In contemporary neuroimaging studies, it has been observed that patients with major depressive disorder (MDD) exhibit aberrant spontaneous neural activity, commonly quantified through the amplitude of low-frequency fluctuations (ALFF). However, the substantial individual heterogeneity among patients poses a challenge to reaching a unified conclusion.

To address this variability, our study adopts a novel framework to parse individualized ALFF abnormalities. We hypothesize that individualized ALFF abnormalities can be portrayed as a unique linear combination of shared differential factors. Our study involved two large multi-center datasets, comprising 2424 patients with MDD and 2183 healthy controls. In patients, individualized ALFF abnormalities were derived through normative modeling and further deconstructed into differential factors using non-negative matrix factorization.

Two positive and two negative factors were identified. These factors were closely linked to clinical characteristics and explained group-level ALFF abnormalities in the two datasets. Moreover, these factors exhibited distinct associations with the distribution of neurotransmitter receptors/transporters, transcriptional profiles of inflammation-related genes, and connectome-informed epicenters, underscoring their neurobiological relevance. Additionally, factor compositions facilitated the identification of four distinct depressive subtypes, each characterized by unique abnormal ALFF patterns and clinical features. Importantly, these findings were successfully replicated in another dataset with different acquisition equipment, protocols, preprocessing strategies, and medication statuses, validating their robustness and generalizability.

This research identifies shared differential factors underlying individual spontaneous neural activity abnormalities in MDD and contributes novel insights into the heterogeneity of spontaneous neural activity abnormalities in MDD.

We aimed to examine the association between dietary Se intake and CVD risk in Chinese adults.

This prospective cohort study included adults above 20 years old in the China Health and Nutrition Survey (CHNS), and they were followed up from 1997 to 2015 (n 16 030). Dietary data were retrieved from CHNS, and a 3-d, 24-h recall of food intake was used to assess the cumulative average intake of dietary Se, which was divided into quartiles. The Cox proportional hazards model was adopted to analyse the association between dietary Se intake and incident CVD risk.

CHNS (1991, 1993, 1997, 2000, 2004, 2006, 2009, 2011 and 2015)

A total of 663 respondents developed CVD after being followed up for a mean of 9·9 years (median 9 years). The incidence of CVD was 4·3, 3·7, 4·6 and 4·0 per 1000 person-years across the quartiles of cumulative Se intake. After adjusting all potential factors, no significant associations were found between cumulative Se intake and CVD risk. No interactions were found between Se intake and income, urbanisation, sex, region, weight, hypertension and CVD risk.

We found no association between dietary Se and CVD.

There is growing evidence that gray matter atrophy is constrained by normal brain network (or connectome) architecture in neuropsychiatric disorders. However, whether this finding holds true in individuals with depression remains unknown. In this study, we aimed to investigate the association between gray matter atrophy and normal connectome architecture at individual level in depression.

In this study, 297 patients with depression and 256 healthy controls (HCs) from two independent Chinese dataset were included: a discovery dataset (105 never-treated first-episode patients and matched 130 HCs) and a replication dataset (106 patients and matched 126 HCs). For each patient, individualized regional atrophy was assessed using normative model and brain regions whose structural connectome profiles in HCs most resembled the atrophy patterns were identified as putative epicenters using a backfoward stepwise regression analysis.

In general, the structural connectome architecture of the identified disease epicenters significantly explained 44% (±16%) variance of gray matter atrophy. While patients with depression demonstrated tremendous interindividual variations in the number and distribution of disease epicenters, several disease epicenters with higher participation coefficient than randomly selected regions, including the hippocampus, thalamus, and medial frontal gyrus were significantly shared by depression. Other brain regions with strong structural connections to the disease epicenters exhibited greater vulnerability. In addition, the association between connectome and gray matter atrophy uncovered two distinct subgroups with different ages of onset.

These results suggest that gray matter atrophy is constrained by structural brain connectome and elucidate the possible pathological progression in depression.

To examine the associations of pregnant women’s dietary and sedentary behaviours with their children’s birth weight.

Secondary data analysis was conducted using data from a randomised controlled trial, Communicating Healthy Beginnings Advice by Telephone, conducted in Australia. Information on mothers’ socio-demographics, dietary and sedentary behaviours during pregnancy was collected by telephone survey at the third trimester. Birth weight data were extracted from the child’s health record book. Multinomial logistic regression models were built to examine the associations of pregnant women’s dietary and sedentary behaviours with children’s birth weight.

Participating families.

Pregnant women and their children.

A total of 1132 mother–child dyads were included in the analysis. The majority of infants (87 %, n 989) were of normal birth weight (2500 g to <4000 g), 4 % (n 50) had low birth weight (<2500 g) and 8 % (n 93) had macrosomia (≥4000 g). Mothers who ate processed meat during pregnancy were more likely to have macrosomia (adjusted risk ratio (ARR) 1·80, 95 % CI (1·12, 2·89)). The risk of macrosomia decreased as the number of dietary recommendations met by mothers increased (ARR 0·84, 95 % CI (0·71, 0·99)). Children’s birth weight was not associated with mothers’ sedentary time. Children’s low birth weight was not associated with mothers’ dietary and sedentary behaviours during pregnancy.

Maternal consumption of processed meat during pregnancy was associated with an increased risk of macrosomia. Increasing number of dietary recommendations met by mothers was associated with a lower risk of macrosomia. The findings suggested encouraging pregnancy women to meet dietary recommendation will benefit children’s birth weight.

Inflammation plays a critical role in the progression of chronic liver diseases, and diet can modulate inflammation. Whether an inflammatory dietary pattern is associated with higher risk of hepatic steatosis or fibrosis remains unclear. We aimed to investigate the associations between inflammatory dietary pattern and the odds of hepatic steatosis and fibrosis.

In this nationwide cross-sectional study, diet was measured using two 24-h dietary recalls. Empirical dietary inflammatory pattern (EDIP) score was derived to assess the inflammatory potential of usual diet, which has been validated to highly predict inflammation markers in the study population. Controlled attenuation parameter (CAP) and liver stiffness measurement (LSM) were derived from FibroScan to define steatosis and fibrosis, respectively.

US National Health and Nutrition Examination Survey.

4171 participants aged ≥18 years.

A total of 1436 participants were diagnosed with S1 steatosis (CAP ≥ 274 dB/m), 255 with advanced fibrosis (LSM ≥ 9·7 kPa). Compared with those in the lowest tertile of EDIP-adherence scores, participants in the highest tertile had 74 % higher odds of steatosis (OR: 1·74, 95 % CI (1·26, 2·41)). Such positive association persisted among never drinkers, or participants who were free of hepatitis B and/or C. Similarly, EDIP was positively associated with CAP in multivariate linear model (P < 0·001). We found a non-significant association of EDIP score with advanced fibrosis or LSM (P = 0·837).

Our findings suggest that a diet score that is associated with inflammatory markers is associated with hepatic steatosis. Reducing or avoiding pro-inflammatory diets intake might be an attractive strategy for fatty liver disease prevention.

As a neuroprogressive illness, depression is accompanied by brain structural abnormality that extends to many brain regions. However, the progressive structural alteration pattern remains unknown.

To elaborate the progressive structural alteration of depression according to illness duration, we recruited 195 never-treated first-episode patients with depression and 130 healthy controls (HCs) undergoing T1-weighted MRI scans. Voxel-based morphometry method was adopted to measure gray matter volume (GMV) for each participant. Patients were first divided into three stages according to the length of illness duration, then we explored stage-specific GMV alterations and the causal effect relationship between them using causal structural covariance network (CaSCN) analysis.

Overall, patients with depression presented stage-specific GMV alterations compared with HCs. Regions including the hippocampus, the thalamus and the ventral medial prefrontal cortex (vmPFC) presented GMV alteration at onset of illness. Then as the illness advanced, others regions began to present GMV alterations. These results suggested that GMV alteration originated from the hippocampus, the thalamus and vmPFC then expanded to other brain regions. The results of CaSCN analysis revealed that the hippocampus and the vmPFC corporately exerted causal effect on regions such as nucleus accumbens, the precuneus and the cerebellum. In addition, GMV alteration in the hippocampus was also potentially causally related to that in the dorsolateral frontal gyrus.

Consistent with the neuroprogressive hypothesis, our results reveal progressive morphological alteration originating from the vmPFC and the hippocampus and further elucidate possible details about disease progression of depression.

Genome-wide association studies (GWAS) have consistently revealed that a variant of microRNA 137 (MIR137) shows a quite significant association with schizophrenia. Identifying the network of genes regulated by MIR137 could provide insights into the biological processes underlying schizophrenia. In addition, DLPFC functional connectivity, a robust correlate of MIR137, may provide plausible endophenotypes. However, the regulatory role of the MIR137 gene network in the disrupted functional connectivity remains unclear. Here, we tested the effects of the MIR137 regulated genes on the risk for schizophrenia and DLPFC functional connectivity.

To evaluate the additive effects of the MIR137 regulated genes (N = 1274), we calculated a MIR137 polygenic risk score (PRS) for schizophrenia and tested its association with the risk for schizophrenia in the genomic data of a Han Chinese population that included schizophrenia patients (N = 589) and normal controls (N = 575). We then investigated the association between MIR137 PRS and DLPFC functional connectivity in two independent young healthy cohorts (N = 356 and N = 314).

We found that the MIR137 PRS successfully captured the differences in genetic structure between the patients and controls, but the single gene MIR137 did not. We then consistently found that a higher MIR137 PRS was correlated with lower functional connectivities between the DLPFC and both the superior parietal cortex and the inferior temporal cortex in two independent cohorts.

The findings suggested that these two functional connectivities of the DLPFC could be important endophenotypes linking the MIR137-regulated genetic structure to schizophrenia.

The purpose of the present study was to examine the influence of maternal pre-pregnancy BMI and gestational weight gain (GWG) on initiation and duration of infant breast-feeding in a prospective birth cohort study.

Breast-feeding information was collected at 1, 3, 6 and 12 months postpartum. The association of pre-pregnancy BMI and GWG with delayed lactogenesis II and termination of exclusive breast-feeding was assessed with logistic regression analysis. The risk of early termination of any breast-feeding during the first year postpartum was assessed with Cox proportional hazards models.

Urban city in China.

Women with infants from the Ma’anshan Birth Cohort Study (n 3196).

The median duration of any breast-feeding in this cohort was 7·0 months. Pre-pregnancy obese women had higher risks of delayed lactogenesis II (risk ratio=1·89; 95 % CI 1·04, 3·43) and early termination of any breast-feeding (hazard ratio=1·38; 95 % CI 1·09, 1·75) adjusted for potential maternal and infant confounders, when compared with normal-weight women. No differences in breast-feeding initiation or duration of exclusive breast-feeding according to pre-pregnancy BMI were found. Moreover, GWG was not associated with any poor breast-feeding outcomes.

The present study indicated that pre-pregnancy obesity increases the risks of delayed lactogenesis II and early termination of any breast-feeding in Chinese women.