claims.
InterpretationreasoningIt is very likely that many important genes for obesity have not yet been discovered, and some of these could operate within the reward system.
“However, because the combined effect of these genes only accounts for less than ∼5% of human obesity, it is very likely that many important genes have not yet been discovered, some of which could operate within the reward system.”
Quote in the paperNot a substantial claimProbably not a substantial claim: may not pass S4 (based). May combine two claims.
Interpretationnone givenThe three mechanisms linking food reward and obesity are not mutually exclusive, and it is highly likely that a combination of all three is operative in most individuals.
“These mechanisms are not mutually exclusive, and it is highly likely that a combination of all three is operative in most individuals.”
Quote in the paperNot a substantial claimClassified as probably not a substantial claim. May combine two claims.
InterpretationreasoningDifferences in reward functions between lean and obese subjects could exist before the development of obesity or could be secondary to the obese state.
“Such differences could exist before the development of obesity or could be secondary to the obese state, but few studies have attempted to dissociate these two mechanisms.”
Quote in the paperSubstantial claimMay combine two claims.
PremisecitationFor nonsweet palatable foods (typically high-fat foods), there is less convincing evidence for development of dependence, although intermittent access to corn oil can stimulate dopamine release in the nucleus accumbens.
“For nonsweet palatable foods (typically high-fat foods), there is less convincing evidence for development of dependence ([21](#B21), [31](#B31)), although intermittent access to corn oil can stimulate dopamine release in the nucleus accumbens ([106](#B106)).”
Quote in the paperNot a substantial claim0 of 3 sources checkedMay combine two claims.
PremisecitationIn Wistar rats, exposure to a palatable cafeteria diet led to sustained hyperphagia over 40 days and lateral hypothalamic electrical self-stimulation threshold increased in parallel to body weight gain.
“In Wistar rats, exposure to a palatable cafeteria diet led to sustained hyperphagia over 40 days and lateral hypothalamic electrical self-stimulation threshold increased in parallel to body weight gain ([89](#B89)).”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [89] source
Not checked in the free run.
May combine two claims.
InterpretationreasoningThe obesity-induced internal toxic environment does not stop at the level of the brain, and within the brain does not stop at the reward circuitry.
“In summary, it seems clear that the obesity-induced internal toxic environment does not stop at the level of the brain, and within the brain does not stop at the reward circuitry.”
Quote in the paperNot a substantial claimMay combine two claims.
InterpretationreasoningThere is considerable indirect and correlative evidence for involvement of the reward system in causing obesity in both animals and humans, but there is no smoking gun for a single specific neural pathway or molecule.
“Although there is considerable indirect and correlative evidence for involvement of the reward system in causing obesity in both animals and humans, there is no smoking gun for a single specific neural pathway or molecule.”
Quote in the paperSubstantial claimMay combine two claims.
PremisecitationAbstinence from sucrose can cause craving and withdrawal symptoms, eventually leading to relapse behavior.
“As with drug ([71](#B71), [96](#B96), [156](#B156)) and alcohol ([18](#B18), [185](#B185)) addiction, abstinence from sucrose can cause craving and withdrawal symptoms ([5](#B5)), eventually leading to relapse behavior ([72](#B72), [73](#B73)).”
Quote in the paperSubstantial claim0 of 3 sources checkedMay combine two claims.
PremisecitationObesity is associated with dysregulated signaling systems, such as leptin and insulin resistance, as well as increased signaling through proinflammatory cytokines and pathways activated by oxidative and endoplasmatic reticulum stress.
“Obesity is associated with dysregulated signaling systems, such as leptin and insulin resistance, as well as increased signaling through proinflammatory cytokines and pathways activated by oxidative and endoplasmatic reticulum stress ([3](#B3)).”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites [3] source
Not checked in the free run.
May combine two claims.
PremisecitationObesity and hypertriglyceridemia produce cognitive impairment in mice, including reduced lever pressing for food reward.
“Obesity and hypertriglyceridemia produce cognitive impairment in mice, including reduced lever pressing for food reward ([59](#B59)), and epidemiological studies show an association of body mass index and risk of Parkinson disease and cognitive decline ([85](#B85)).”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [59] source
Not checked in the free run.
May combine two claims.
Interpretationnone givenObesity is a multifactorial disease with a number of potential causes, and the involvement of recent environmental changes including overabundance of palatable food and little opportunity to work off the extra energy seems undeniable.
“Obesity clearly is a multifactorial disease with a number of potential causes, but the involvement of recent environmental changes including overabundance of palatable food and little opportunity to work off the extra energy seems undeniable.”
Quote in the paperSubstantial claimMay combine two claims.
PremisecitationEpidemiological studies show an association of body mass index and risk of Parkinson disease and cognitive decline.
“Obesity and hypertriglyceridemia produce cognitive impairment in mice, including reduced lever pressing for food reward ([59](#B59)), and epidemiological studies show an association of body mass index and risk of Parkinson disease and cognitive decline ([85](#B85)).”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [85] source
Not checked in the free run.
Probably not a substantial claim: may not pass S2 (checkable).
InterpretationreasoningThe lack of a smoking gun is most likely because the reward system is complex and cannot be easily manipulated with drugs or genetic deletions.
“This is most likely because the reward system is complex and cannot be easily manipulated with drugs or genetic deletions.”
Quote in the paperNot a substantial claim- Rests on an assumption: The reward system is complex and cannot be easily manipulated with drugs or genetic deletions.
May combine two claims.
PremisecitationAfter 14 days of abstinence from the palatable diet, reward threshold did not normalize even though the rats were hypophagic and lost ∼10% body weight.
“Interestingly, after 14 days of abstinence from the palatable diet, reward threshold did not normalize even though the rats were hypophagic and lost ∼10% body weight ([89](#B89)).”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [89] source
Not checked in the free run.
May combine two claims.
InterpretationreasoningThe end effects of these changes are central insulin and leptin resistance and impaired hypothalamic regulation of energy balance, further favoring the development of obesity and in turn, neurodegeneration.
“The end effects of these changes are central insulin and leptin resistance and impaired hypothalamic regulation of energy balance, further favoring the development of obesity and in turn, neurodegeneration.”
Quote in the paperSubstantial claimMay combine two claims.
InterpretationreasoningGiven external conditions and the strong inherent bias of the homeostatic regulatory system to defend against energy depletion more strongly than energy surplus, weight is easily gained but not so easily lost.
“Given these external conditions together with the strong inherent bias of the homeostatic regulatory system to defend against energy depletion more strongly than energy surplus, weight is easily gained but not so easily lost.”
Quote in the paperSubstantial claim- Rests on an assumption: The homeostatic regulatory system has a strong inherent bias to defend against energy depletion more strongly than energy surplus.
May combine two claims.
Interpretationown dataBoth obesity per se and high-fat diet can cause alterations in mesolimbic dopamine signaling and reward behaviors.
“These results suggest that both obesity per se and high-fat diet can cause alterations in mesolimbic dopamine signaling and reward behaviors.”
Quote in the paperSubstantial claim
The paper relies on this without support.
The anatomy, chemistry, and functions of the elaborate neural systems involved in food reward and their interactions with the hypothalamic homeostatic regulator are poorly understood.
“Regrettably, the anatomy, chemistry, and functions of these elaborate neural systems and their interactions with the homeostatic regulator in the hypothalamus are poorly understood.”
The paper relies on this without support.
Dysregulated brain reward pathways may contribute to increased intake of palatable foods and ultimately obesity.
“recent studies in rodents and humans suggest that dysregulated brain reward pathways may be contributing not only to drug addiction but also to increased intake of palatable foods and ultimately obesity.”
The paper relies on this without support.
Eating is typically experienced as pleasurable and rewarding.
“Eating is typically experienced as pleasurable and rewarding”
The paper relies on this without support.
Food is a powerful natural reinforcer that outcompetes most other behaviors, particularly when an individual is metabolically hungry.
“Thus, food is a powerful natural reinforcer that out competes most other behaviors, particularly when an individual is metabolically hungry.”
The paper relies on this without support.
Metabolic hunger increases motivation to find food and to eat.
“It has long been known that metabolic hunger increases motivation to find food and to eat, but the neural mechanisms involved were obscure.”
The paper relies on this without support.
The hypothalamus is the epicenter of homeostatic regulation.
“Given that the hypothalamus was recognized as the epicenter of homeostatic regulation, it was assumed that the metabolic hunger signal originates in this brain area and propagates through neural projections to other areas important for the organization of goal-directed behavior.”
The paper relies on this without support.
There is no hunger center and no pleasure center in the brain.
“Just as there is no hunger center, there is no pleasure center in the brain.”
The paper relies on this without support.
In animals, only the subconscious components of pleasure (core “liking”) and aversion are experimentally accessible.
“In animals, only the subconscious components of pleasure (Berridge's core “liking”) and aversion are experimentally accessible, and one of the few specific test paradigms is measurement of positive and negative orofacial expressions when tasting pleasurable (typically sweet) or aversive stimuli ([11](#B11)).”
The paper relies on this without support.
A general feeling of satisfaction lingers long after meal termination and contributes to the reinforcing power of a meal.
“Rather than the acute pleasure of tasty food in the mouth, there is a general feeling of satisfaction that lingers on long after termination, and most likely contributes to the reinforcing power of a meal.”
The paper relies on this without support.
Leptin and other metabolic signals act on a large number of brain systems.
“However, during the last few years it became increasingly clear that leptin and the plethora of other metabolic signals not only act on the hypothalamus, but on a large number of brain systems.”
The paper relies on this without support.
Not all subjects exposed to the same toxic environment gain weight.
“this simple explanation does not account for the fact that not all subjects exposed to the same toxic environment gain weight.”
The paper relies on this without support.
Environmental pressure pushes the general population to higher food intake and body weight.
“Although environmental pressure undoubtedly pushes the general population to higher food intake and body weight”
The paper relies on this without support.
Obesity-prone rats develop some degree of obesity even on regular chow diet.
“Because obesity-prone rats develop some degree of obesity even on regular chow diet, it is also not clear to what extent the genetic difference depends on availability of palatable diet vs. chow, to be phenotypically expressed (susceptibility genes).”
The paper relies on this without support.
The homeostatic regulatory system has a strong inherent bias to defend against energy depletion more strongly than energy surplus.
“Given these external conditions together with the strong inherent bias of the homeostatic regulatory system to defend against energy depletion more strongly than energy surplus, weight is easily gained but not so easily lost.”
The paper relies on this without support.
The reward system is complex and cannot be easily manipulated with drugs or genetic deletions.
“This is most likely because the reward system is complex and cannot be easily manipulated with drugs or genetic deletions.”
The paper relies on this without support.
The concept of food addiction is still not generally accepted, and its behavioral and neurological mechanisms remain obscure.
“While the field of drug addiction has a long tradition (e.g., Refs. [96](#B96), [132](#B132)), the concept of food addiction is still not generally accepted, and its behavioral and neurological mechanisms remain obscure.”
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?
Ingestive behavior is regulated not only homeostatically but also by nonhomeostatic brain circuits that process the reward-related qualities of food intake.
“Ingestive behavior is not only regulated homeostatically (i.e., by central nervous pathways that respond to energy depletion) but also by nonhomeostatic brain circuits that process the reward-related, “hedonic” qualities of food intake (19).”
From Oxytocin Reduces Reward-Driven Food Intake in Humans (2013) · cites this paper as [19]
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Central nervous system control of food intake
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- Authors
- Berthoud, H.-R., Lenard, N. R., & Shin, A. C.
- Affiliations
- Pennington Biomedical Research Center (US)
- Corresponding author
- Berthoud, Hans-Rudolf
- Venue
- American Journal of Physiology-Regulatory, Integrative and Comparative Physiology
- Publisher
- American Physiological Society
- Published
- 2011-06
- Volume
- 300
- Issue
- 6
- Pages
- R1266-R1277
- ISSN
- 0363-6119 (ISSN-L)
- 1522-1490
- PMC
- PMC3119156
- OpenAlex
- W2141794225
- Cited by
- 275
- References
- 208
- Citations by year
- 2026: 8 · 2025: 8 · 2024: 4 · 2023: 16 · 2022: 10 · 2021: 24 · 2020: 18 · 2019: 52 · 2018: 11 · 2017: 12 · 2016: 17 · 2015: 20 · 2014: 27 · 2013: 25 · 2012: 18
- FWCI
- 2.47
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- American Journal of Physiology-Regulatory, Integrative and Comparative Physiology (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institute of Diabetes and Digestive and Kidney Diseases (DK-47348, R01DK071082, DK071082, R01DK047348)
- Topics
- Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Regulation of Appetite and Obesity
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neurotransmitter Receptor Influence on Behavior
- Social Sciences › Psychology › Clinical Psychology › Eating Disorders and Behaviors
- Keywords
- food reward, hyperphagia, obesity, incentive salience, palatable food intake, brain reward system, sensitization, inflammatory signaling, oxidative stress, mitochondrial stress, drug addiction, alcoholism, eating disorders, obesity-related comorbidities
- MeSH terms
- Animals, Humans, Hyperphagia, Neural Pathways, Obesity, Reward, Signal Transduction, Behavior, Addictive, Models, Animal
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