Comorbid Major Depressive Disorder Research Articles

Comorbidity between major depressive disorder and physical diseases: a comprehensive review of epidemiology, mechanisms and management.

Populations with common physical diseases - such as cardiovascular diseases, cancer and neurodegenerative disorders - experience substantially higher rates of major depressive disorder (MDD) than the general population. On the other hand, people living with MDD have a greater risk for many physical diseases. This high level of comorbidity is associated with worse outcomes, reduced adherence to treatment, increased mortality, and greater health care utilization and costs. Comorbidity can also result in a range of clinical challenges, such as a more complicated therapeutic alliance, issues pertaining to adaptive health behaviors, drug-drug interactions and adverse events induced by medications used for physical and mental disorders. Potential explanations for the high prevalence of the above comorbidity involve shared genetic and biological pathways. These latter include inflammation, the gut microbiome, mitochondrial function and energy metabolism, hypothalamic-pituitary-adrenal axis dysregulation, and brain structure and function. Furthermore, MDD and physical diseases have in common several antecedents related to social factors (e.g., socioeconomic status), lifestyle variables (e.g., physical activity, diet, sleep), and stressful live events (e.g., childhood trauma). Pharmacotherapies and psychotherapies are effective treatments for comorbid MDD, and the introduction of lifestyle interventions as well as collaborative care models and digital technologies provide promising strategies for improving management. This paper aims to provide a detailed overview of the epidemiology of the comorbidity of MDD and specific physical diseases, including prevalence and bidirectional risk; of shared biological pathways potentially implicated in the pathogenesis of MDD and common physical diseases; of socio-environmental factors that serve as both shared risk and protective factors; and of management of MDD and physical diseases, including prevention and treatment. We conclude with future directions and emerging research related to optimal care of people with comorbid MDD and physical diseases.

Altered resting-state brain activity in major depressive disorder comorbid with subclinical hypothyroidism: A regional homogeneity analysis

BackgroundMajor depressive disorder (MDD), a common mental disorder worldwide, frequently coexists with various physical illnesses, and recent studies have shown an increased prevalence of subclinical hypothyroidism (SHypo) among MDD patients. However, the neural mechanisms shared and unique to these disorders and the associated alterations in brain function remain largely unknown. This study investigated the potential brain function mechanisms underlying comorbid MDD and SHypo. MethodThirty MDD patients (non-comorbid group), 30 MDD patients comorbid with SHypo (comorbid group), 26 patients with SHypo, and 30 healthy controls were recruited for resting-state functional magnetic resonance imaging (rs-fMRI). We used regional homogeneity (ReHo) to examine differences in internal cerebral activity across the four groups. ResultsCompared with the non-comorbid group, the comorbid group exhibited significantly higher ReHo values in the right orbital part of the middle frontal gyrus (ORBmid) and bilateral middle frontal gyrus; decreased ReHo values in the right middle temporal gyrus, right thalamus, and right superior temporal gyrus, and right insula. Within the comorbid group, serum TSH levels were negatively associated with the ReHo values of the right insula; the ReHo values of the right Insula were negatively associated with the retardation factor score; the ReHo values of the right ORBmid were positively correlated with the anxiety/somatization factor scores. ConclusionsThese findings provide valuable clues for exploring the shared neural mechanisms between MDD and SHypo and have important implications for understanding the pathophysiological mechanisms of the comorbidity of the two disorders.

Association of serotonin reuptake inhibitors with asthma control.

Background: Clinical trials demonstrated that selective serotonin reuptake inhibitors (SSRI) can improve asthma control in patients with comorbid major depressive disorder (MDD) and that this effect may be greater than the effect of SSRIs on depression. These findings suggest that SSRIs may improve asthma control in patients without MDD. Objective: The current retrospective study examined the effect of SSRIs and serotonin and norepinephrine reuptake inhibitors (SNRI) on asthma control in adult patients. We hypothesized that patients would have fewer asthma exacerbations after treatment with an SSRI or SNRI. Methods: Electronic health record data of adult patients (N = 592) who were seen at a University of Texas Southwestern (UTSW) hospital or clinic and had (1) an SSRI or SNRI prescription, (2) a previous asthma diagnosis, and (3) no mood disorder diagnosis were extracted by using the UTSW Clinical Data Exchange Network. Wilcoxon signed rank tests were used to compare oral corticosteroid prescriptions and asthma-related emergency department (ED) visits and hospitalizations in the 12 months before and after the start of an SSRI/SNRI. Results: Therapy with SSRIs/SNRIs was associated with a significant decrease in oral corticosteroid use (p = 0.003), ED visits (p = 0.002), and hospitalizations (p < 0.001). Conclusion: Results from the current study add to the existing literature by demonstrating a reduced rate of severe exacerbations in patients with asthma by using an SSRI/SNRI without limiting the analytic sample to a high-illness-severity subgroup defined by symptoms of asthma or depression. Future work should include a prospective, placebo controlled study with individuals who have asthma and no comorbid mental health condition, verified by a mental health professional.

Toward a Precision Treatment Approach for Metabolic Depression: Integrating Epidemiology, Neuroscience, and Psychiatry

BackgroundIndividuals with comorbid major depressive disorder and type 2 diabetes represent an important subgroup of patients for whom conventional treatment may be insufficient. A precision treatment approach that addresses insulin resistance with an outcome of a positive response to antidepressants may prove beneficial. MethodsThis study utilized an emulated target trial on a large dataset from the Optum Clinformatics Data Mart Database. We evaluated the effect of adjuvant pioglitazone, an insulin-sensitizing drug, on antidepressant response among 4696 people with type 2 diabetes, comparing it with DPP4 (dipeptidyl peptidase-4) inhibitors (non–insulin-sensitizing). An additional analysis involving 6518 participants was conducted to assess the efficacy of pioglitazone versus sulfonylureas. ResultsThe instrumental variable analysis indicated that the initiation of an antidepressant with pioglitazone was superior to DPP4 inhibitors in terms of antidepressant response, with fewer treatment shifts and/or additions of new antidepressant or antipsychotic over a 1-year period. This result was consistent when pioglitazone was compared with sulfonylureas in a supplemental analysis. ConclusionsOur findings suggest that pioglitazone may be more effective than DPP4 inhibitors or sulfonylureas in enhancing antidepressant response among people with comorbid major depressive disorder and type 2 diabetes. This provides a strong case for the use of pioglitazone in patients with these conditions, emphasizing the potential of precision medicine strategies. The results should be interpreted with caution due to inherent limitations associated with observational data.

The differences of event-related potential components in patients with comorbid depression and anxiety, depression, or anxiety alone

BackgroundThere was a high comorbidity rate of major depressive disorder (MDD) and generalized anxiety disorder (GAD), showing a poor prognosis and significant detrimental impact on functioning. The study aimed to find whether patients with comorbid GAD and MDD had some differences in cognitive functions from patients with MDD or GAD alone. Methods360 adult patients were enrolled from inpatient department of psychiatry from 2020 to 2022. They were divided into three groups with 120 patients for each group: MDD, GAD, and MDD + GAD. All the patients completed psychological evaluation scales including patient health questionnaire-9 (PHQ-9) and 7-item generalized anxiety disorder (GAD-7). All the patients underwent examinations of auditory brainstem response and event-related potentials (ERPs). ResultsIn MDD + GAD group, P3b latency was significantly longer than patients with MDD alone, and P300 reaction time was positively correlated with total score of GAD-7 and PHQ-9, and PHQ-9 total score was also significantly positively correlated with P2-P3b amplitude (all p < 0.05). In addition, MDD patients had significantly longer P300 reaction time and lower P2-P3b amplitude than the GAD group (p < 0.05). LimitationsIt was a single-center and cross-sectional study, and we used self-report scales as assessment tools. ConclusionsPatients with MDD and GAD comorbidity might have a worse cognitive function than MDD patients, and the severity of cognitive impairments was positively correlated with the severity of anxiety and depression symptoms.

Prevalence of substance use disorders among patients with systemic lupus erythematous and major depressive disorder

AbstractBackgroundMajor depressive disorder (MDD) has a higher prevalence among patients with systemic lupus erythematous (SLE). Patients with SLE struggle with stressors such as social stigma and reduced employment. Furthermore, substance use disorders (SUD) are strongly associated with MDD.ObjectivesThis research investigated whether comorbid MDD among patients with SLE is associated with an increased prevalence of SUD diagnoses. Rates of various SUD diagnoses were compared among patients with SLE.MethodsThis was a retrospective comparison study of the medical record. All data were extracted from I2B2, a deidentified dataset from an academic hospital in an urban setting. Upon stratifying patients with SLE into two groups with or without MDD, chi‐squared test comparing SUD was completed. An additional analysis stratified patients with MDD into two groups with or without comorbid SLE and completed the chi‐squared test to compare SUD.ResultsPatients with SLE and comorbid MDD were more likely to have diagnoses of tobacco, alcohol, and opioid disorders, among others. The most common SUD was tobacco (prevalence 59.94%). Furthermore, the diagnosis of SLE among patients with MDD was not associated with increased rates of SUD diagnosis. However, patients diagnosed with comorbid SLE and MDD were more likely to have tobacco use and opioid use disorder diagnosis.ConclusionsThis study demonstrates a consistently higher rate of SUD diagnoses among patients diagnosed with SLE and comorbid MDD versus SLE alone. Rates of both tobacco and opioid use disorder were higher among patients with MDD and comorbid SLE when compared to MDD alone. Our study is limited by its retrospective analysis and does not include an analysis of the treatment of comorbid depression on SUD. For clinicians who take care of patients with SLE, when they have comorbid MDD, SUD should be screened.

Comparison of behavioral activation-enhanced cognitive processing therapy and cognitive processing therapy among U.S. service members: A randomized clinical trial

Posttraumatic stress disorder (PTSD) and major depressive disorder (MDD) frequently co-occur and can cause significant impairment. Data are lacking as to whether interventions targeting both PTSD and MDD may improve treatment outcomes among individuals with this comorbidity compared with existing evidence-based PTSD treatments alone. This randomized trial compared the effectiveness of cognitive processing therapy (CPT) enhanced with behavioral activation (BA+CPT) versus CPT among 94 service members (52 women and 42 men; age M = 28.5 years) with comorbid PTSD and MDD. The primary outcome was clinician-administered depression symptom severity on the Montgomery-Åsberg Depression Rating Scale (MADRS) from pretreatment through 3-month follow-up. Intent-to-treat analyses using multilevel models showed statistically and clinically significant decreases in MADRS scores for both conditions over time, with no significant differences between BA+CPT and CPT. Secondary depression and PTSD symptom outcomes followed a similar pattern of results. For diagnostic MDD and PTSD outcomes using available data, no statistically significant differences between treatments emerged at posttreatment or 3-month follow-up. Sessions attended, dropout rate, and treatment satisfaction did not significantly differ between treatments. Outcomes were comparable for both treatments, suggesting that BA+CPT and CPT were similarly effective psychotherapy options for comorbid PTSD and MDD.

Cross-sectional field study comparing hippocampal subfields in patients with post-traumatic stress disorder, major depressive disorder, post-traumatic stress disorder with comorbid major depressive disorder, and adjustment disorder using routine clinical data.

The hippocampus is a central brain structure involved in stress processing. Previous studies have linked stress-related mental disorders, such as post-traumatic stress disorder (PTSD) and major depressive disorder (MDD), with changes in hippocampus volume. As PTSD and MDD have similar symptoms, clinical diagnosis relies solely on patients reporting their cognitive and emotional experiences, leading to an interest in utilizing imaging-based data to improve accuracy. Our field study aimed to determine whether there are hippocampal subfield volume differences between stress-related mental disorders (PTSD, MDD, adjustment disorders, and AdjD) using routine clinical data from a military hospital. Participants comprised soldiers (N = 185) with PTSD (n = 50), MDD (n = 70), PTSD with comorbid MDD (n = 38), and AdjD (n = 27). The hippocampus was segmented and volumetrized into subfields automatically using FreeSurfer. We used ANCOVA models with estimated total intracranial volume as a covariate to determine whether there were volume differences in the hippocampal subfields cornu ammonis 1 (CA1), cornu ammonis 2/3 (CA2/3), and dentate gyrus (DG) among patients with PTSD, MDD, PTSD with comorbid MDD, and AdjD. Furthermore, we added self-reported symptom duration and previous psychopharmacological and psychotherapy treatment as further covariates to examine whether there were associations with CA1, CA2/3, and DG. No significant volume differences in hippocampal subfields between stress-related mental disorders were found. No significant associations were detected between symptom duration, psychopharmacological treatment, psychotherapy, and the hippocampal subfields. Hippocampal subfields may distinguish stress-related mental disorders; however, we did not observe any subfield differences. We provide several explanations for the non-results and thereby inform future field studies.

The association between the CCDC88A gene polymorphism at rs1437396 and alcohol use disorder, with or without major depression disorder.

Girdin is a protein involved in neuronal migration and hippocampal development. It is encoded by the coiled-coil domain-containing 88A (CCDC88A) gene, located on the short arm of chromosome 2 (2p). The CCDC88A gene is modulated by the intergenic single-nucleotide polymorphism (SNP) of the rs1437396, situated 9.5 kb downstream from its transcription stop site. As recent genome-wide research has associated the T allele of the SNP with increased risk of alcohol use disorder (AUD), we wanted to validate this finding in an independent cohort and to test further for an association with comorbid major depressive disorder (MDD). The study included 226 AUD patients (AUD group), 53 patients with comorbid MDD, and 391 controls selected randomly. The participants were genotyped for the rs1437396 polymorphism using the real-time polymerase chain reaction. The association between the rs1437396 polymorphism and increased risk of AUD and AUD+MDD was tested with logistic regression. Our results show significantly higher frequency of the T risk allele in the AUD group (p=0.027) and even higher in the AUD+MDD group (p=0.016). In conclusion, this is the first study that has validated the association between the rs1437396 polymorphism of the CCDC88A gene and AUD with or without MDD. Studies on larger samples of patients are needed to further investigate the mechanism of this association.

Prevalence of overweight and obesity in patients with major depressive disorder with anxiety: Mediating role of thyroid hormones and metabolic parameters

BackgroundsAnxiety is a common comorbidity in major depressive disorder (MDD); however, its role in overweight and obesity in MDD patients remains unclear. We examined the relationship between severe anxiety and overweight and obesity, as well as the mediating role of thyroid hormones and metabolic parameters in MDD patients. MethodsThis cross-sectional study recruited 1718 first-episode drug-naïve MDD outpatients. All participants were rated on the Hamilton Depression Rating Scale for depression and Hamilton Anxiety Rating Scale for anxiety and measured in thyroid hormones and metabolic parameters. ResultsA total of 218 (12.7 %) individuals had severe anxiety. The prevalence of overweight and obesity in patients with severe anxiety was 62.8 % and 5.5 %, respectively. Severe anxiety symptoms were associated with overweight (Odds Ratio [OR]: 1.47, 95 % CI: 1.08, 2.00) and obesity (OR: 2.10, 95 % CI: 1.07, 4.15). The association between severe anxiety and overweight was mainly attenuated by thyroid hormones (40.4 %), blood pressure (31.9 %), and plasma glucose (19.1 %). For obesity, the association with severe anxiety was mainly attenuated by thyroid hormones (48.2 %), blood pressure (39.1 %), and total cholesterol (28.2 %). LimitationsDue to the cross-sectional design, no causal relationship could be derived. ConclusionsThyroid hormones and metabolic parameters can explain the risk of overweight and obesity associated with severe anxiety in MDD patients. These findings add to the knowledge of the pathological pathway of overweight and obesity in MDD patients with comorbid severe anxiety.

Body mass index and clinical outcomes in individuals with major depressive disorder: Findings from the GSRD European Multicenter Database

BackgroundIndividuals with major depressive disorder (MDD) are at higher risk for obesity. In turn, weight gain is a predisposing factor for depression. Although clinical data are sparse, suicide risk also appears to be elevated in obese patients. This study used data from the European Group for the Study of Resistant Depression (GSRD) to investigate clinical outcomes associated with body mass index (BMI) in MDD. MethodsData were drawn from 892 participants with MDD over the age of 18 years (580 female, 50.5 ± 13.6 years). Response and resistance to antidepressant medication, depression rating scale scores, and further clinical and sociodemographic variables were compared using multiple logistic and linear regressions controlled for age, sex, and risk of weight gain due to psychopharmacotherapy. ResultsOf the 892 participants, 323 were categorized as treatment-responsive and 569 as treatment-resistant. Within this cohort, 278 (31.1 %) were overweight (BMI = 25–29.9 kg/m2) and 151 (16.9 %) were obese (BMI > 30 kg/m2). Elevated BMI was significantly associated with higher suicidality, longer duration of psychiatric hospitalizations over their lifetimes, earlier age of onset of MDD, and comorbidities. There was a trend-wise association of BMI with treatment resistance. LimitationsData were analyzed in a retrospective, cross-sectional design. BMI was used as an exclusive measure of overweight and obesity. ConclusionsParticipants with comorbid MDD and overweight/obesity were at risk for worse clinical outcomes, suggesting that weight gain should be closely monitored in individuals with MDD in daily clinical practice. Further studies are needed to explore the neurobiological mechanisms linking elevated BMI to impaired brain health.

Symptoms of major depressive disorder and post-traumatic stress disorder in veterans with mild traumatic brain injury: A network analysis.

Mild Traumatic Brain Injury (mTBI, or concussion) is a debilitating condition that often leads to persistent cognitive and mental health problems post-injury. Post-traumatic Stress Disorder (PTSD) and Major Depressive Disorder (MDD) are two most commonly occurring mental health problems following mTBI and are suggested to be strong contributors to the persistent post-concussion symptoms. Thus, it is important to understand the symptomatology of PTSD and MDD post-mTBI, to better inform targets for behavioral health interventions. Therefore, the current study examined the symptom structure of post-mTBI co-morbid PTSD and MDD through network approaches; we compared the network structure of participants with a positive mTBI screen (N = 753) to the network structure of participants with a negative mTBI screen (N = 2044); lastly, we examined a network of PTSD and MDD symptoms with clinical covariates in a positive mTBI sample. We found that feeling distant/cutoff (P10) and difficulty concentrating (P15) were the most central symptoms in the positive mTBI network and sleep problems were the most prominent bridge nodes across the disorders. No significant difference between the positive and negative mTBI network were found through network comparison tests. Moreover, anxiety and insomnia were strongly associated with sleep symptoms and irritability symptoms, and emotional support and resilience were potential buffers against most of the PTSD and MDD symptoms. The results of this study might be particularly useful for identifying targets (i.e., feeling distant, concentration and sleep problems) for screening, monitoring and treatment after concussion to better inform post-mTBI mental health care and to improve treatment outcomes.

Novel implication of the prolactin (PRL) gene in the comorbidity of type 2 diabetes and depression.

The prolactin (PRL) system plays important behavioral, social, and metabolic roles, such as mediating social bonding and insulin secretion. Inherited dysfunction of the PRL pathway-related genes is associated with psychopathology and insulin resistance. We have previously suggested that the PRL system might be implicated in the comorbidity of psychiatric (depression) and type 2 diabetes (T2D) owing to the pleiotropy of PRL pathway-related genes. To our knowledge, no PRL variants have so far been reported in patients with either major depressive disorder (MDD) and/or T2D. In this study, we analyzed 6 variants within the PRL gene and tested them for the presence of parametric linkage and/or linkage disequilibrium (LD, i.e., linkage and association) with familial MDD, T2D, and their comorbidity. We found, for the first time, that the PRL gene and its novel risk variants are linked to and in LD (i.e., linkage and association) with familial MDD, T2D, and MDD-T2D comorbidity. PRL might play a key role in mental-metabolic comorbidity and can be considered a novel gene in MDD and T2D.

Serum Angiotensin-Converting Enzyme Methylation Level and Its Significance in Patients With Comorbid Major Depressive Disorder and Hypertension.

Major depressive disorder (MDD) often coexists with hypertension (HYT). DNA methylation has elicited vital functionality in their development. Angiotensin-converting enzyme (ACE) is a vital enzyme in blood pressure. This study investigated the effect of ACE methylation on depression and HYT severity in patients with comorbid MDD and HYT (MDD + HYT). A total of 119 patients (41 men, 78 women, average age: 56.8 ± 9.1 years) with MDD + HYT were enrolled, with 89 healthy subjects (29 men, 60 women, average age: 57.4 ± 9.7 years) were enrolled. The Hamilton Depression Rating Scale-17 and self-rating depression scale scoring scales were used to assess the depression degree of patients, serum ACE methylation level in MDD + HYT patients was measured by means of bisulfite sequencing polymerase chain reaction, with subsequent analysis of the diagnostic efficacy of ACE methylation for MDD + HYT. The independent risk factors for sMDD + HYT were explored. Serum ACE methylation levels were significantly increased in MDD + HYT patients. The area under the curve of serum ACE methylation level for accurate diagnosis of MDD + HYT was 0.8471, and the cut-off value was 26.9 (sensitivity 83.19%, specificity 73.03%). ACE methylation was an independent risk factor for sMDD + HYT (P = 0.014; odds ratio, 1.071; 95% confidence interval = 1.014-1.131). The elevated serum ACE methylation level (P < 0.001) in patients with MDD + HYT elicited definite diagnostic values for MDD + HYT, and ACE methylation level was independently correlated with sMDD + HYT (P < 0.05).

Fronto-central resting-state 15-29 Hz transient beta events change with therapeutic transcranial magnetic stimulation for posttraumatic stress disorder and major depressive disorder

Repetitive transcranial magnetic stimulation (rTMS) is an established treatment for major depressive disorder (MDD) and shows promise for posttraumatic stress disorder (PTSD), yet effectiveness varies. Electroencephalography (EEG) can identify rTMS-associated brain changes. EEG oscillations are often examined using averaging approaches that mask finer time-scale dynamics. Recent advances show some brain oscillations emerge as transient increases in power, a phenomenon termed “Spectral Events,” and that event characteristics correspond with cognitive functions. We applied Spectral Event analyses to identify potential EEG biomarkers of effective rTMS treatment. Resting 8-electrode EEG was collected from 23 patients with MDD and PTSD before and after 5 Hz rTMS targeting the left dorsolateral prefrontal cortex. Using an open-source toolbox (https://github.com/jonescompneurolab/SpectralEvents), we quantified event features and tested for treatment associated changes. Spectral Events in delta/theta (1–6 Hz), alpha (7–14 Hz), and beta (15–29 Hz) bands occurred in all patients. rTMS-induced improvement in comorbid MDD PTSD were associated with pre- to post-treatment changes in fronto-central electrode beta event features, including frontal beta event frequency spans and durations, and central beta event maxima power. Furthermore, frontal pre-treatment beta event duration correlated negatively with MDD symptom improvement. Beta events may provide new biomarkers of clinical response and advance the understanding of rTMS.

Identification of novel biomarkers linking depressive disorder and Alzheimer’s disease based on an integrative bioinformatics analysis

BackgroundPrevious reports revealed that a history of major depressive disorder (MDD) increased the risk of Alzheimer’s disease (AD). The immune disorder is associated with MDD and AD pathophysiology. We aimed to identify differentially expressed immune-related genes (DEIRGs) that are involved in the pathogenesis of MDD and AD.MethodsWe downloaded mRNA expression profiles (GSE76826 and GSE5281) from the Gene Expression Omnibus (GEO) database. The R software was used to identify DEIRGs for the two diseases separately. Functional enrichment analysis and PPI network of DEIRGs were performed. Finally, the relationship between shared DEIRGs and immune infiltrates of AD and MDD were analyzed, respectively.ResultsA total of 121 DEIRGs linking AD and MDD were identified. These genes were significantly enriched in immune-related pathways, such as the JAK-STAT signaling pathway, regulation of chemotaxis, chemotaxis, cytokine-cytokine receptor interaction, and primary immunodeficiency. Furthermore, three shared DEIRGs (IL1R1, CHGB, and NRG1) were identified. Correlation analysis between DEIRGs and immune cells revealed that IL1R1 and NRG1 had a negative or positive correlation with some immune cells both in AD and MDD.ConclusionBoth DEIRGs and immune cell infiltrations play a vital role in the pathogenesis of AD and MDD. Our findings indicated that there are common genes and biological processes between MDD and AD, which provides a theoretical basis for the study of the comorbidity of MDD and AD.

Preliminary evidence that individuals with remitted alcohol use disorder and major depressive disorder exhibit enhanced neural responses to reward: An EEG study

IntroductionDisruptions in neural responses to reward are implicated in risk for Alcohol Use Disorder (AUD) and Major Depressive Disorder (MDD). It is not clear whether these findings extend to those in remission from AUD and MDD, a critical question as studies of remission can (a) rule out effects due to current symptoms, and (b) can reveal potential trait-like differences. MethodsIndividuals with and without remitted AUD (rAUD) and/or rMDD (rMDD) were drawn from a larger study to create four groups: rAUD (n = 54), rMDD (n = 66), rAUD + rMDD (n = 53), and a community control group (CCG; n = 81). Participants completed a validated monetary reward task during electroencephalogram (EEG). Multilevel models examined group differences in event-related potentials and time–frequency indices of reward and loss responsiveness, namely, reward positivity (RewP), feedback negativity (FN), reward-related delta power, and loss-related theta power. ResultsAnalyses revealed that the rAUD + rMDD group had significantly higher reward-related delta activity than the three other groups (p-values < 0.01), which did not differ from each other. Sensitivity analyses revealed this relationship fell just above the threshold set for significance after controlling for residual current MDD and AUD symptoms (p =.05). There were no other group differences or significant interactions (p-values > 0.05). ConclusionsTo our knowledge, this is the first study to show that individuals with remitted AUD and MDD demonstrate increased sensitivity to rewards compared to individuals with remitted AUD alone, MDD alone, and without AUD or MDD. These findings suggest heightened motivational salience to reward might be an important factor in comorbid AUD and MDD.

PTSD and comorbid MDD is associated with activation of the right frontoparietal network

There is growing evidence of abnormalities in intrinsic functional connectivity (FC) in posttraumatic stress disorder (PTSD) and major depressive disorder (MDD). However, there has been less work on the commonly occurring co-presentation of PTSD and MDD. Characterising intrinsic FC abnormalities in this clinical population is important for understanding how they may contribute towards impairments underpinned by different networks. Participants were mothers enroled in the Drakenstein Child Health Study from Western Cape, South Africa. Mothers between 18 and 50 years of age were recruited and divided into 4 groups: PTSD, MDD, PTSD with MDD, and healthy controls. Participants underwent resting-state fMRI at the 18-month postpartum time point. Functional connectivity within and between higher order cognitive control networks, including the salience, dorsal attention, frontoparietal, and default mode networks were compared across the 4 groups. PTSD with comorbid MDD was associated with greater intrinsic FC within the R FPAR, relative to controls and the mono-diagnostic groups. Intrinsic FC differences were observed within the default mode network for the MDD group. No group differences in connectivity between networks were observed. Differential intrinsic connectivity in participants with comorbidity are consistent with evidence that such individuals have more severe illness and require more robust intervention.

Prevalence, risk factors and clinical correlates of glucose disturbances in a large sample of Han Chinese patients with first-episode drug-naïve major depressive disorder.

Glucose disturbances are a common comorbidity of major depressive disorder (MDD) patients and have been extensively studied in the past. However, few studies have explored glucose disturbances in first-episode drug-naïve (FEDN) MDD patients. The purpose of this study was to examine the prevalence and risk factors of glucose disturbances in FEDN MDD patients to understand the relationship between MDD and glucose disturbances in the acute early phase and provide important implications for therapeutic interventions. Using a cross-sectional design, we recruited a total of 1718 MDD patients. We collected their socio-demographic information, clinical data, and blood glucose indicators.17-item Hamilton Depression Rating Scale (HAMD), 14-item Hamilton Anxiety Rating Scale (HAMA), and the positive symptom subscale of the Positive and Negative Syndrome Scale (PANSS) were used to assess their depression, anxiety, psychotic symptoms, respectively. The prevalence of glucose disturbances in FEDN MDD patients was 13.6%. Depression, anxiety and psychotic symptoms, body mass index (BMI) levels and suicide attempts rates were higher in the group with glucose disorders than in the group without glucose disorders among patients with first-episode drug-naive MDD. Correlation analysis showed that glucose disturbances were associated with HAMD score, HAMA score, BMI, psychotic symptoms and suicide attempts. Furthermore, binary logistic regression showed that HAMD score and suicide attempts were independently associated with glucose disturbances in MDD patients. Our findings suggest that the prevalence of comorbid glucose disturbances is very high in FEDN MDD patients. Moreover, more severe depressive symptoms and higher suicide attempts are correlated with glucose disturbances in MDD FEDN patients in the early stage.

A Brief History of Transcranial Magnetic Stimulation

A Brief History of Transcranial Magnetic Stimulation