Various studies have examined associations between maternal vitamin D (VD) deficiency and offspring health, including offspring brain health. The purpose of this review was to summarize current evidence concerning the impact of maternal VD deficiency on brain development and function in offspring. A systematic search was conducted within Medline (on Ovid) for studies published through 7 May 2015. Animal and human studies that examined associations between maternal VD status or developmental VD deficiency and offspring brain development and function were included. A total of 26 animal studies and 10 human studies met the inclusion criteria. Several animal studies confirmed the hypothesis that low prenatal VD status may affect brain morphology and physiology as well as behavioral outcomes. In humans, subtle cognitive and psychological impairments in offspring of VD-deficient mothers were observed. However, data obtained from animal and human studies provide inconclusive evidence, and results seem to depend on strain or race and age of offspring. To conclude, prenatal VD status is thought to play an important role in brain development, cognitive function, and psychological function. However, results are inconclusive; validation of these findings and investigation of underlying mechanisms are required. Thus, more investigation is needed before recommending supplementation of VD during pregnancy to promote brain health of offspring.

The majority of patients with epilepsy report that seizures are sometimes triggered or provoked. Stress is the most frequently self-reported seizure-precipitant. The mechanisms underlying stress-sensitivity of seizures are currently unresolved. We hypothesized that stress-sensitivity of seizures relates to alteration of the stress response, which could affect neuronal excitability and hence trigger seizures. To study this, children with epilepsy between 6 and 17 years of age and healthy controls, with similar age, sex and intelligence, were exposed to a standardized acute psychosocial stressor (the Trier Social Stress Test for Children), during which salivary cortisol and sympathetic parameters were measured. Beforehand, the relation between stress and seizures in children with epilepsy was assessed by (i) a retrospective questionnaire; and (ii) a prospective 6-week diary on stress and seizure occurrence. Sixty-four children with epilepsy and 40 control subjects were included in the study. Of all children with epilepsy, 49% reported that seizures were precipitated by acute stress. Diary analysis showed a positive association between acute stress and seizures in 62% of children who experienced at least one seizure during the diary period. The acute social stress test was completed by 56 children with epilepsy and 37 control subjects. Children with sensitivity of seizures for acute stress, either determined by the questionnaire or by the prospective diary, showed a blunted cortisol response to stress compared with patients without acute stress-precipitated seizures and healthy controls (questionnaire-based F = 2.74, P = 0.018; diary-based F = 4.40, P = 0.007). No baseline differences in cortisol were observed, nor differences in sympathetic stress response. The relation between acute stress-sensitivity of seizures and the cortisol response to stress remained significant in multivariable analysis (β = -0.30, P = 0.03). Other variables associated with the acute stress response were the number of anti-epileptic drugs (β = -0.27, P = 0.05) and sleep quality (β = 0.30, P = 0.03). In conclusion, we show that children with acute stress-sensitive seizures have a decreased cortisol response to stress. These results support our hypothesis that stress-sensitivity of seizures is associated with alterations of the stress response, thereby providing a first step in unravelling the mechanisms behind the seizure-precipitating effects of stress. Increased knowledge of the relation between stress and seizures in childhood epilepsy might benefit our understanding of the fundamental processes underlying epilepsy and ictogenesis in general, and provide valuable clues to direct the development of new therapeutic strategies for epilepsy.

Subjects with MS had impaired premorbid cognition in adolescence and lower educational achievement, irrespective of parental SES. This suggests poor premorbid cognitive functioning is a risk factor for metabolic complications later in life. Future studies are needed to examine whether cognitive interventions have beneficial effects on general health in schizophrenia.

BackgroundIn schizophrenia about 40% of patients have an additional diagnosis of metabolic syndrome (MetS). In this present study the effect of MetS on cognition in a relatively young group of patients with schizophrenia was examined.Methods290 schizophrenia patients (age/sd = 30/6.37 years old) were included in the study. Patients were divided into two groups, those with and those without MetS (MetS+/MetS-). Neuropsychological performance was assessed with the Wechsler Adult Intelligence Scale-III, the Continuous Performance Test-HQ, the Word Learning Task and the Response Shifting Task.Results124 (42%) patients with schizophrenia met the criteria for MetS. MetS+ and MetS- groups did not differ on amount of cigarettes, alcohol, drug use, severity of illness, socioeconomic status and antipsychotic medication. MetS+ had a significantly lower estimated IQ (sd) 94.9 (17.4) compared to MetS- 100.1(16.3) (t=2,54; p=0.012). MetS+ performed significantly worse on immediate (t=3,12; p=0.002) and delayed recall (t=2,92; p=0.004) and processing speed (t=-2,80; p=0.006) as compared to MetS-. Linear regression analyses revealed that WAIS IQ scores (p=0.026) and immediate memory (p=0.003) were associated with waist circumference.DiscussionPatients with schizophrenia and an additional diagnosis of MetS had lower IQ, performed worse on immediate and delayed recall and processing speed as compared to patients without MetS. This suggests that, even at a relatively young age, metabolic abnormalities are related to poor cognition in schizophrenia. Future studies are needed to examine whether treatment of MetS will also have a beneficial effect on cognitive performance in schizophrenia.