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.
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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.
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- Load-bearing: passes — 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
“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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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.
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- 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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- 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.
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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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- 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.
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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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- 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
“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.
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- Load-bearing: fails — The paper’s conclusions may not depend on it.
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Probably not a substantial claim. The paper’s conclusions may not depend on it. 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.
- 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.
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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.
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.
- 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.
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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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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.
- 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.
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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
“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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- 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.
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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.
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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].”
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- Not checked yetcites [119] source
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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
“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.
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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.”
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- Not checked yetcites [110] source
hedgeddirect- Asserted: passes — The authors put it forward as true.
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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.
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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]
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“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].”
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“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].”
Antidepressant therapies inhibit inflammation and microglial M1-polarization
Kalkman, H. O., & Feuerbach, D. (2016) · Pharmacology & Therapeutics · doi:10.1016/j.pharmthera.2016.04.001 · Cited by 212 · cited 1×
“Consistently, suppression of microglia [80] and astrocyte [81] reactivity is implicated in the response to antidepressant therapies.”
BackgroundMilaneschi, Y., Lamers, F., Bot, M., Drent, M. L., & Penninx, B. W. J. H. (2017) · Biological Psychiatry · doi:10.1016/j.biopsych.2015.10.023 · Cited by 209 · cited 1×
“In a corresponding manner, 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].”
BackgroundGafoor, R., Booth, H., & Gulliford, M. C. (2018) · BMJ · doi:10.1136/bmj.k1951 · Cited by 207 · cited 1×
“Treatment options Antidepressant medications serve as the standard line of treatment; however, these drugs can be ineffective andmost augment the risk of weight gain [147].”
BackgroundInhibiting microglia expansion prevents diet-induced hypothalamic and peripheral inflammation
André, C., Guzman-Quevedo, O., Rey, C., Rémus-Borel, J., Clark, S., Castellanos-Jankiewicz, A., Ladeveze, E., Leste-Lasserre, T., Nadjar, A., Abrous, D. N., et al. (2017) · Diabetes · doi:10.2337/db16-0586 · Cited by 182 · cited 1×
“Reversing neuroinflammation via targeted genetic [96,97], pharmacological [98,99], or dietary [49,100] approaches that rescue behavioral anomalies offers convincing support for a causal role of neuroinflammation in obesity-induced neuropathophysiology.”
BackgroundHigh-fat diet-induced metabolic disorders impairs 5-HT function and anxiety-like behavior in mice
Zemdegs, J., Quesseveur, G., Jarriault, D., Pénicaud, L., Fioramonti, X., & Guiard, B. P. (2016) · British Journal of Pharmacology · doi:10.1111/bph.13343 · Cited by 180 · cited 1×
“Chronic HFD in male mice, leading to increased anxiety-like behavior, has been shown to impair the basal electrical activity and excitability of serotonin neurons as well as serotonin-mediated neurotransmission in the hippocampus [33,35].”
BackgroundSelf-citationThe role of depressive subtypes within the neuroinflammation hypothesis of major depressive disorder
Woelfer, M., Kasties, V., Kahlfuss, S., & Walter, M. (2019) · Neuroscience · doi:10.1016/j.neuroscience.2018.03.034 · Cited by 171 · cited 2×
“This form of depression has stronger links to peripheral [10,11] and central [12] inflammation.”
BackgroundInsulin-mediated synaptic plasticity in the CNS: Anatomical, functional and temporal contexts
Ferrario, C. R., & Reagan, L. P. (2017) · Neuropharmacology · doi:10.1016/j.neuropharm.2017.12.001 · Cited by 163 · cited 9×
“The effects of DIO on the hippocampus have received considerable attention because of the well-reported effects of HFD to elicit cognitive and emotional impairments [102].”
InfluentialTreatment of depression with atypical features: a meta-analytic approach
Henkel, V., Mergl, R., Allgaier, A.-K., Kohnen, R., Möller, H.-J., & Hegerl, U. (2006) · Psychiatry Research · doi:10.1016/j.psychres.2005.07.012 · Cited by 161 · cited 1×
“Individuals with atypical depression often have a more unrelenting course of depression [13], in part because they show a poorer response to antidepressants [14].”
BackgroundSobesky, J. L., Barrientos, R. M., May, H. S. D., Thompson, B. M., Weber, M. D., Watkins, L. R., & Maier, S. F. (2014) · Brain Behavior and Immunity · doi:10.1016/j.bbi.2014.06.017 · Cited by 160 · cited 1×
“Corroborating and extending findings in humans, rodent investigations illustrate the impact of high-fat and -sugar diet to stimulate reactive gliosis and upregulate cytokine and chemokine gene expression in mouse hypothalamus [89], hippocampus [90,91], nucleus accumbens [34], and ventral tegmental area [92].”
BackgroundSchur, E. A., Melhorn, S. J., Oh, S.-K., Lacy, J. M., Berkseth, K. E., Guyenet, S. J., Sonnen, J. A., Tyagi, V., Leon, M. R. B. D., Leon, B. D., et al. (2015) · Obesity · doi:10.1002/oby.21248 · Cited by 155 · cited 1×
“Radiologic evidence of brain gliosis that links to insulin resistance in obese adults has also been reported [87].”
BackgroundZemdegs, J., Martin, H., Pintana, H., Bullich, S., Manta, S., Marqués, M. A., Moro, C., Layé, S., Ducrocq, F., Chattipakorn, N., et al. (2019) · The Journal of Neuroscience · doi:10.1523/jneurosci.2904-18.2019 · Cited by 151 · cited 2×
“In particular, it has been proposed that peripheral insulin resistance increases branch-chained amino acids that limit the reuptake of tryptophan through the BBB, thereby limiting serotonin synthesis in the hippocampus [35].”
BackgroundSelf-citationOpel, N., Thalamuthu, A., Milaneschi, Y., Grotegerd, D., Flint, C., Leenings, R., Goltermann, J., Richter, M., Hahn, T., Woditsch, G., et al. (2021) · Molecular Psychiatry · doi:10.1038/s41380-020-0774-9 · Cited by 148
Brain insulin resistance: A treatment target for cognitive impairment and anhedonia in depression
Hamer, J., Testani, D. A., Mansur, R. B., Lee, Y. L., Subramaniapillai, M., & McIntyre, R. S. (2019) · Experimental Neurology · doi:10.1016/j.expneurol.2019.01.016 · Cited by 142 · cited 1×
“In turn, a high percentage of patients with depression exhibit insulin resistance [124].”
BackgroundFish oil supplementation and insulin sensitivity: a systematic review and meta-analysis
Gao, H., Geng, T., Huang, T., & Zhao, Q. (2017) · Lipids in Health and Disease · doi:10.1186/s12944-017-0528-0 · Cited by 140 · cited 1×
“Increased dietary n-3 intake can improve insulin sensitivity [43] and significantly diminish plasma CRP, interleukin-6 (IL-6), and tumor necrosis factor alpha (TNFα) levels in humans [44].”
BackgroundOpel, N., Redlich, R., Grotegerd, D., Dohm, K., Heindel, W., Kugel, H., Arolt, V., & Dannlowski, U. (2015) · Psychoneuroendocrinology · doi:10.1016/j.psyneuen.2014.10.001 · Cited by 138 · cited 1×
“Both obesity and depression share similar morphometric anomalies in medial prefrontal cortex [104], and 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].”
BackgroundXu, Q., Anderson, D., & Lurie-Beck, J. (2011) · Obesity Research & Clinical Practice · doi:10.1016/j.orcp.2011.04.007 · Cited by 136 · cited 7×
“This sex distinction in incidence narrows considerably in conditions of severe obesity (BMI ≥ 40) [1].”
BackgroundInfluentialMa, J., Rosas, L. G., Lv, N., Xiao, L., Snowden, M. B., Venditti, E. M., Lewis, M. A., Goldhaber-Fiebert, J. D., & Lavori, P. W. (2019) · JAMA · doi:10.1001/jama.2019.0557 · Cited by 133 · cited 1×
“For example, adding a dietary weight loss intervention and psychotherapy has been shown to enhance the efficacy of antidepressant medications in obese individuals [148].”
BackgroundTreatment of cytokine-induced depression
Capuron, L., Hauser, P., Hinze-Selch, D., Miller, A. H., & Neveu, P. J. (2002) · Brain Behavior and Immunity · doi:10.1016/s0889-1591(02)00007-7 · Cited by 132 · cited 1×
“observations that inflammatory interventions can lead to symptoms of these disorders, such as in the case of patients receiving interferon (IFN) alpha treatment [64].”
BackgroundHamer, M., Batty, G. D., & Kivimaki, M. (2012) · Molecular Psychiatry · doi:10.1038/mp.2012.30 · Cited by 132 · cited 1×
“blood pressure, C-reactive protein, triglycerides, and glycaemia) present either no increased risk [161] or a modest elevated”
BackgroundJokela, M., Hamer, M., Singh-Manoux, A., Batty, G. D., & Kivimäki, M. (2014) · Molecular Psychiatry · doi:10.1038/mp.2013.162 · Cited by 132 · cited 3×
“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].”
BackgroundObesity-mediated inflammation may damage the brain circuit that regulates food intake
Cazettes, F., Cohen, J. I., Yau, P. L., Talbot, H., & Convit, A. J. (2010) · Brain Research · doi:10.1016/j.brainres.2010.12.008 · Cited by 131 · cited 1×
“Both waist circumference [84] and circulating markers of inflammation [85] in obesity correlate negatively with cortical grey matter volume.”
BackgroundDietary sugars, not lipids, drive hypothalamic inflammation
Gao, Y., Bielohuby, M., Fleming, T., Grabner, G. F., Foppen, E., Bernhard, W., Guzmán-Ruiz, M., Layritz, C., Legutko, B., Zinser, E., et al. (2017) · Molecular Metabolism · doi:10.1016/j.molmet.2017.06.008 · Cited by 131 · cited 1×
“The presence of excess sugar in a HFD was shown to be necessary for hypothalamic inflammatory responses in mice, including the activation of microglia, the resident immune cells of the brain [58].”
BackgroundLiukkonen, T., Räsänen, P., Jokelainen, J., Leinonen, M., Järvelin, M.-R., Meyer-Rochow, V. B., & Timonen, M. (2011) · European Psychiatry · doi:10.1016/j.eurpsy.2011.02.001 · Cited by 127 · cited 1×
“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].”
BackgroundSpichak, S., Bastiaanssen, T. F. S., Berding, K., Vlckova, K., Clarke, G., Dinan, T. G., & Cryan, J. F. (2021) · Neuroscience & Biobehavioral Reviews · doi:10.1016/j.neubiorev.2021.02.044 · Cited by 127 · cited 1×
“Chronic changes in microbiota composition in obesity (dysbiosis) are associated with inflammation, insulin resistance, and mental health deficits [72].”
BackgroundMilos, G. F., Antel, J., Kaufmann, L., Barth, N., Koller, A., Tan, S., Wiesing, U., Hinney, A., Libuda, L., Wabitsch, M., et al. (2020) · Translational Psychiatry · doi:10.1038/s41398-020-00977-1 · Cited by 125 · cited 1×
“While studies in humans are limited, treatment with a leptin analog (metreleptin) has rapid antidepressant effects in individuals with anorexia nervosa marked by very low leptin levels [143].”
BackgroundDietary inflammatory index and depression: a meta-analysis
Wang, J., Zhou, Y., Chen, K., Jing, Y., He, J., Sun, H., & Hu, X. (2018) · Public Health Nutrition · doi:10.1017/s1368980018002628 · Cited by 122 · cited 1×
“Dietary fat overload Several lines of evidence link poor diet, inflammation, and depressive symptomology [21,22].”
BackgroundHryhorczuk, C., Florea, M., Rodaros, D., Poirier, I., Daneault, C., Des Rosiers, C., Arvanitogiannis, A., Alquier, T., & Fulton, S. (2016) · Neuropsychopharmacology · doi:10.1038/npp.2015.207 · Cited by 119 · cited 1×
“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].”
BackgroundSelf-citationTang, F., Wang, G., & Lian, Y. (2017) · Psychoneuroendocrinology · doi:10.1016/j.psyneuen.2016.11.025 · Cited by 117 · cited 1×
“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].”
BackgroundScott, K. M., Von Korff, M., Alonso, J., Angermeyer, M., Bromet, E. J., Bruffaerts, R., de Girolamo, G., de Graaf, R., Fernandez, A., Gureje, O., et al. (2008) · Psychological Medicine · doi:10.1017/s0033291708003413 · Cited by 116 · cited 1×
“obese men [1,157], a divergence that corresponds with lifetime prevalence independent of body weight.”
BackgroundEffects of adiposity and metabolic dysfunction on cognition: A review
Farruggia, M. C., & Small, D. M. (2019) · Physiology & Behavior · doi:10.1016/j.physbeh.2019.112578 · Cited by 112 · cited 1×
“In this review, we focus on how obesity increases the risk for depression and anxiety (for cognitive corollaries, see [7,8]), with the aim to illuminate the diverse metabolic culprits of obesity and their influence on the neural and behavioral processes giving rise to mood and emotional deficits.”
BackgroundJanowitz, D., Wittfeld, K., Terock, J., Freyberger, H. J., Hegenscheid, K., Völzke, H., Habes, M., Hosten, N., Friedrich, N., Nauck, M. A., et al. (2015) · NeuroImage · doi:10.1016/j.neuroimage.2015.07.086 · Cited by 111 · cited 1×
“Both waist circumference [84] and circulating markers of inflammation [85] in obesity correlate negatively with cortical grey matter volume.”
BackgroundRole of the Brain's Reward Circuitry in Depression
Nestler, E. J. (2015) · International review of neurobiology · doi:10.1016/bs.irn.2015.07.003 · Cited by 108 · cited 3×
“In contrast, increasing brain-derived neurotrophic factor in the nucleus accumbens or ventral tegmental area produces a depressive-like phenotype, whereas animals with selective knockout of brain-derived neurotrophic factor in ventral tegmental area are protected from depressive effects produced by social defeat stres…”
BackgroundHarrell, C. S., Burgado, J., Kelly, S. D., Johnson, Z. P., & Neigh, G. N. (2015) · Psychoneuroendocrinology · doi:10.1016/j.psyneuen.2015.08.025 · Cited by 107
Décarie-Spain, L., Sharma, S., Hryhorczuk, C., Issa-Garcia, V., Barker, P. A., Arbour, N., Alquier, T., & Fulton, S. (2018) · Molecular Metabolism · doi:10.1016/j.molmet.2018.01.018 · Cited by 107 · cited 4×
“Corroborating and extending findings in humans, rodent investigations illustrate the impact of high-fat and -sugar diet to stimulate reactive gliosis and upregulate cytokine and chemokine gene expression in mouse hypothalamus [89], hippocampus [90,91], nucleus accumbens [34], and ventral tegmental area [92].”
BackgroundInfluentialSelf-citationWang, F., Wang, S., Zong, Q. ‐., Zhang, Q., Ng, C. H., Ungvari, G. S., & Xiang, Y. ‐. (2019) · Diabetic Medicine · doi:10.1111/dme.14042 · Cited by 105 · cited 1×
“betes [159] and more than threefold higher in people with type 1 diabetes than those without, with greater rates in diabetic”
BackgroundKetamine’s effect on inflammation and kynurenine pathway in depression: A systematic review
Kopra, E. I., Mondelli, V., Pariante, C. M., & Nikkheslat, N. (2021) · Journal of Psychopharmacology · doi:10.1177/02698811211026426 · Cited by 105 · cited 6×
“Adipose-derived inflammatory molecules such as TNFα disrupt insulin signaling to promote resistance and impaired vascular health.”
BackgroundInfluentialSelective deletion of leptin receptors in adult hippocampus induces depression-related behaviours
Guo, M., Huang, T.-Y., Garza, J. C., Chua, S. C., & Lu, X. (2012) · The International Journal of Neuropsychopharmacology · doi:10.1017/s1461145712000703 · Cited by 102 · cited 1×
“The anxiolytic action of leptin in mice has been tied to leptin receptor signaling in mesolimbic dopamine neurons [137,138], whereas its effects to inhibit behavioral despair are attributed to signaling actions in the hippocampus [139].”
BackgroundRecognition and diagnosis of atypical depression.
Thase, M. E. (2007) · PubMed · Cited by 97
Role of brain transmigrating neutrophils in depression-like behavior during systemic infection
Aguliar-Valles, A., Kim, J., Jung, S., Woodside, B., & Luheshi, G. N. (2014) · Molecular Psychiatry · doi:10.1038/mp.2013.137 · Cited by 97 · cited 1×
“DIO [163] and that favors depressive behaviors [164,165].”
BackgroundCarraça, E. V., Encantado, J., Battista, F., Beaulieu, K., Blundell, J. E., Busetto, L., van Baak, M., Dicker, D., Ermolao, A., Farpour‐Lambert, N., et al. (2021) · Obesity Reviews · doi:10.1111/obr.13261 · Cited by 97 · cited 1×
“Although there is limited evidence for depression and obesity comorbidity, exercise has been shown to enhance mental health outcomes in obesity via ameliorating self-efficacy and autonomous motivation [156].”
BackgroundKokras, N., & Dalla, C. (2017) · Journal of Neuroscience Research · doi:10.1002/jnr.23861 · Cited by 94 · cited 2×
“A dietary approach that includes anti-inflammatory foods and supplements, such as those containing high EPA n-3 PUFA and probiotics, could help attenuate psychological stress in obesity [149,150].”
BackgroundSivanathan, S., Thavartnam, K., Arif, S., Elegino, T., & McGowan, P. O. (2015) · Behavioural Brain Research · doi:10.1016/j.bbr.2015.02.036 · Cited by 93
Kadriu, B., Farmer, C., Yuan, P., Park, L. T., Deng, Z., Moaddel, R., Henter, I. D., Shovestul, B. J., Ballard, E. D., Kraus, C., et al. (2019) · Molecular Psychiatry · doi:10.1038/s41380-019-0589-8 · Cited by 93 · cited 1×
“The influence of inflammation on IDO shifts kynurenine metabolism towards microglial byproducts, such as 3-hydroxykynurenine and quinolinic acid, a change associated with elevated oxidative stress and glutamate excitotoxicity that could contribute to depressive symptoms [111,112].”
BackgroundHickman, R. J., Khambaty, T., & Stewart, J. C. (2014) · Journal of Behavioral Medicine · doi:10.1007/s10865-013-9510-0 · Cited by 90
Leptin regulates leukocyte recruitment into the brain following systemic LPS-induced inflammation
Rummel, C., Inoue, W., Poole, S., & Luheshi, G. N. (2010) · Molecular Psychiatry · doi:10.1038/mp.2009.98 · Cited by 88 · cited 1×
“DIO [163] and that favors depressive behaviors [164,165].”
BackgroundSamara, A., Murphy, T., Strain, J. F., Rutlin, J. R., Sun, P., Neyman, O., Sreevalsan, N., Shimony, J. S., Ances, B. M., Song, S., et al. (2020) · Frontiers in Human Neuroscience · doi:10.3389/fnhum.2019.00464 · Cited by 88 · cited 1×
“Obese adults exhibit increased cellularity in the hippocampus and amygdala [86], whereas greater cell density in the nucleus accumbens, dorsal striatum, pallidum, hypothalamus, amygdala, and hippocampus correlates positively with waist circumference in adolescents [5].”
BackgroundFinger, B. C., Dinan, T. G., & Cryan, J. F. (2010) · Psychopharmacology · doi:10.1007/s00213-010-1858-z · Cited by 79
Hypervulnerability of the adolescent prefrontal cortex to nutritional stress via reelin deficiency
Labouesse, M. A., Lassalle, O., Richetto, J., Iafrati, J., Weber‐Stadlbauer, U., Notter, T., Gschwind, T., Pujadas, L., Soriano, E., Reichelt, A. C., et al. (2016) · Molecular Psychiatry · doi:10.1038/mp.2016.193 · Cited by 79 · cited 1×
“Adolescence is considered a sensitive period for prefrontal cortex functional modulation by obesity, as HFD can inhibit prefrontal cortex synaptic plasticity to induce local perturbations in excitatory transmission in adolescent mice [106].”
BackgroundNucleus accumbens cytoarchitecture predicts weight gain in children
Rapuano, K. M., Laurent, J. S., Hagler, D. J., Hatton, S. N., Thompson, W. K., Jernigan, T. L., Dale, A. M., Casey, B. J., & Watts, R. (2020) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.2007918117 · Cited by 79 · cited 2×
“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].”
BackgroundObesity and cortisol: New perspectives on an old theme
van Rossum, E. F. C. (2017) · Obesity · doi:10.1002/oby.21774 · Cited by 76 · cited 2×
“Not all obese individuals have elevated cortisol and obesity development coincides with an increase in factors that enhance cortisol production, such as chronic stress, consumption of food high in sugar and fat, and reduced sleep [118,119].”
BackgroundSartorius, T., Ketterer, C., Kullmann, S., Balzer, M., Rotermund, C., Binder, S., Hallschmid, M., Machann, J., Schick, F., Somoza, V., et al. (2012) · Diabetes · doi:10.2337/db11-1521 · Cited by 73
Rudolf, S., Greggersen, W., Kahl, K. G., Hüppe, M., & Schweiger, U. (2014) · Psychiatry Research · doi:10.1016/j.psychres.2014.02.016 · Cited by 71 · cited 1×
“This form of depression has stronger links to peripheral [10,11] and central [12] inflammation.”
BackgroundRole of macrophages in the endocrine system
Rehman, A., Pacher, P., & Haskó, G. (2021) · Trends in Endocrinology & Metabolism · doi:10.1016/j.tem.2020.12.001 · Cited by 71 · cited 1×
“It is namely resident macrophages and T-lymphocyte immune cells that perpetuate the inflammatory situation in adipose tissue [68], and dietary saturated fatty acids can be a direct source of metabolic stress that can promote inflammation by increasing TLR4 signaling.”
BackgroundGariepy, G., Wang, J., Lesage, A. D., & Schmitz, N. (2010) · Obesity · doi:10.1038/oby.2009.333 · Cited by 70 · cited 1×
“, dread, unease) by 30% and 40%, respectively [1,20].”
Leptin treatment ameliorates anxiety in ob/ob obese mice
Asakawa, A., Inui, A., Inui, T., Katsuura, G., Fujino, M., & Kasuga, M. (2003) · Journal of Diabetes and its Complications · doi:10.1016/s1056-8727(02)00185-x · Cited by 70
Leptin/LepRb in the Ventral Tegmental Area Mediates Anxiety-Related Behaviors
Liu, J., Guo, M., & Lu, X. (2015) · The International Journal of Neuropsychopharmacology · doi:10.1093/ijnp/pyv115 · Cited by 68 · cited 1×
“The anxiolytic action of leptin in mice has been tied to leptin receptor signaling in mesolimbic dopamine neurons [137,138], whereas its effects to inhibit behavioral despair are attributed to signaling actions in the hippocampus [139].”
BackgroundInsulin and ghrelin: peripheral hormones modulating memory and hippocampal function
McNay, E. C. (2007) · Current Opinion in Pharmacology · doi:10.1016/j.coph.2007.10.009 · Cited by 67 · cited 1×
“The direct effects of insulin to increase neurogenesis may also contribute to its antidepressant-like and procognitive properties [131].”
BackgroundDown-regulation of cholinergic signaling in the habenula induces anhedonia-like behavior
Han, S., Yang, S. H., Kim, J. Y., Mo, S., Yang, E., Song, K. M., Ham, B., Mechawar, N., Turecki, G., Lee, H. W., et al. (2017) · Scientific Reports · doi:10.1038/s41598-017-01088-6 · Cited by 67 · cited 1×
“Neuronal activity in the lateral habenula is associated with encoding value of cues previously paired with aversive outcomes and is posited to contribute to anhedonia [82].”
BackgroundRebelos, E., Rinne, J. O., Nuutila, P., & Ekblad, L. L. (2021) · Journal of Clinical Medicine · doi:10.3390/jcm10071532 · Cited by 66 · cited 2×
“Reductions in glucose uptake in the hippocampus have been connected to cognitive deficits in obesity [59].”
BackgroundRole of cytokines in atypical depression
Yoon, H.-K., Kim, Y.-K., Lee, H.-J., Kwon, D.-Y., & Kim, L. (2012) · Nordic Journal of Psychiatry · doi:10.3109/08039488.2011.611894 · Cited by 65 · cited 1×
“This form of depression has stronger links to peripheral [10,11] and central [12] inflammation.”
BackgroundIncreased anxiety-like behavior is associated with the metabolic syndrome in non-stressed rats
Rebolledo-Solleiro, D., Roldán-Roldán, G., Díaz, D., Velasco, M., Larqué, C., Rico-Rosillo, G., Vega-Robledo, G. B., Zambrano, E., Hiriart, M., & Pérez de la Mora, M. (2017) · PLoS ONE · doi:10.1371/journal.pone.0176554 · Cited by 64
Unravelling the impacts of western-style diets on brain, gut microbiota and cognition
Kendig, M. D., Leigh, S., & Morris, M. J. (2021) · Neuroscience & Biobehavioral Reviews · doi:10.1016/j.neubiorev.2021.05.031 · Cited by 63
Xu, M.-X., Yu, R., Shao, L.-F., Zhang, Y.-X., Ge, C.-X., Liu, X.-M., Wu, W.-Y., Li, J.-M., & Kong, L.-D. (2016) · Brain Behavior and Immunity · doi:10.1016/j.bbi.2016.01.001 · Cited by 61 · cited 1×
“Reversing neuroinflammation via targeted genetic [96,97], pharmacological [98,99], or dietary [49,100] approaches that rescue behavioral anomalies offers convincing support for a causal role of neuroinflammation in obesity-induced neuropathophysiology.”
BackgroundChan, R. F., Turecki, G., Shabalin, A. A., Guintivano, J., Zhao, M., Xie, L. Y., van Grootheest, G., Kaminsky, Z. A., Dean, B., Penninx, B. W. J. H., et al. (2019) · Biological Psychiatry · doi:10.1016/j.biopsych.2019.10.014 · Cited by 61 · cited 12×
“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].”
BackgroundInfluentialEndothelium as a gatekeeper of fatty acid transport
Mehrotra, D., Wu, J., Papangeli, I., & Chun, H. J. (2014) · Trends in Endocrinology & Metabolism · doi:10.1016/j.tem.2013.11.001 · Cited by 60 · cited 1×
“Brain transport of fatty acids is elevated in individuals with metabolic syndrome [48].”
BackgroundAuguste, S., Fisette, A., Fernandes, M. F., Hryhorczuk, C., Poitout, V., Alquier, T., & Fulton, S. (2016) · International Journal of Neuropsychopharmacology · doi:10.1093/ijnp/pyw014 · Cited by 59 · cited 13×
“The effects of DIO on the hippocampus have received considerable attention because of the well-reported effects of HFD to elicit cognitive and emotional impairments [102].”
BackgroundInfluentialSelf-citationGuo, M., & Lu, X.-Y. (2014) · Translational Psychiatry · doi:10.1038/tp.2014.126 · Cited by 57 · cited 2×
“Correspondingly, several lines of evidence point to hypodopaminergic states in MDD. Blunted mesolimbic dopamine signaling has been more directly implicated in anhedonia, a cardinal symptom of MDD that is ineffectively treated by SSRIs [114].”
BackgroundChen, G.-Q., Peng, C.-L., Lian, Y., Wang, B.-W., Chen, P.-Y., & Wang, G.-P. (2021) · Frontiers in Nutrition · doi:10.3389/fnut.2021.662357 · Cited by 55 · cited 1×
“Dietary fat overload Several lines of evidence link poor diet, inflammation, and depressive symptomology [21,22].”
BackgroundLi, X., Liang, S., Li, Z., Li, S., Xia, M., Verkhratsky, A., & Li, B. (2019) · Frontiers in Psychiatry · doi:10.3389/fpsyt.2018.00734 · Cited by 54 · cited 2×
“Correspondingly, several lines of evidence point to hypodopaminergic states in MDD. Blunted mesolimbic dopamine signaling has been more directly implicated in anhedonia, a cardinal symptom of MDD that is ineffectively treated by SSRIs [114].”
Transcriptomic predictors of inflammation-induced depressed mood
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“Reversing neuroinflammation via targeted genetic [96,97], pharmacological [98,99], or dietary [49,100] approaches that rescue behavioral anomalies offers convincing support for a causal role of neuroinflammation in obesity-induced neuropathophysiology.”
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“Similarly, 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.”
BackgroundRecent Advances in the Cellular and Molecular Mechanisms of Hypothalamic Neuronal Glucose Detection
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“Reversing neuroinflammation via targeted genetic [96,97], pharmacological [98,99], or dietary [49,100] approaches that rescue behavioral anomalies offers convincing support for a causal role of neuroinflammation in obesity-induced neuropathophysiology.”
BackgroundEndocrine factors in key structural and intracellular changes in depression
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“Leptin Plasma levels of the adipose-derived hormone leptin negatively correlate with symptoms of anxiety and depression in women and men [116].”
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Anxiety-like behavior in female mice is modulated by STAT3 signaling in midbrain dopamine neurons
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Cited by
Sorted by citations
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“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…”
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BackgroundObesity: pathophysiology and therapeutic interventions
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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
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