Evidence from high-income countries suggests that childhood trauma is associated with schizophrenia. Studies of childhood trauma and schizophrenia in low and middle income (LMIC) countries are limited. This study examined the prevalence of childhood traumatic experiences among cases and controls and the relationship between specific and cumulative childhood traumatic experiences and schizophrenia in a sample in South Africa.

Data were from the Genomics of Schizophrenia in the South African Xhosa people study. Cases with schizophrenia and matched controls were recruited from provincial hospitals and clinics in the Western and Eastern Cape regions in South Africa. Childhood traumatic experiences were measured using the Childhood Trauma Questionnaire (CTQ). Adjusted logistic regression models estimated associations between individual and cumulative childhood traumatic experiences and schizophrenia.

Traumatic experiences were more prevalent among cases than controls. The odds of schizophrenia were 2.44 times higher among those who experienced any trauma than those who reported no traumatic experiences (95% CI 1.77–3.37). The odds of schizophrenia were elevated among those who experienced physical/emotional abuse (OR 1.59, CI 1.28–1.97), neglect (OR 1.39, CI 1.16–1.68), and sexual abuse (OR 1.22, CI 1.03–1.45) compared to those who did not. Cumulative physical/emotional abuse and neglect experiences increased the odds of schizophrenia as a dose–response relationship.

Childhood trauma is common in this population. Among many other benefits, interventions to prevent childhood trauma may contribute to a decreasing occurrence of schizophrenia.

To examine the association of psychological distress with serum C-reactive protein (CRP) in a South African cohort.

Data were analysed on individuals aged ≥15 years from the South African National Health and Nutrition Examination Survey (SANHANES) of 2012. Psychological distress was evaluated using the Kessler Psychological Distress Scale. Linear regression models assessed the association of psychological distress with serum CRP, adjusting for possible confounding factors.

The analytic sample comprised n = 3944 individuals (mean age = 40 and sex = 36% males). Psychological distress was significantly associated with increased serum CRP levels (B = 0.31 and p = 0.001). This association was no longer significant after adjusting for demographic variables, lifestyle factors, cardiac disease, diabetes, hypertension, trauma and anti-inflammatory medication use (B = 0.15 and p = 0.062).

Psychological distress was associated with elevated levels of CRP among South African adults. However, the association was confounded by a range of factors, with demographic variables (age, sex and population group) having the largest confounding effect. These findings indicate that CRP is not a useful biomarker of psychological distress, and that additional work is needed on the underlying psychobiology of psychological distress.

Bipolar disorder (BD) and obsessive compulsive disorder (OCD) are prevalent, comorbid, and disabling conditions, often characterized by early onset and chronic course. When comorbid, OCD and BD can determine a more pernicious course of illness, posing therapeutic challenges for clinicians. Available reports on prevalence and clinical characteristics of comorbidity between BD and OCD showed mixed results, likely depending on the primary diagnosis of analyzed samples.

We assessed prevalence and clinical characteristics of BD comorbidity in a large international sample of patients with primary OCD (n = 401), through the International College of Obsessive–Compulsive Spectrum Disorders (ICOCS) snapshot database, by comparing OCD subjects with vs without BD comorbidity.

Among primary OCD patients, 6.2% showed comorbidity with BD. OCD patients with vs without BD comorbidity more frequently had a previous hospitalization (p < 0.001) and current augmentation therapies (p < 0.001). They also showed greater severity of OCD (p < 0.001), as measured by the Yale–Brown Obsessive Compulsive Scale (Y-BOCS).

These findings from a large international sample indicate that approximately 1 out of 16 patients with primary OCD may additionally have BD comorbidity along with other specific clinical characteristics, including more frequent previous hospitalizations, more complex therapeutic regimens, and a greater severity of OCD. Prospective international studies are needed to confirm our findings.

Childhood maltreatment (CM) plays an important role in the development of major depressive disorder (MDD). The aim of this study was to examine whether CM severity and type are associated with MDD-related brain alterations, and how they interact with sex and age.

Within the ENIGMA-MDD network, severity and subtypes of CM using the Childhood Trauma Questionnaire were assessed and structural magnetic resonance imaging data from patients with MDD and healthy controls were analyzed in a mega-analysis comprising a total of 3872 participants aged between 13 and 89 years. Cortical thickness and surface area were extracted at each site using FreeSurfer.

CM severity was associated with reduced cortical thickness in the banks of the superior temporal sulcus and supramarginal gyrus as well as with reduced surface area of the middle temporal lobe. Participants reporting both childhood neglect and abuse had a lower cortical thickness in the inferior parietal lobe, middle temporal lobe, and precuneus compared to participants not exposed to CM. In males only, regardless of diagnosis, CM severity was associated with higher cortical thickness of the rostral anterior cingulate cortex. Finally, a significant interaction between CM and age in predicting thickness was seen across several prefrontal, temporal, and temporo-parietal regions.

Severity and type of CM may impact cortical thickness and surface area. Importantly, CM may influence age-dependent brain maturation, particularly in regions related to the default mode network, perception, and theory of mind.

The aim of this paper was to provide a systematic review and update on the available longitudinal studies on the impact of prenatal alcohol exposure (PAE) on language, speech and communication development, as well as associated potential environmental confounders during the preschool period.

A literature search was restricted to English, full‐text, peer‐reviewed, longitudinal studies in from 1970 until present: PUBMed, Scopus, Web of Science {C-e Collection, Biological Abstracts, KCI-Kean Journal Database, Russian Science Citation Index, SciELO Citation Index, Zoological Rec-d}, Academic Search Premier (Africa-Wide Information, CINAHL, MEDLINE, PsycINFO. Keywords included: prenatal alcohol exposure (PAE); speech or language or communication outcomes; neurocognitive or neurodevelopment or neurobehavioral or neurobehavioural; infant or baby or toddler or preschooler; longitudinal or follow-up. The inclusion criteria included (i) longitudinal cohorts with at least 2 time-points; (ii) association of light, moderate or heavy PAE on language, speech or communication delay, development or disorder; (iii) environmental confounders; (iv) infants up to preschool age.

Six studies satisfied the threshold for inclusion. Three studies reported that PAE was significantly associated with receptive or expressive delay. These studies demonstrated lower scores on either receptive or expressive communication in the alcohol group in comparison to the non-alcohol group, even after controlling for environmental factors up to 36 months.

Evidence from the longitudinal studies reviewed suggest that PAE influenced delays in receptive and expressive communication up to 36 months. Contextual risk factors played a significant role in language development over time and especially as children approached school age.