Associations between thyroid hormones and biochemical metabolism in major depressive disorder patients with and without comorbid eating disorders.

Thyroid-stimulating hormone, fasting blood glucose and suicidal ideation in Chinese adolescents with major depressive disorder: a cross-sectional study

Background Thyroid function and glycolipid metabolic alterations are often associated with major depressive disorder (MDD), yet their roles in suicide risk among adolescents with MDD remain unclear. This study aimed to investigate thyroid-stimulating hormone (TSH) levels, glycolipid metabolism parameters, and their associations with suicidal ideation (SI) in adolescents with MDD. Methods This cross-sectional study was conducted at one general hospital and one psychiatric hospital in Anhui Province, China. Socio-demographic data and laboratory parameters were collected from participants, and the patients’ depressive symptoms and SI severity were assessed using the 24-item Hamilton Depression Rating Scale (HAMD-24) and the Positive and Negative Suicide Ideation Inventory (PANSI), respectively. TSH levels and glycolipid metabolism parameters were also measured. Results A total of 146 adolescents with MDD and 70 healthy controls (HCs) were enrolled in this study. Compared with HCs, patients had lower fasting blood glucose (FBG) levels (P < 0.001). Logistic regression analyses showed that a worse relationship with family, a higher HAMD-24 total score, and higher TSH and FBG levels were independently associated with concurrent SI in adolescents with MDD (all P < 0.05). Furthermore, receiver operating characteristic (ROC) curve analysis showed that the combination of these four factors had a good discriminatory ability for SI, with an area under the curve (AUC) of 0.851. Conclusion In this cross-sectional study, TSH and FBG levels were associated with SI in adolescents with MDD. Nevertheless, whether these parameters can serve as clinically useful biomarkers requires further validation in larger prospective studies.

Neurometabolic alterations in the anterior cingulate gyrus and putamen: Insights from adolescents with insomnia and depression.

BACKGROUND Sleep disorders are common in adolescents with major depressive disorder (MDD), with an incidence rate surpassing that of low mood. Nonetheless, the effects of sleep disturbances on brain function in adolescent MDD remain unclear. METHOD 97 right-handed, untreated adolescents with MDD and 63 healthy controls (HCs) underwent proton magnetic resonance spectroscopy (1H-MRS) scans of the anterior cingulate cortex (ACC) and putamen. Differential and association analysis examined the relationship between sleep quality, depression severity, and neurometabolic ratios of ACC and putamen in MDD groups. RESULTS Among 97 MDD patients, 64 were categorized into the insomnia symptom (IS) group, with an insomnia item score ≥ 1 on Hamilton Depression Rating Scale (HDRS) and a Pittsburgh Sleep Quality Index score ≥ 6. IS group exhibited significantly lower choline-to-creatine (Cho/Cr) ratios in the right ACC compared with the NIS group and HCs, and a higher Cho/Cr ratio in the right putamen compared with HCs. NIS group showed lower N-acetylaspartate-to-creatine (NAA/Cr) ratios in the right putamen compared with the IS group and HCs. Within the IS group, HDRS scores showed nominal negative correlations with NAA/Cr ratios in the bilateral ACC and Cho/Cr ratios in the right ACC. Insomnia item scores were nominally correlated with Cho/Cr ratios in the left ACC. However, these correlations did not survive FDR correction. CONCLUSION A substantial proportion of adolescents with depression experience sleep disturbances, which may be associated with altered brain neurometabolism. These preliminary findings highlight the need for further investigation into the neurobiological relevance of sleep disturbances in adolescent MDD.

Neuroimmune lipidome dysregulation in major depressive disorder: A meta-analysis of peripheral endocannabinoid and n-acylethanolamine signaling.

Major depressive disorder (MDD) is a prevalent psychiatric condition characterized by substantial biological heterogeneity. Evidence suggests that the endocannabinoid system (ECS), which regulates stress responses, emotional processing, and neuroimmune signaling, may contribute to depression pathophysiology. However, clinical studies examining circulating endocannabinoids (eCBs) and N-acylethanolamines (NAEs) in MDD have produced inconsistent findings. We therefore conducted a systematic review and meta-analysis to quantify peripheral alterations in eCBs and NAEs in individuals with MDD. Following PRISMA guidelines, case-control and cross-sectional studies comparing circulating levels of eCBs and NAEs between patients with MDD and healthy controls were identified. Standardized mean differences (SMDs) with 95 % confidence intervals (CIs) were calculated using a random-effects model. Between-study heterogeneity was assessed by using Cochran's Q test and further explored in subgroups analysis. Nine studies, including 514 individuals with MDD and 417 healthy controls, met the inclusion criteria. Patients with MDD exhibited significantly higher circulating levels of anandamide (AEA; SMD = 0.32, 95 % CI: 0.10---0.54, p = 0.005) and palmitoylethanolamide (PEA; SMD = 0.35, 95 % CI: 0.04---0.65, p = 0.03) compared with controls, whereas no significant differences were observed for 2-arachidonoylglycerol (2-AG) or oleoylethanolamide (OEA). Subgroup analyses indicated that the elevation in AEA levels were more pronounced among medicated patients and individuals with psychiatric comorbidities. These findings suggest selective alterations in ECS-related lipid mediators in individuals with MDD and support dysregulation of the ECS-NAE signaling axis in depression. Circulating lipid signaling molecules such as AEA and PEA may represent potential peripheral biomarkers of MDD, although longitudinal and mechanistic studies are needed to clarify the influence of treatment and comorbidities.

Gut Microbiome in Depression with and without REM Sleep Behavior Disorder.

Gut microbiome provides a candidate approach for potential risk stratification in psychiatric populations, and MDD + RBD may represent a biologically distinct depression subtype associated with potential neurodegenerative risk.

MS-based metabolic profiling in serum for bipolar disorder

Compensatory neurochemical adaptation in first-episode, drug-naïve depression: Integrating cortical and systemic metabolism using multivoxel 1H-MRS.

BACKGROUND Major depressive disorder (MDD) involves both central neurotransmission and systemic metabolic disturbances. This study investigated how body mass index (BMI) modulates prefrontal neurometabolic profiles and their relationship with depressive severity in depression. METHODS 66 first-episode, drug-naïve Han Chinese patients with MDD and 79 Han Chinese healthy controls were recruited. Using multi-voxel proton magnetic resonance spectroscopy, we quantified tissue-corrected metabolite-to-creatine ratios in the anterior cingulate cortex (ACC) and bilateral dorsolateral prefrontal cortex (DLPFC). Serum lipid profiles and 17-item Hamilton Depression Rating Scale (HAMD) scores were collected. Patients were stratified into low-BMI and normal-BMI subgroups. RESULTS Within the MDD cohort, the low-BMI subgroup showed lower HAMD-17 scores, triglyceride levels, and LDL-C levels and higher HDL-C levels than the normal-BMI subgroup. Nominally higher ACC GABA/Cr and DLPFC NAA/Cr ratios were observed in the low-BMI subgroup, although these differences did not survive FDR correction. In the additional comparison with low-BMI healthy controls, no neurometabolite difference survived false discovery rate correction. BMI subgroup significantly moderated the association between DLPFC Glu/Cr and HAMD-17 scores: the association was positive in the normal-BMI subgroup but negative in the low-BMI subgroup. CONCLUSIONS These findings suggest a possible compensatory neurochemical pattern associated with low BMI in depression. However, the cross-sectional design cannot determine whether this pattern reflects compensatory adaptation or a pre-existing neurobiological subtype, and low BMI alone should not be interpreted as evidence of metabolic stress. TRIAL REGISTRATION Chinese Clinical Trial Registry; URL: https://www.chictr.org.cn/; Registration number: ChiCTR2500109138.