The DOI matches its Crossref record; 167 of the 173 references it cites were found in a registry or an index; none of the 136 sources its claims cite is checked for support yet.
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
AI snapshot
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.
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
92 Not checked yet · 21 Own interpretation · 1 No basis given
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.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“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.
- 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.
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.
- 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.
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.
- 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.
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.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“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.
- 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.
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.
- Based: passes — The paper gives a reason why it holds.
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.
- 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.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“The incidence of depression and anxiety is amplified by obesity.”
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. 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.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“The 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.
- 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
“Neuroinflammation alters structure, excitability, and connectivity in corticolimbic networks controlling mood, motivation, and emotion.”
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.
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.
- 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
“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.
- 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
“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.
- 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
“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.
- 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
“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.
- 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
“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.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
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.
- 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
“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.
- 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
“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.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“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.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
None of the sources cited for this claim have been checked yet.
In the paper
“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.
- 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
“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.
- 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
“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.
- 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
“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.
- 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
“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.
- 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
“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.
- 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
“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.
- 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
“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.
- 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
“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.
- 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
“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.
- 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
“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.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“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.
- 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
“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.
- 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
“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.
- 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
“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].”
BackgroundBizzozero‐Peroni, B., Martínez‐Vizcaíno, V., Fernández‐Rodríguez, R., Jiménez‐López, E., de Arenas‐Arroyo, S. N., Saz‐Lara, A., Goñi, V. D., & Mesas, A. E. (2023) · Nutrition Reviews · doi:10.1093/nutrit/nuad176 · Cited by 92
Shared biological mechanisms of depression and obesity: focus on adipokines and lipokines
Fu, X., Wang, Y., Zhao, F., Cui, R., Xie, W., Liu, Q., & Yang, W. (2023) · Aging · doi:10.18632/aging.204847 · Cited by 86
The impact of obesity: a narrative review
Lam, B. C. C., Lim, A. Y. L., Chan, S. L., Yum, M. P. S., Koh, N. S. Y., & Finkelstein, E. A. (2023) · Singapore Medical Journal · doi:10.4103/singaporemedj.smj-2022-232 · Cited by 74
“either directly or indirectly impact the control of emotions and mood.[73,74] Hence, the causal relationship between obesity and”
Backgroundde Paiva, I. H. R., Maciel, L. M., da Silva, R. S., Mendonça, I. P., de Souza, J. R. B., & Peixoto, C. A. (2024) · Food Research International · doi:10.1016/j.foodres.2024.114153 · Cited by 73
Zhang, Q., Jin, K., Chen, B., Liu, R., Cheng, S., Zhang, Y., & Lü, J. (2022) · Frontiers in Neuroscience · doi:10.3389/fnins.2022.884579 · Cited by 65
“The resulting metabolic and inflammatory dysfunction of obesity played a role in developing depression with an impact on the neuroimmune status and neural circuits controlling mood and emotional states (Fulton et al., 2022).”
BackgroundDoes intermittent fasting impact mental disorders? A systematic review with meta-analysis
Fernández‐Rodríguez, R., Martínez‐Vizcaíno, V., Mesas, A. E., Notario‐Pacheco, B., Medrano, M., & Heilbronn, L. K. (2022) · Critical Reviews in Food Science and Nutrition · doi:10.1080/10408398.2022.2088687 · Cited by 64
“In this sense, prevalence of obesity is also rapidly increasing (Grannell et al. 2021) with a bidirectional relationship between mental disorders and metabolic dysfunction caused by excess adiposity (Fulton et al. 2022).”
BackgroundKokka, I., Mourikis, I., & Bacopoulou, F. (2023) · Children · doi:10.3390/children10020285 · Cited by 64
“In addition, manifestations of these disorders at a cognitive and behavioral level may complicate and obstruct compliance to health management interventions, such as weight regulation [73].”
Backgroundde Wit, L. M., ten Have, M., Cuijpers, P. J., & de Graaf, R. (2022) · BMC Psychiatry · doi:10.1186/s12888-022-04077-w · Cited by 54
“Both psychological as well as biological factors seem to have an influence on the association [15, 16, 18, 19].”
BackgroundHigh-fat diet and neuroinflammation: The role of mitochondria
Song, M., Bai, Y., & Song, F. (2025) · Pharmacological Research · doi:10.1016/j.phrs.2025.107615 · Cited by 60
Pharmacologic Treatment of Obesity in Reproductive Aged Women
Nuako, A. A., Tu, L., Reyes, K. J. C., Chhabria, S. M., & Stanford, F. C. (2023) · Current Obstetrics and Gynecology Reports · doi:10.1007/s13669-023-00350-1 · Cited by 57
Lin, M.-H., Cheng, P.-C., Hsiao, P.-J., Chen, S.-C., Hung, C.-H., Kuo, C.-H., Huang, S.-K., & Clair Chiou, H.-Y. (2023) · International Immunopharmacology · doi:10.1016/j.intimp.2022.109653 · Cited by 42
Depression and obesity: Focus on factors and mechanistic links
Selman, A., Dai, J., Driskill, J., Reddy, A. P., & Reddy, P. H. (2024) · Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease · doi:10.1016/j.bbadis.2024.167561 · Cited by 48
Wang, Z., Cheng, Y., Li, Y., Han, J., Yuan, Z., Li, Q., Zhong, F., Wu, Y., Fan, X., Bo, T., et al. (2022) · Frontiers in Endocrinology · doi:10.3389/fendo.2022.880230 · Cited by 42
“org 5 contribute to the occurrence and development of depression (13).”
BackgroundIt’s not the thought that counts: Allostasis at the core of brain function
Theriault, J. E., Katsumi, Y., Reimann, H. M., Zhang, J., Deming, P., Dickerson, B. C., Quigley, K. S., & Barrett, L. F. (2025) · Neuron · doi:10.1016/j.neuron.2025.09.028 · Cited by 64
Comorbidity of Anxiety and Hypertension: Common Risk Factors and Potential Mechanisms
Qiu, T., Jiang, Z., Chen, X., Dai, Y., & Zhao, H. (2023) · International Journal of Hypertension · doi:10.1155/2023/9619388 · Cited by 69
GDF15 links adipose tissue lipolysis with anxiety
Townsend, L. K., Wang, D., Knuth, C. M., Fayyazi, R., Mohammad, A., Becker, L. J., Tsakiridis, E. E., Desjardins, E. M., Patel, Z., Valvano, C. M., et al. (2025) · Nature Metabolism · doi:10.1038/s42255-025-01264-3 · Cited by 42
“48).”
Valentin‐Escalera, J., Leclerc, M., & Calon, F. (2024) · Journal of Alzheimer s Disease · doi:10.3233/jad-230118 · Cited by 37
The global prevalence of overweight and obesity among nurses: A systematic review and meta‐analyses
Sadali, U. B., Kamal, K. K. B. N., Park, J., Chew, H. S. J., & Devi, M. K. (2023) · Journal of Clinical Nursing · doi:10.1111/jocn.16861 · Cited by 36
Lama, A., Piano, F. D., Annunziata, C., Comella, F., Opallo, N., Melini, S., Grumetto, L., Pirozzi, C., Raso, G. M., Meli, R., et al. (2022) · Life Sciences · doi:10.1016/j.lfs.2022.121301 · Cited by 29
Mindful eating for weight loss in women with obesity: a randomised controlled trial
Pepe, R. B., Coelho, G. S. D. M. A., Miguel, F. D. S., Gualassi, A. C., Sarvas, M. M., Cercato, C., Mancini, M. C., & de Melo, M. E. (2022) · British Journal Of Nutrition · doi:10.1017/s0007114522003932 · Cited by 30
“Mental health is also a concern in individuals with obesity, with studies reporting high rates of depression(3,4), stress(5) and anxiety(6) among this population.”
BackgroundGe, Z., Hu, Y., Kan, W., Li, L., Xu, J., Zhang, Y., Zheng, N., Wang, G., & Du, J. (2025) · Frontiers in Immunology · doi:10.3389/fimmu.2025.1625087 · Cited by 34
McCall, K. L., Mastro, K. A., Casey, R. T., Samana, T. N., Sulicz, E. K., Tso, S. Y., Yalanzhi, E. R., & Piper, B. J. (2025) · Expert Opinion on Drug Safety · doi:10.1080/14740338.2025.2499670 · Cited by 31
“Depression itself is associated with chronic diseases such as diabetes and obesity [24,25].”
Qi, R., Sheng, B., Zhou, L., Chen, Y., Sun, L., & Zhang, X. (2023) · Nutrients · doi:10.3390/nu15122721 · Cited by 29
The enigma of vascular depression in old age: a critical update
Jellinger, K. A. (2022) · Journal of Neural Transmission · doi:10.1007/s00702-022-02521-5 · Cited by 27
Gallagher, C., Pirkis, J., Lambert, K. A., Perret, J. L., Ali, G. B., Lodge, C., Bowatte, G., Hamilton, G. S., Matheson, M. C., Bui, D., et al. (2023) · International Journal of Obesity · doi:10.1038/s41366-023-01312-6 · Cited by 26
“as a key catalyst for depression, and possibly anxiety, by triggering dysregulation of the hypothalamic-pituitary-adrenal axis, with activated immune-inflammatory pathways inducing neuroendocrine abnormalities [24].”
BackgroundFan, Y., Zhao, L., Deng, Z., Li, M., Huang, Z., Zhu, M., & Xu, W. (2022) · Frontiers in Psychiatry · doi:10.3389/fpsyt.2022.936283 · Cited by 25
“The prevalence of depression is known to be increased in the setting of obesity, a condition that promotes inflammation as well as resistance to insulin and leptin (43, 44).”
BackgroundGains and Losses: Resilience to Social Defeat Stress in Adolescent Female Mice
Pantoja-Urbán, A. H., Richer, S., Mittermaier, A., Giroux, M., Nouel, D., Hernández, G., & Flores, C. (2023) · Biological Psychiatry · doi:10.1016/j.biopsych.2023.06.014 · Cited by 29
Pinel, A., Guillet, C., Capel, F., Pouget, M., De Antonio, M., Pereira, B., Topinkova, E., Eglseer, D., Barazzoni, R., Cruz-Jentoft, A. J., et al. (2024) · Clinical Nutrition · doi:10.1016/j.clnu.2024.04.033 · Cited by 24
Zhao, D., Chen, Y., Xia, J., Li, Z., Kang, Y., Xiao, Z., & Niu, Y. (2024) · Trends in Food Science & Technology · doi:10.1016/j.tifs.2024.104602 · Cited by 25
Zheng, Y., Yin, K., Li, L., Wang, X., Li, H., Li, W., & Fang, Z. (2024) · Journal of Affective Disorders · doi:10.1016/j.jad.2024.06.103 · Cited by 24
Glucose metabolism impairment in major depressive disorder
Meng, F., Wang, J., Wang, L., & Zou, W. (2025) · Brain Research Bulletin · doi:10.1016/j.brainresbull.2025.111191 · Cited by 26
Zhang, W., Nan, N., He, Y., Zuo, H., Song, X., Zhang, M., & Zhou, Y. (2022) · Psychology Health & Medicine · doi:10.1080/13548506.2022.2104885 · Cited by 25
“The link between obesity and depression and anxiety has also been proved by some studies (Fulton et al., 2022; Wang et al., 2019).”
ResultZhang, S., Lin, T., Zhang, Y., Liu, X., & Huang, H. (2022) · PLoS ONE · doi:10.1371/journal.pone.0276469 · Cited by 27
Yu, H., Yu, B., Qin, X., & Shan, W. (2023) · Journal of Affective Disorders · doi:10.1016/j.jad.2023.07.005 · Cited by 25
Nakajima, S., Demers, G., Machuca‐Parra, A. I., Pour, Z. D., Bairamian, D., Bouyakdan, K., Fisette, A., Kabahizi, A., Robb, J. L., Rodaros, D., et al. (2023) · Journal of Neuroinflammation · doi:10.1186/s12974-023-02978-5 · Cited by 25
“…and if GPR120 stimulation protects against the activation of NAc microglia in response to central of TNF-α and IL-1β—two cytokines required for the innate immune response, that influence affective states and that are upregulated in the brain in response to systemic LPS, stress and obesity [2, 29].”
BackgroundSelf-citationMiao, C., Wang, L., Wang, H., Shen, Y., Man, C., Zhang, W., Zhang, Y., Zhao, Q., & Jiang, Y. (2024) · Food & Function · doi:10.1039/d4fo03591g · Cited by 27
Kaner, G., Depboylu, G. Y., Çalık, G., Yalçın, T., & Nalçakan, T. (2022) · Public Health Nutrition · doi:10.1017/s1368980022002579 · Cited by 24
“Studies have shown that depression, stress and anxiety are higher in obese participants (33 – 35) .”
BackgroundFemale obesity: clinical and psychological assessment toward the best treatment
Guglielmi, V., Grave, R. D., Leonetti, F., & Solini, A. (2024) · Frontiers in Endocrinology · doi:10.3389/fendo.2024.1349794 · Cited by 33
Body composition, lifestyle, and depression: a prospective study in the UK biobank
Lv, X., Cai, J., Li, X., Wang, X., Ma, H., Heianza, Y., Qi, L., & Zhou, T. (2024) · BMC Public Health · doi:10.1186/s12889-024-17891-6 · Cited by 25
“…the risk of depression than those who lead an unfavorable lifestyle [15, 16, 25, 48, 49], and the adverse lifestyles could be a risk factor for adverse body composition and may share similar pathways with adverse body composition, such as metabolic dysfunction, that contribute to depression [50].”
BackgroundWang, X., Liang, X., Jiang, M., Wei, L., Shi, X., Fang, F., & Cang, J. (2025) · BMC Psychiatry · doi:10.1186/s12888-025-06892-3 · Cited by 26
“Psychosocial factors such as body image dissatisfaction, diminished self-esteem, and social stigma may contribute to the increased risk of depression in individuals with obesity [18, 19].”
Hamasaki, H. (2023) · Medicines · doi:10.3390/medicines10090053 · Cited by 26
“Mindfulness could be a feasible and supportive practice for people with diabetes who also suffer from stress, depression, and anxiety; however, more rigorous scientific evidence will be needed in the future.”
BackgroundLi, D., Liang, W., Zhang, W., Huang, Z., Liang, H., & Liu, Q. (2024) · Frontiers in Microbiology · doi:10.3389/fmicb.2023.1241309 · Cited by 23
Lv, Y., Peng, X., Lee, Y., et al. (2024) · Food Research International · doi:10.1016/j.foodres.2024.114900 · Cited by 20
Chang, Z., Zhu, Y., Wang, P., Du, L., Wu, M., Wang, X., Kong, C., Huang, D., Xie, R., Guo, J., et al. (2025) · 中国科学通报：英文版 · doi:10.1016/j.scib.2025.04.010 · Cited by 20
Magdy, Y., Kamar, S. A., Habib, M. Z., Rady, H. Y., Rabei, M. R., & Khedr, S. A. (2025) · Psychopharmacology · doi:10.1007/s00213-025-06834-7 · Cited by 20
“It is no wonder that the incidence of both conditions has increased steadily over the past few years (Fulton et al. 2022 ).”
Huang, J., Li, R.-H., & Tsai, L. (2022) · Nutrients · doi:10.3390/nu14194200 · Cited by 23
“Growing evidence suggests that obesity may increase the risk of depression [14,42].”
Backgroundde Ceglia, M., Bonaventura, M. V. M. D., Romano, A., Friuli, M., Bonaventura, E. M. D., Gavito, A., Botticelli, L., Gaetani, S., de Fonseca, F. R., & Cifani, C. (2023) · International Journal of Eating Disorders · doi:10.1002/eat.23917 · Cited by 21
Liu, S., Jiang, W., Liu, C., Guo, S., Wang, H., & Chang, X. (2023) · Food & Function · doi:10.1039/d3fo00604b · Cited by 20
Prevalence and Determinants of Depression, Anxiety, and Stress Among Secondary School Students
Barnawi, M. M., Sonbaa, A. M., Barnawi, M. M., Alqahtani, A. H., & Fairaq, B. A. (2023) · Cureus · doi:10.7759/cureus.44182 · Cited by 20
Landgraaf, R. G., Bloem, M. N., Fumagalli, M., Benninga, M. A., de Lorijn, F., & Nieuwdorp, M. (2023) · Frontiers in Endocrinology · doi:10.3389/fendo.2023.1236370 · Cited by 21
“Additionally, there is a bidirectional link between anxiety, depression, and obesity (88, 89).”
Obesity and Depression: A Pathophysiotoxic Relationship
Monsalve, F. A., Fernández-Tapia, B., Arriagada, O., González, D. R., & Delgado‐López, F. (2025) · International Journal of Molecular Sciences · doi:10.3390/ijms262311590 · Cited by 22
“…is complex, as not all obese individuals have elevated cortisol levels, and the development of obesity coincides with an increase in factors that enhance cortisol production, such as chronic stress, chronic low-grade inflammation, consumption of sugar-and fat-rich foods, and reduced sleep [51].”
InfluentialGallagher, C., Waidyatillake, N. T., Pirkis, J., Lambert, K. A., Cassim, R., Dharmage, S. C., & Erbas, B. (2023) · Obesity Reviews · doi:10.1111/obr.13566 · Cited by 20
“Within this growing evidence base, obesity has garnered much attention, with mental disorders thought to be a possible consequence of weight-related stigma and discrimination,(2) low selfesteem,(3) functional impairment,(3) and metabolic disturbance.(4) Indeed, several systematic reviews and meta-analyses of longitudi…”
BackgroundCustodio, R. J. P., Hobloss, Z., Myllys, M., Hassan, R. A. R. A., González, D., Reinders, J., Bornhorst, J., Weishaupt, A.-K., Seddek, A., Abbas, T., et al. (2023) · Cells · doi:10.3390/cells12182331 · Cited by 19
Obesogenic diet induces circuit-specific memory deficits in mice
Bakoyiannis, I., Ducourneau, E., N’diaye, M., Fermigier, A., Ducroix-Crepy, C., Bosch‐Bouju, C., Coutureau, É., Trifilieff, P., & Ferreira, G. (2024) · eLife · doi:10.7554/elife.80388 · Cited by 17
Liu, H., Dong, H., Zhou, Y., Jin, M., Hao, H., Yuan, Y., & Jia, H. (2024) · Frontiers in Endocrinology · doi:10.3389/fendo.2024.1482003 · Cited by 18
“When it comes to depression in women, those who are obese are more likely to experience it than those who are not (1, 9).”
BackgroundLin, Y., Cheng, S., Liu, W., Zailani, H., Wu, S., Hung, M., & Su, K. (2024) · Brain Behavior and Immunity · doi:10.1016/j.bbi.2024.10.028 · Cited by 20
Han, X., Zhang, H., Xu, T., Liu, L. L., Cai, H., Liu, Z., Li, Q., Zheng, H., Xu, T., & Yuan, T. (2022) · Frontiers in Psychiatry · doi:10.3389/fpsyt.2022.873953 · Cited by 17
“Especially when anxiety and depression themselves are highly correlated with obesity (49), it is a very dangerous move to try to eliminate the major factors, which may be the abnormal phenotypes shared by anxiety and depression with obesity.”
BackgroundRelationship of perceived depression, stress, anxiety levels and hedonic hunger
Yalçın, T., Ayyıldız, F., Yılmaz, M. V., & Asil, E. (2023) · International Journal of Obesity · doi:10.1038/s41366-023-01315-3 · Cited by 18
“Studies have shown that depression, stress and anxiety are higher in people with obesity [42, 43].”
BackgroundAalipanah, E., Askarpour, M., Eskandari, M. H., Zare, M., Famouri, M., Bedeltavana, A., Mohsenpour, M. A., & Sohrabi, Z. (2025) · Clinical Nutrition ESPEN · doi:10.1016/j.clnesp.2025.05.045 · Cited by 19
Zhang, C., Ma, W., Chen, Z., He, C., Zhang, Y., & Tao, Q. (2022) · Nutrients · doi:10.3390/nu14214508 · Cited by 21
“Obese adults have increased odds of depressive and anxiety symptoms compared with non-obese people [56,57].”
BackgroundPotential Benefits of Anthocyanins in Chronic Disorders of the Central Nervous System
Panchal, S. K., & Brown, L. (2022) · Molecules · doi:10.3390/molecules28010080 · Cited by 18
“Obesity defined as an increased body mass index predicts chronic anxiety and depression symptoms likely related to prolonged inflammation due to poor dietary lifestyle and inactivity [80].”
BackgroundWu, S., Chen, W.-J., Chang, J. P., Guu, T., Hsin, M.-C., Huang, C., Mischoulon, D., Capuron, L., & Su, K. (2023) · Journal of Personalized Medicine · doi:10.3390/jpm13061003 · Cited by 19
“Depression is notorious for being a risk factor for metabolic dysfunction associated with obesity, including an inflammatory response, high blood pressure, impaired insulin sensitivity, and impaired leptin sensitivity [11].”
BackgroundOn behalf of The By-Band-Sleeve Collaborating Group (2024) · BMJ Open · doi:10.1136/bmjopen-2022-071231 · Cited by 19
Inhibition of Pancreatic Lipase by Flavonoid Derivatives: In Vitro and In Silico Investigations
Tran, T., Mai, T. T., Ho, T.-T.-T., Le, T.-N.-D., Cao, T., Thai, K., & Tran, T.-S. (2024) · Advances in Pharmacological and Pharmaceutical Sciences · doi:10.1155/2024/6655996 · Cited by 18
“Scientifc investigations consistently elucidate a robust association between obesity and mental health issues, such as depression [10], anxiety [11], and low self-esteem [12].”
BackgroundAhmed, F., Arshad, M. T., Maqsood, S., Ikram, A., & Gnedeka, K. T. (2025) · Food Science & Nutrition · doi:10.1002/fsn3.70689 · Cited by 22
“Obese individuals tend to experience mood disorders, and individuals who experience anxiety or depression tend to gain weight, which is partly brought about by emotional eating and inactivity (Fulton et al. 2022; Dakanalis et al. 2023).”
Neural encoding of food and monetary reward delivery
Oren, S., Tittgemeyer, M., Rigoux, L., Schlamann, M. U., Schönberg, T., & Kuzmanovic, B. (2022) · NeuroImage · doi:10.1016/j.neuroimage.2022.119335 · Cited by 20
“interplay between food intake, reward-related processing, gustatory processing, and homeostatic regulation have been suggested to underlie metabolic disorders such as obesity — and its severe medical and psychiatric comorbidities (Beutler et al., 2020; Fulton et al., 2021; Pantalone et al., 2017; Plassmann et al., 202…”
BackgroundSulaiman, S. K., Tsiga-Ahmed, F. I., Arora, T., Faris, M. E., Musa, M. S., Kareem, Y. A., Dayyab, F. M., Hussein, A., Sale, S., Javaid, S. F., et al. (2023) · Brain and Behavior · doi:10.1002/brb3.2990 · Cited by 20
“This is because obesity and being over-weight have been positively correlated to increased incidence of both anxiety and depression (Fulton et al., 2022; Sharafi et al., 2020).”
BackgroundWittekind, D. A., Kratzsch, J., Biemann, R., Mergl, R., Riedel-Heller, S. G., Witte, A. V., Villringer, A., & Kluge, M. (2022) · Frontiers in Psychiatry · doi:10.3389/fpsyt.2022.891325 · Cited by 15
“A leptin analog, metreleptin, even exhibited swift antidepressant action in depressed anorexia-nervosa patients, which is associated with low leptin levels (65, 73).”
BackgroundChinese medicinal herbs as potential prodrugs for obesity
Law, S., Wang, Y., Lu, X., Au, D. C. T., Chow, W. Y. L., Leung, A. W., & Xu, C. (2022) · Frontiers in Pharmacology · doi:10.3389/fphar.2022.1016004 · Cited by 15
“An abnormally accumulated fat is positively associated with diabetes, cardiovascular diseases, hyperlipidemia, hypertension, metabolic syndrome, fatty liver disease, a certain type of cancer, depression, and anxiety (Fulton et al., 2022).”
BackgroundLipids in major depressive disorder: new kids on the block or old friends revisited?
van der Heijden, A. R., & Houben, T. (2023) · Frontiers in Psychiatry · doi:10.3389/fpsyt.2023.1213011 · Cited by 15
“However, the relationship between obesity and depression seems rather bidirectional as underlying mechanisms are very closely intertwined (see the examples of inflammation and HPA-axis here above) (158, 162).”
BackgroundJing, X., Hong, F., Xie, Y., Xie, Y., Shi, F., Wang, R., Wang, L., Chen, Z., & Liu, X. (2023) · Biomedicine & Pharmacotherapy · doi:10.1016/j.biopha.2023.115796 · Cited by 16
Poly-Agonist Pharmacotherapies for Metabolic Diseases: Hopes and New Challenges
Allard, C., Cota, D., & Quarta, C. (2023) · Drugs · doi:10.1007/s40265-023-01982-6 · Cited by 15
“Psychological support before and after surgery is as important as metabolic monitoring, as following strict dietary guidelines can be difficult, especially for those who are more prone to anxiety-related problems [29].”
Wang, Y., Wang, H., Cheng, B., & Xia, J. (2025) · Journal of Affective Disorders · doi:10.1016/j.jad.2025.04.134 · Cited by 17
Yan, L., & Li, J. (2022) · Brain Research Bulletin · doi:10.1016/j.brainresbull.2022.04.015 · Cited by 16
Al-Amin, M., Rinky, F., Bhuiyan, M. N. H., Yeasmin, R., Akter, T., Hoque, N., & Reza, S. (2025) · BMJ Open · doi:10.1136/bmjopen-2024-097745 · Cited by 20
“108 The consumption patterns and dietary habits— including the intake of 6–8 food groups, as well as the consumption of wheat or rice, pulses, fats and oils, and sugar-sweetened foods and beverages—were significantly associated with the development of anxiety.”
Guo, J.-J., Hang, Q.-Q., Xu, T., Liang, W.-X., Gao, J.-K., Ou, H.-B., Jiang, F.-Z., Qiu, X.-C.-H., Tian, Z.-Z., Zhang, Y., et al. (2025) · Lipids in Health and Disease · doi:10.1186/s12944-025-02619-1 · Cited by 15
“Excess visceral fat promotes chronic inflammation via adipokine dysregulation and macrophage infiltration, exacerbating both periodontal and cardiovascular pathologies [13].”
Tsirmpas, C., Andrikopoulos, D., Fatouros, P., Eleftheriou, G., Anguera, J. A., Kontoangelos, K. A., & Papageorgiou, C. (2022) · Frontiers in Digital Health · doi:10.3389/fdgth.2022.868970 · Cited by 14
The prevalence of anxiety in adult endocrinology outpatients: A systematic review and meta–analysis
Kershaw, K. A., Storer, B., Braund, T. A., Chakouch, C., Coleshill, M. J., Haffar, S., Harvey, S. B., Newby, J. M., Sicouri, G., & Murphy, M. (2023) · Psychoneuroendocrinology · doi:10.1016/j.psyneuen.2023.106357 · Cited by 17
Saffari, M., Lin, Y.-C., Huang, P., Huang, Y.-T., Huang, R.-Y., Huang, C. H., Chen, J., Poon, W. C., Griffiths, M. D., & Lin, C. (2024) · International Journal of Mental Health Promotion · doi:10.32604/ijmhp.2024.053432 · Cited by 14
“Moreover, psychological stress may concurrently be considered as one of the causes and outcomes of WS [8,20].”
BackgroundLiu, X., Xu, L., Luo, R., et al. (2022) · Journal of Food Processing and Preservation · doi:10.1111/jfpp.16528 · Cited by 14
Recent advances in biomimetic nanodelivery systems for the treatment of depression
Jiang, P., & Li, J. (2025) · Materials Today Bio · doi:10.1016/j.mtbio.2025.101781 · Cited by 17
“In the alarm phase, the internal balance of the organism is disrupted, and it begins to react to external stressors [42 – 44].”
Xanthine-induced deficits in hippocampal behavior and abnormal expression of hemoglobin genes
Kambe, J., Miyata, S., Li, C., Yamamoto, Y., & Nagaoka, K. (2023) · Behavioural Brain Research · doi:10.1016/j.bbr.2023.114476 · Cited by 13
Kozhuharov, V. R., Ivanov, K., Karcheva-Bahchevanska, D. P., Prissadova, N. A., & Ivanova, S. (2023) · Processes · doi:10.3390/pr11082337 · Cited by 13
Valenta, S. T., Stecchi, M., Perazza, F., Nuccitelli, C., Villanova, N., Pironi, L., Atti, A. R., & Petroni, M. L. (2023) · Eating and Weight Disorders - Studies on Anorexia Bulimia and Obesity · doi:10.1007/s40519-023-01625-5 · Cited by 13
“Overall, the recurrent co-occurrence of obesity, anxiety-depressive syndromes, and the use of antidepressant therapies often results in a complex interplay, both in clinical presentation and adherence to treatment [37].”
BackgroundLonergan, C., Millar, S., & Kabir, Z. (2024) · PLoS ONE · doi:10.1371/journal.pone.0299029 · Cited by 18
Assessing the state of obesity care: Quality, access, guidelines, and standards
Kaplan, L. M., Apovian, C. M., Ard, J. D., Allison, D. B., Aronne, L. J., Batterham, R. L., Busetto, L., Dicker, D., Horn, D. B., Kelly, A. S., et al. (2024) · Obesity Science & Practice · doi:10.1002/osp4.765 · Cited by 15
“36 40 Endocrine dysfunctions, including hypogonadism, polycystic ovarian syndrome, and infertility, are common in patients with obesity, and low levels of sex steroids and growth hormone may exacerbate body composition abnormalities.”
BackgroundSchell, M., Wardelmann, K., Hauffe, R., Rath, M., Chopra, S., & Kleinridders, A. (2023) · Biological Psychiatry Global Open Science · doi:10.1016/j.bpsgos.2023.02.011 · Cited by 14
“The intake of an unhealthy high-calorie diet causes dysbiosis and is linked to altered emotional behavior in humans (20).”
BackgroundThe Melanocortin System: A Promising Target for the Development of New Antidepressant Drugs
Markov, D. D., Dolotov, O. V., & Grivennikov, I. A. (2023) · International Journal of Molecular Sciences · doi:10.3390/ijms24076664 · Cited by 14
“Indirectly, the possible involvement of the melanocortin system in depression is indicated by studies demonstrating a close relationship between depression and obesity [306,307].”
BackgroundLazarevich, I., Irigoyen‐Camacho, M. E., Vázquez, C. C. R., Tolentino, R. G., Velázquez-Alva, M. C., & Zepeda‐Zepeda, M. A. (2025) · Behavioral Sciences · doi:10.3390/bs15050669 · Cited by 13
“The bidirectional relationship between obesity and depression has been reported previously (Fulton et al., 2021; Vittengl, 2018), and anxiety is considered the most frequent condition related to unhealthy dietary patterns.”
Depression Following Acute Coronary Syndrome: A Review
Pan, R., Fan, Q., & Tao, R. (2023) · Reviews in Cardiovascular Medicine · doi:10.31083/j.rcm2409247 · Cited by 13
“sion, obesity and ACS are all associated with lifestyle risk factors, such as poor diet and physical inactivity [46].”
BackgroundLi, Y., Shi, N., & Tao, Y. (2025) · Frontiers in Sports and Active Living · doi:10.3389/fspor.2025.1638381 · Cited by 12
Paraventricular ThalamicMC3RCircuits Link Energy Homeostasis with Anxiety-Related Behavior
Cho, D., O'Berry, K., Possa‐Paranhos, I. C., Butts, J., Palanikumar, N., & Sweeney, P. (2023) · Journal of Neuroscience · doi:10.1523/jneurosci.0704-23.2023 · Cited by 11
Zilkha, N., Chuartzman, S. G., Fishman, R., Ben‐Dor, S., & Kimchi, T. (2024) · Scientific Reports · doi:10.1038/s41598-024-70062-w · Cited by 13
Menichetti, F., Battezzati, A., Bertoli, S., Amicis, R. S. D., Foppiani, A., Sileo, F., & Leone, A. (2024) · European Journal of Clinical Nutrition · doi:10.1038/s41430-024-01536-3 · Cited by 13
“First, in fl ammation and oxidative stress are common among patients with anxiety or depression [44].”
Age and an obesogenic diet affect mouse behaviour in a sex‐dependent manner
Mort, E. J., Fordington, S., Heritage, S., Fowden, A. L., Jones, S., & Camm, E. J. (2023) · European Journal of Neuroscience · doi:10.1111/ejn.16070 · Cited by 11
“In particular, obesity is associated with increased anxiety (Fulton et al., 2022) and risk-taking behaviours in both adolescent and adult human populations (Ratcliff et al., 2011).”
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).
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.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review
