Pathways linking obesity to neuropsychiatric disorders

Martins, Laís Bhering; Monteze, Nayara Mussi; Calarge, Chadi A.; Ferreira, Adaliene Versiani Matos; Teixeira, Antônio Lúcio

doi:10.1016/j.nut.2019.03.017

Cited by 72 publications

(52 citation statements)

References 86 publications

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“…A study conducted among British university students showed a positive correlation between depressive symptoms and consumption of highly palatable and high-calorie food, mainly high in carbohydrates, including sweets, biscuits, snacks and fast food [21]. In fact, high carbohydrate meals can temporarily improve mood, particularly because the consumption of highly palatable foods activates the brain opioid system, producing hedonic responses and stimulates the serotonergic system since the consumption of carbohydrates can increase the production of serotonin in the brain due to the increased availability of tryptophan [22,23].…”

Section: Psychological and Behavioral Aspectsmentioning

confidence: 99%

“…As in obese patients, also in depressed patients, an increase in the translocation of intestinal bacteria is detected which, by passing the intestinal mucosa, favors the activation of immune responses [120]. The excessive presence of lipopolysaccharide (LPS), a substance present in the outer membrane of bacteria, can cause metabolic endotoxemia that activates systemic macrophages through the binding of LPS to its specific receptor which triggers the immune system by inducing an inflammatory response [23,28]. On the contrary, after weight loss in obese individuals, reduced serum levels of the LPS-binding protein, a marker of endotoxemia, were found [28,121].…”

Section: Microbiotamentioning

confidence: 99%

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Depression and Obesity: Analysis of Common Biomarkers

Milano¹,

Paola²,

Carizzone³

et al. 2020

Diseases

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Depression and obesity are very common pathologies. Both cause significant problems of both morbidity and mortality and have decisive impacts not only on the health and well-being of patients, but also on socioeconomic and health expenditure aspects. Many epidemiological studies, clinical studies and meta-analyses support the association between mood disorders and obesity in relationships to different conditions such as the severity of depression, the severity of obesity, gender, socioeconomic status, genetic susceptibility, environmental influences and adverse experiences of childhood. Currently, both depression and obesity are considered pathologies with a high-inflammatory impact; it is believed that several overlapping factors, such as the activation of the cortico-adrenal axis, the exaggerated and prolonged response of the innate immune system and proinflammatory cytokines to stress factors and pathogens—as well as alterations of the intestinal microbiota which promote intestinal permeability—can favor the expression of an increasingly proinflammatory phenotype that can be considered a key and common phenomenon between these two widespread pathologies. The purpose of this literature review is to evaluate the common and interacting mechanisms between depression and obesity.

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Section: Psychological and Behavioral Aspectsmentioning

confidence: 99%

Section: Microbiotamentioning

confidence: 99%

Depression and Obesity: Analysis of Common Biomarkers

Milano¹,

Paola²,

Carizzone³

et al. 2020

Diseases

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“…The primary causes of BDs in dementia are unclear. APP, MAPT, APOE, and other variants in pathogenic genes (Table 1) as well as the presence of schizophrenia-and/or depression-related SNPs [25][26][27], together with additional metabolic disorders [28], cerebrovascular risk or consolidated vascular damage [4,[29][30][31], premorbid personality [32], and inappropriate management may contribute to BDs in AD. BDs partially correlate with conventional biomarkers of dementia [33,34]; however, agitation/aggression correlates with AD cerebrospinal fluid (CSF) biomarkers, and depression is inversely associated with core AD CSF pathology (low Aβ42, high Tau, and high pTau) [35,36].…”

Section: Introductionmentioning

confidence: 99%

Pharmacogenomics of Cognitive Dysfunction and Neuropsychiatric Disorders in Dementia

Cacabelos

2020

IJMS

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Symptomatic interventions for patients with dementia involve anti-dementia drugs to improve cognition, psychotropic drugs for the treatment of behavioral disorders (BDs), and different categories of drugs for concomitant disorders. Demented patients may take >6–10 drugs/day with the consequent risk for drug–drug interactions and adverse drug reactions (ADRs >80%) which accelerate cognitive decline. The pharmacoepigenetic machinery is integrated by pathogenic, mechanistic, metabolic, transporter, and pleiotropic genes redundantly and promiscuously regulated by epigenetic mechanisms. CYP2D6, CYP2C9, CYP2C19, and CYP3A4/5 geno-phenotypes are involved in the metabolism of over 90% of drugs currently used in patients with dementia, and only 20% of the population is an extensive metabolizer for this tetragenic cluster. ADRs associated with anti-dementia drugs, antipsychotics, antidepressants, anxiolytics, hypnotics, sedatives, and antiepileptic drugs can be minimized by means of pharmacogenetic screening prior to treatment. These drugs are substrates, inhibitors, or inducers of 58, 37, and 42 enzyme/protein gene products, respectively, and are transported by 40 different protein transporters. APOE is the reference gene in most pharmacogenetic studies. APOE-3 carriers are the best responders and APOE-4 carriers are the worst responders; likewise, CYP2D6-normal metabolizers are the best responders and CYP2D6-poor metabolizers are the worst responders. The incorporation of pharmacogenomic strategies for a personalized treatment in dementia is an effective option to optimize limited therapeutic resources and to reduce unwanted side-effects.

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“…Of course, the metabolic syndrome itself, without accompanying schizophrenia, may negatively affect cognitive functions. This was observed in middle-aged people with a diagnosis of MS, without mental illness, who, in comparison to their peers without MS, have greater problems in psychomotor efficiency and speed, creating concepts, decision making and intellectual functioning (19). Individuals with pathological obesity, in comparison to the group with BMI in normal range, obtain worse results in terms of operating memory and executive functions.…”

Section: Introductionmentioning

confidence: 94%

Metabolic Syndrome and Cognitive Functions in Schizophrenia—Implementation of Dietary Intervention

et al. 2020

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Introduction: The coexistence of schizophrenia and metabolic syndrome is a widely described phenomenon that contributes to the worse functioning of patients in everyday life. A relatively new area of research is the relationship between metabolic syndrome (MS) and cognitive function in patients with schizophrenia. The aim of the study was to verify the relationship between the presence of metabolic syndrome and cognitive function of patients with schizophrenia and to assess the possibility of changing cognitive function by introducing appropriate dietary intervention.

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Pathways linking obesity to neuropsychiatric disorders

Cited by 72 publications

References 86 publications

Depression and Obesity: Analysis of Common Biomarkers

Depression and Obesity: Analysis of Common Biomarkers

Pharmacogenomics of Cognitive Dysfunction and Neuropsychiatric Disorders in Dementia

Metabolic Syndrome and Cognitive Functions in Schizophrenia—Implementation of Dietary Intervention

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