The DOI matches its Crossref record; 167 of the 173 references it cites were found in a registry or an index; 1 of the 136 sources its claims cite were checked for support.
The menace of obesity to depression and anxiety prevalence
Open accessAbstract
The incidence of depression and anxiety is amplified by obesity. Mounting evidence reveals that the psychiatric consequences of obesity stem from poor diet, inactivity, and visceral adipose accumulation. Resulting metabolic and vascular dysfunction, including inflammation, insulin and leptin resistance, and hypertension, have emerged as key risks to depression and anxiety development. Recent research advancements are exposing the important contribution of these different corollaries of obesity and their impact on neuroimmune status and the neural circuits controlling mood and emotional states. Along these lines, this review connects the clinical manifestations of depression and anxiety in obesity to our current understanding of the origins and biology of immunometabolic threats to central nervous system function and behavior.
Overview
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Written from the paper’s full text.
TL;DR
This review argues that obesity raises the risk of depression and anxiety mainly through immunometabolic and neuroinflammatory consequences of poor diet, inactivity, and visceral adiposity, rather than body weight alone. It synthesizes human epidemiological and rodent mechanistic evidence linking adipose and gut inflammation, neuroinflammation, neuroplastic and monoamine changes, and endocrine dysfunction to mood disorders.
Key findings
- Obesity increases depression risk: a meta-analytic overview cited by the review reports that obese adults self-reporting symptoms have 23–36% increased odds of developing depressed mood versus nonobese controls, while clinically diagnosed MDD is elevated by 14–34%; obese adolescents have a 40% increased risk of being depressed.
- Obesity also increases anxiety risk: the review states obesity heightens the odds of an anxiety disorder or anxiety symptoms by 30% and 40%, respectively, with a stronger relationship for severe obesity (BMI ≥ 35); diabetes is associated with a 48% greater likelihood of anxiety symptoms and a 20% higher risk of developing an anxiety disorder.
- Sex and metabolic status matter: depression and anxiety disorder diagnoses are approximately double for obese women compared with obese men, and metabolically healthy obese individuals show either no increased risk or a modest elevated risk of depression diagnosis versus nonobese controls.
- Proposed mechanisms include saturated fat and sugar intake, visceral adipose expansion, gut dysbiosis, peripheral inflammation (e.g., CRP, IL-6, TNFα), insulin and leptin resistance, HPA dysregulation, neuroinflammation, altered corticolimbic circuits, monoamine imbalances, and reduced hippocampal neurogenesis.
Methods
- Narrative review; no primary data collection, systematic search, or meta-analysis is reported.
- Synthesizes clinical and epidemiological observations with rodent models of diet-induced obesity, high-fat/high-sugar feeding, and depressive- or anxiety-like behaviors.
- Main analysis is qualitative integration of evidence across immunometabolic, neuroinflammatory, neural circuit, monoamine, and endocrine domains.
Limitations
- Stated: the causal relationship of diet-induced obesity to depression and anxiety in human studies is indirect; the literature linking inflammation to anxiety is much sparser; microbiota alterations across studies are conflicting and mechanisms remain unclear; the precise contribution of HPA activity and insulin’s role in mood circuits remain to be established; and it remains poorly understood to what degree particular changes are causal or a consequence of mood and metabolic changes.
- Stated: human leptin studies are limited, and evidence for depression and obesity comorbidity is described as limited in the concluding remarks.
- Evident: as a narrative review, it does not systematically quantify or appraise the evidence, and much mechanistic support comes from rodent models, so human causality and effect sizes are not established by this paper itself.
Model-written summary. Check it against the paper before relying on it.
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Claims the paper makes
91 Not checked yet · 21 Own interpretation · 1 Partly supported · 1 No basis given · accuracy not yet measured
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Chronic changes in microbiota composition in obesity (dysbiosis) are associated with inflammation, insulin resistance, and mental health deficits [72].”
What the sources say
- Partly supportedcites [72] sourceExperimental — accuracy not yet measured
Section 3.8.1.1 reports associations between gut microbes and a wellbeing score in people with morbid obesity, supporting the mental-health aspect in a limited sense. It does not establish that chronic dysbiosis in obesity is associated with inflammation or insulin resistance; the search for insulin resistance found it only in a reference title. Section 4.11.1 also says evidence linking microbial-derived metabolites to psychological measures in obesity is insufficient. No page numbers were available in our copy. (LLM, conf=0.84)
plaincorrelational- Asserted: passes — The authors put it forward as true.
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- Partly supported
In the paper
“Emphasizing the importance of early detection and treatment, a longitudinal meta-analysis suggests that obese adolescents have a 40% increased risk of being depressed [19].”
What the sources say
- Not checked yetcites [19] source
hedgedcorrelational- Asserted: passes — The authors put it forward as true.
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- 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
“A meta-analytic overview illustrates that obese adults self-reporting symptoms have 23-36% increased odds of developing depressed mood as compared with nonobese controls, whereas clinically diagnosed MDD is elevated by 14-34% [2].”
What the sources say
- Not checked yetcites [2] source
plaincorrelational- 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
“Obesity is coupled to various structural and functional changes in the brain that are remarkably similar to those observed in depressive disorders, such as regionspecific increases in cell density and compromised neural connectivity and excitability [5,6].”
plaincorrelational- 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
“The odds of developing major depressive disorder (MDD) and anxiety increase as a function of the number of coexisting metabolic impairments, such as those characteristic of metabolic syndrome [3,4].”
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 similar positive relationship is observed with anxiety: obesity heightens the odds of an anxiety disorder or anxiety symptoms (e.g., dread, unease) by 30% and 40%, respectively [1,20].”
plaindirect- Asserted: passes — The authors put it forward as true.
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- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
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In the paper
“The odds of depression are higher when evaluating the waist-to-hip ratio [16,17] which provides a better estimate of visceral adiposity and metabolic dysfunction than BMI [18].”
What the sources say
- Not checked yetcites [18] source
plaincorrelational- Asserted: passes — The authors put it forward as true.
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- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
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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
“Mounting evidence reveals that the psychiatric consequences of obesity stem from poor diet, inactivity, and visceral adipose accumulation.”
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: unclear — It is unclear why the paper says it holds.
None of the sources cited for this claim have been checked yet.
In the paper
“This form of depression has stronger links to peripheral [10,11] and central [12] inflammation.”
What the sources say
boostedcorrelational- 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
“An elevated body mass index (BMI) is predictive of a chronic course of depressive and anxiety symptoms [1,2].”
plaincorrelational- Asserted: passes — The authors put it forward as true.
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- It may state two separate claims as one. 38
- Probably not a substantial claim. 4
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
“As atypical depression is predictive of overeating and weight gain, and metabolic risks can be intensified by antidepressant treatments that encourage weight gain, a vicious cycle can promote disease progression.”
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 odds of depression are higher when evaluating the waist-to-hip ratio [16,17] which provides a better estimate of visceral adiposity and metabolic dysfunction than BMI [18].”
- Also stated in: § Adipose expansion · plain
“Correspondingly, depression incidence is higher when assessing abdominal adiposity or the waist-to-hip ratio as compared with BMI [17].”
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.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Also stated in: § Adipose expansion · plain
In the paper
“There is a bidirectional association between being overweight (BMI ≥ 25-29.99)and depression in men and women, a relationship that is stronger for obesity (BMI ≥ 30) [15].”
What the sources say
- Not checked yetcites [15] source
plaincorrelational- 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
“Neuroinflammation alters structure, excitability, and connectivity in corticolimbic networks controlling mood, motivation, and emotion.”
plaindirect- Asserted: passes — The authors put it forward as true.
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- 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.
- Rests on an assumption: Findings from rodent models of obesity and depressive- and anxiety-like behaviors translate to human depression and anxiety.
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
“Adipose-and gut-derived inflammation and changes in brain nutrient composition stimulate neuroinflammation.”
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: fails — The paper may give no reason why it holds.
Probably not a substantial claim. The paper may give no reason why it holds.
- Rests on an assumption: Findings from rodent models of obesity and depressive- and anxiety-like behaviors translate to human depression and anxiety.
- Rests on an assumption: Gut microbiota alterations observed in diet-induced obese mice translate to human obesity-related mood dysfunction.
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
“Diets that include excess saturated fat and sugar intake promote metabolic dysfunction, neuroinflammation, and mental health impairments.”
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: unclear — It is unclear why the paper says it holds.
It may state two separate claims as one.
- Rests on an assumption: Findings from rodent models of obesity and depressive- and anxiety-like behaviors translate to human depression and anxiety.
None of the sources cited for this claim have been checked yet.
In the paper
“Individuals with atypical depression often have a more unrelenting course of depression [13], in part because they show a poorer response to antidepressants [14].”
What the sources say
- Not checked yetcites [13]
- Not checked yetcites [14] source
plaindirect- Asserted: passes — The authors put it forward as true.
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- 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.
In the paper
“Both EPA and DHA limit the inflammatory effect of eicosanoids derived from arachidonic acid, an omega-6 fatty acid with plasma levels that positively correlate with MDD severity and reduced serotonin transporter binding in the brain [50].”
What the sources say
- Not checked yetcites [50] source
plaincorrelational- Asserted: passes — The authors put it forward as true.
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- 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.
In the paper
“Moreover, chronic saturated high-fat feeding increases saturated fatty acid levels and appreciably decreases PUFA levels in the brain of rodents [49], changes that are likely one means by which saturated dietary fats generate neuroinflammatory responses and mood deficits.”
What the sources say
- Not checked yetcites [49] source
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.
- Rests on an assumption: Findings from rodent models of obesity and depressive- and anxiety-like behaviors translate to human depression and anxiety.
None of the sources cited for this claim have been checked yet.
In the paper
“Consumption of saturated fats [26] and plasma concentrations of the saturated fatty acid palmitate [27] positively correlate with depressive symptoms and plasma levels of the acute phase reactant C-reactive protein (CRP) in humans.”
plaincorrelational- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
In the paper
“In contrast, low levels of blood n-3 PUFA correlate with heightened inflammatory status and depression risk in humans, whereas imposed dietary n-3 deficiency in rodents diminishes brain n-3 levels and stimulates neuroinflammation and anxiety-and depressive-like behaviors [47].”
What the sources say
- Not checked yetcites [47] source
plaindirect- Asserted: passes — The authors put it forward as true.
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- 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.
- Rests on an assumption: Findings from rodent models of obesity and depressive- and anxiety-like behaviors translate to human depression and anxiety.
None of the sources cited for this claim have been checked yet.
In the paper
“Several reports link higher n-3 consumption with lower prevalence and severity of mood disturbances in humans [45] and demonstrate that n-3 supplementation dampens neuroinflammation and attenuates behavioral indices of mood deficits in rodents [46,47].”
boosteddirect- 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.
- Rests on an assumption: Findings from rodent models of obesity and depressive- and anxiety-like behaviors translate to human depression and anxiety.
None of the sources cited for this claim have been checked yet.
In the paper
“To this end, rodent research has revealed that prolonged high-fat diet (HFD) elicits metabolic dysfunction and increases anxiety-and depressive-like behaviors [28][29][30][31][32][33][34][35][36], heightens stress and hypothalamic-pituitary-adrenal (HPA) responses [37,38], and triggers neurobehavioral deficits associated with blunted mesolimbic dopamine function [39][40][41].”
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.
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It may state two separate claims as one.
- Rests on an assumption: Findings from rodent models of obesity and depressive- and anxiety-like behaviors translate to human depression and anxiety.
In the paper
“Correspondingly, the prevalence of MDD is nearly twice as high in people with type 2 diabetes [159] and more than threefold higher in people with type 1 diabetes than those without, with greater rates in diabetic women than men [160].”
What the sources say
- Not checked yetcites [160] source
plaincorrelational- Asserted: passes — The authors put it forward as true.
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Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
In the paper
“In contrast, low levels of blood n-3 PUFA correlate with heightened inflammatory status and depression risk in humans, whereas imposed dietary n-3 deficiency in rodents diminishes brain n-3 levels and stimulates neuroinflammation and anxiety-and depressive-like behaviors [47].”
What the sources say
- Not checked yetcites [47] source
plaincorrelational- Asserted: passes — The authors put it forward as true.
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- 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
“Oleate, a monounsaturated fatty acid enriched in olive oil, can improve glycemic control and plasma lipid profiles in humans and protect against inflammation, hyperphagia, and anxiodepressive behaviors in mice [34,42].”
plaindirect- Asserted: passes — The authors put it forward as true.
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- 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.
- Rests on an assumption: Findings from rodent models of obesity and depressive- and anxiety-like behaviors translate to human depression and anxiety.
None of the sources cited for this claim have been checked yet.
In the paper
“Diet is the primary effector of microbiota composition, but psychological stress can also modulate flora in rodents and in patients with MDD [69,70].”
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
“Likewise, individuals suffering from anxiety disorders can exhibit elevated circulating levels of inflammatory markers, including CRP, IL-1β, IL-6, and TNFα [63]; however, the literature linking inflammation to anxiety is much sparser.”
plaincorrelational- Asserted: passes — The authors put it forward as true.
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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
“Notably, both the obese phenotype [73] and anxiodepressive behaviors [74] are transmissible by transplanting gut microbiota of DIO to normal-weight, germ-free mice.”
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.
- Rests on an assumption: Gut microbiota alterations observed in diet-induced obese mice translate to human obesity-related mood dysfunction.
In the paper
“Notably, large cohort studies report higher CRP concentrations in depressed patients, making heightened CRP levels in obesity one of the best predictors of depression onset, particularly atypical depression [66].”
What the sources say
- Not checked yetcites [66] source
boostedcorrelational- Asserted: passes — The authors put it forward as true.
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In the paper
“Hypertension is a leading risk factor for depression incidence in obesity and causes neurovascular changes that involve the actions of perivascular macrophages to stimulate oxidative stress and inflammation that lead to cognitive dysfunction [166].”
What the sources say
- Not checked yetcites [166] 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
“Several bacteria can produce other metabolites that can impact physiology and health, such as short-chain fatty acids, and several molecules with that can affect neural signaling and excitability in mood networks, including serotonin and gamma-aminobutyric acid (GABA) [69].”
What the sources say
- Not checked yetcites [69] source
plaindirect- Asserted: passes — The authors put it forward as true.
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- 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
“The breakdown of the BBB produced by peripheral immune challenge (LPS) permits passage of bone marrow-derived immune cells into the brain, a process enhanced by DIO [163] and that favors depressive behaviors [164,165].”
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.
- Rests on an assumption: Findings from rodent models of obesity and depressive- and anxiety-like behaviors translate to human depression and anxiety.
In the paper
“Microglia dominate as contributors to neuroinflammation and several reports underscore their role in the neuroimmune pathogenesis of depression [77].”
What the sources say
- Not checked yetcites [77] source
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“Deletion of T cell-dependent immunoglobulin A production enhances obesity, while reducing the abundance and diversity of Clostridium [75].”
What the sources say
- Not checked yetcites [75] 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
“However, in the absence of obesity development, these diets can still potentiate HPA reactivity [37] and feedback [38] and suppress behavioral responses to rewards [41].”
What the sources say
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.
- Rests on an assumption: Findings from rodent models of obesity and depressive- and anxiety-like behaviors translate to human depression and anxiety.
In the paper
“Interestingly, significant reduction of Clostridium is also observed in MDD patients and its abundance is negatively correlated to the severity of anxiety and depression [70].”
What the sources say
- Not checked yetcites [70] source
plaincorrelational- Asserted: passes — The authors put it forward as true.
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In the paper
“Obese individuals exhibiting elevated inflammation, particularly increases in CRP, are more likely to meet criteria for metabolic syndrome and to develop MDD and anxiety [65].”
What the sources say
- Not checked yetcites [65] source
hedgedcorrelational- Asserted: passes — The authors put it forward as true.
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In the paper
“Excess fat and sugar consumption favor the accumulation of visceral adipose tissue, which comprises a higher concentration of saturated fatty acids and is especially vulnerable to immune insults as compared with subcutaneous fat [18].”
What the sources say
- Not checked yetcites [18] 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
“In addition, monocytes can infiltrate the brain and differentiate into microglia that produce an inflammatory response that contributes to anxiety-like behavior [78].”
What the sources say
- Not checked yetcites [78] 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.
- Rests on an assumption: Findings from rodent models of obesity and depressive- and anxiety-like behaviors translate to human depression and anxiety.
None of the sources cited for this claim have been checked yet.
In the paper
“Dietary-derived saturated fatty acids [26] and erythrocyte content of saturated fatty acids (indicator of long-term consumption) [27], positively correlate with circulating measures of CRP and can contribute to inflammation by favoring TLR4 signaling in macrophages [67].”
What the sources say
plainconditional- 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
“Moreover, the microbiota from DIO mice can weaken endothelial tight junctions and trigger inflammation in both intestine and brain and promote brain insulin resistance [73,74].”
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.
- Rests on an assumption: Gut microbiota alterations observed in diet-induced obese mice translate to human obesity-related mood dysfunction.
In the paper
“As these immunometabolic consequences heighten the risk of depression [3], abdominal adipose expansion plays a central role in the transmission of peripheral inflammation to the CNS.”
What the sources say
- Not checked yetcites [3] source
plaindirect- Asserted: passes — The authors put it forward as true.
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- Load-bearing: passes — The paper’s conclusions depend on it.
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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
“Peripheral immune activation figures prominently in the pathophysiology of psychiatric and metabolic disorders and resonates as a prime instigator of depression onset in obesity.”
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
“In turn, both diet and serum indices of inflammation associate with indices of emotional distress.”
plaincorrelational- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
In the paper
“While changes in microbiota composition are reported in individuals with MDD and can correlate with disease severity, the nature of microbiota alterations across studies are conflicting [76].”
What the sources say
- Not checked yetcites [76] source
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.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“chronic HFD exposure in rodents, leading to obesity, gives rise to impairments in prefrontal cortex-dependent functions that are accompanied by changes in dendritic spine density and synaptic remodeling [105].”
What the sources say
- Not checked yetcites [105] source
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.
In the paper
“HPA dysregulation contributes to weight gain in stressed individuals via the actions of cortisol to trigger palatable food intake through brain GC receptors, an effect that leads to reduced HPA activity and short-term relief of negative affective states [119].”
What the sources say
- Not checked yetcites [119] source
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.
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
“These collective findings suggest that diabetes treatments could be repositioned to improve both depressive symptoms and diabetes concurrently and perhaps as an add-on strategy to improve the efficacy of other antidepressant drugs.”
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.
In the paper
“obesity-induced increases in neuroinflammation were recently shown to suppress serotonin signaling by increasing its clearance from the synaptic cleft in the hippocampus [110], findings that provide a potential synaptic mechanism for reduced SSRI responsiveness in obese individuals with depression.”
What the sources say
- Not checked yetcites [110] source
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.
None of the sources cited for this claim have been checked yet.
In the paper
“leptin resistance can elicit depressive-like behaviors in rats [144] and is associated with atypical features of depression (increased appetite and weight) in humans [145].”
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.
The paper relies on this without support.
Findings from rodent models of obesity and depressive- and anxiety-like behaviors translate to human depression and anxiety.
“Clinical observations combined with rodent models of obesity exhibiting depressive-and anxiety-like behaviors are proving valuable for uncovering the immunometabolic and neural mechanisms”
“To this end, rodent research has revealed that prolonged high-fat diet (HFD) elicits metabolic dysfunction and increases anxiety-and depressive-like behaviors [28][29][30][31][32][33][34][35][36], heightens stress and hypothalamic-pituitary-adrenal (HPA) responses [37,38], and triggers neurobehavioral deficits associated with blunted mesolimbic dopamine function [39][40][41].”
The paper relies on this without support.
Gut microbiota alterations observed in diet-induced obese mice translate to human obesity-related mood dysfunction.
“Notably, both the obese phenotype [73] and anxiodepressive behaviors [74] are transmissible by transplanting gut microbiota of DIO to normal-weight, germ-free mice.”
The paper relies on this without support.
Findings from rodent models of diet-induced obesity and depressive/anxiety-like behaviors can be generalized to human obesity-induced depression and anxiety.
“The collective findings in rodents, along with reports of structural and functional changes in obese humans, support the clinical relevance of this mechanism.”
The paper relies on this without support.
Obesity causally contributes to the development of depression and anxiety, rather than being solely a consequence or correlated.
“New research developments uncovering the metabolic and neurobiological mechanisms by which obesity heightens the risk of depression and anxiety will prove valuable for evaluating new treatment strategies”
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
“Even if depression is known to be associated with obesity [56,57], evidences are lacking in SO.”
From Identification of factors associated with sarcopenic obesity development: Literature review and expert panel voting (2024) · cites this paper as [57]
Citations
Cites
Physiology and neurobiology of stress and adaptation: central role of the brain
McEwen, B. S. (2007) · Physiological Reviews · doi:10.1152/physrev.00041.2006 · Cited by 5,429 · cited 1×
“life stress presents a particular risk for the development of clinical depression or anxiety disorders in adulthood [117].”
BackgroundOverweight, Obesity, and Depression: A Systematic Review and Meta-analysis of Longitudinal Studies
Luppino, F. S., de Wit, L. M., Bouvy, P. F., Stijnen, T., Cuijpers, P., Penninx, B. W. J. H., & Zitman, F. G. (2010) · Archives of General Psychiatry · doi:10.1001/archgenpsychiatry.2010.2 · Cited by 4,322 · cited 1×
“99) and depression in men and women, a relationship that is stronger for obesity (BMI ≥ 30) [15].”
BackgroundThe role of inflammation in depression: from evolutionary imperative to modern treatment target
Miller, A. H., & Raison, C. L. (2016) · Nature Reviews Immunology · doi:10.1038/nri.2015.5 · Cited by 3,942
TLR4 links innate immunity and fatty acid-induced insulin resistance
Shi, H., Kokoeva, M. V., Inouye, K., Tzameli, I., Yin, H., & Flier, J. S. (2006) · Journal of Clinical Investigation · doi:10.1172/jci28898 · Cited by 3,690
Ross, R., Neeland, I. J., Yamashita, S., Shai, I., Seidell, J., Magni, P., Santos, R. D., Arsenault, B., Cuevas, A., Hu, F. B., et al. (2020) · Nature Reviews Endocrinology · doi:10.1038/s41574-019-0310-7 · Cited by 1,966 · cited 8×
“This sex distinction in incidence narrows considerably in conditions of severe obesity (BMI ≥ 40) [1].”
BackgroundInfluentialChronic stress, glucocorticoid receptor resistance, inflammation, and disease risk
Cohen, S., Janicki-Deverts, D., Doyle, W. J., Miller, G. E., Frank, E., Rabin, B. S., & Turner, R. B. (2012) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1118355109 · Cited by 1,419 · cited 1×
“However, chronic stress is associated with downregulation of GC receptormediated transcriptional activity, resulting in GC insensitivity and loss of anti-inflammatory feedback [120].”
BackgroundEpidemiology of depression and diabetes: a systematic review
Roy, T., & Lloyd, C. E. (2012) · Journal of Affective Disorders · doi:10.1016/s0165-0327(12)70004-6 · Cited by 1,229
Depression and obesity: evidence of shared biological mechanisms
Milaneschi, Y., Simmons, W. K., van Rossum, E. F. C., & Penninx, B. W. (2019) · Molecular Psychiatry · doi:10.1038/s41380-018-0017-5 · Cited by 1,073 · cited 2×
“A meta-analytic overview illustrates that obese adults self-reporting symptoms have 23–36% increased odds of developing depressed mood as compared with nonobese controls, whereas clinically diagnosed MDD is elevated by 14–34% [2].”
BackgroundSocial stress induces neurovascular pathology promoting depression
Menard, C., Pfau, M. L., Hodes, G. E., Kana, V., Wang, V. X., Bouchard, S., Takahashi, A., Flanigan, M. E., Aleyasin, H., LeClair, K. B., et al. (2017) · Nature Neuroscience · doi:10.1038/s41593-017-0010-3 · Cited by 1,028
Targeting abnormal neural circuits in mood and anxiety disorders: from the laboratory to the clinic
Ressler, K. J., & Mayberg, H. S. (2007) · Nature Neuroscience · doi:10.1038/nn1944 · Cited by 1,007 · cited 1×
“As targets of deep-brain stimulation therapy, both nucleus accumbens and ventral anterior cingulate cortex stimulation are associatedwith strong antidepressant effects in treatment-resistant MDD patients [83].”
Background
Cited by
Sorted by citations
Kunugi, H. (2023) · Psychiatry and Clinical Neurosciences · doi:10.1111/pcn.13551 · Cited by 117
“In addition to inflammation, insulin resistance and leptin resistance are supposed to be involved in the pathophysiology of the bidirectional relationship between depression and excessive energy intake.(196) A molecular basis underlying the antidepressant actions of calorie restriction might involve orexin signaling a…”
BackgroundNeural interfaces: Bridging the brain to the world beyond healthcare
Xu, S., Liu, Y., Lee, H., & Li, W. (2024) · Exploration · doi:10.1002/exp.20230146 · Cited by 102
Tobaiqy, M. A., & Elkout, H. (2024) · International Journal of Clinical Pharmacy · doi:10.1007/s11096-023-01694-7 · Cited by 119
“Although obesity may increase the risk of psychiatric disorders, mental health conditions also contribute to the development or worsening of obesity through various mechanisms such as emotional eating and decreased motivation for physical activity [34, 35].”
BackgroundObesity: pathophysiology and therapeutic interventions
Kong, Y., Yang, H., Nie, R., Zhang, X., Zuo, F., Zhang, H., & Nian, X. (2025) · Molecular Biomedicine · doi:10.1186/s43556-025-00264-9 · Cited by 89
GLP-1 agonists for weight loss: pharmacology and clinical implications.
Moore, P. W., Malone, K., VanValkenburg, D., Rando, L. L., Williams, B. C., Matejowsky, H. G., Ahmadzadeh, S., Shekoohi, S., Cornett, E. M., & Kaye, A. D. (2023) · Advances in Therapy · doi:10.1007/s12325-022-02394-w · Cited by 86
“Regarding the mental consequences of obesity, poor diet and lack of exercise, chronic inflammation, and insulin and leptin resistance have been identified as key risk factors for developing depression and anxiety [6].”
Background
Metadata
- Authors
- Fulton, S., Décarie-Spain, L., Fioramonti, X., Guiard, B., & Nakajima, S.
- Affiliations
- Centre Hospitalier de l’Université de Montréal (CA)
- Université de Bordeaux (FR)
- Centre National de la Recherche Scientifique (FR)
- Corresponding author
- Fulton, Stephanie
- Venue
- Trends in Endocrinology & Metabolism
- Publisher
- Elsevier BV
- Published
- 2022-01
- Volume
- 33
- Issue
- 1
- Pages
- 18-35
- ISSN
- 1043-2760 (ISSN-L)
- OpenAlex
- W3213132689
- Semantic Scholar
- 7810f6a48f94176d175f9ea2f8ab49f150c84578
- Cited by
- 441
- References
- 173
- Citations by year
- 2026: 75 · 2025: 135 · 2024: 100 · 2023: 92 · 2022: 39
- FWCI
- 5.46
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Trends in Endocrinology and Metabolism (publishedVersion, cc-by-nc-nd)
- PubMed (publishedVersion)
- HAL (submittedVersion, cc-by-nc-nd)
- Oskar-Bordeaux (Universite de Bordeaux) (submittedVersion, cc-by-nc-nd)
- Funders
- Fonds de Recherche du Québec - Santé
- Japan Society for the Promotion of Science
- Topics
- Life Sciences › Neuroscience › Biological Psychiatry › Tryptophan and brain disorders
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Adipokines, Inflammation, and Metabolic Diseases
- Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Regulation of Appetite and Obesity
- Keywords
- obesity, depression, anxiety, neuroinflammation, insulin resistance, leptin resistance, visceral adipose tissue, hypertension, metabolic dysfunction, neuroimmune dysfunction, mood regulation
- MeSH terms
- Anxiety, Depression, Humans, Inflammation, Obesity, Prevalence
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.
A language model drew the claims from the paper on 2026-10-09, under version 3 of the claim definition (model deepseek-v4.1-flash, prompt extract-v3).
A second model labelled each claim on 2026-10-09 (model jev-1.13-20260917, definition revision gold-guideline-v0.2).
Cited sources are checked with a language model’s help (gpt-6-sol).
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
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