No known studies have tested the hypothesis that a blunted pattern of cortisol reactivity to stress, which is often found following exposure to chronic life stressors, is associated with a higher body mass index (BMI) in very young children. Low-income children (n = 218, mean age 56.6 (range: 38.1 to 78.5; SD 7.0) months, 49.1% male, 56.4% white, 16.1% black, 11.5% Hispanic/Latino) participated in a series of behavioral tasks designed to elicit stress. Cortisol was sampled in saliva 5 times during the protocol, and area under the curve (AUC), representing total cortisol output during stress elicitation, was calculated. Children were weighed and height measured and body mass index (BMI) z-score was calculated. Linear regression was used to evaluate the association between cortisol AUC and BMI z-score, controlling for child age, sex, and race/ethnicity (non-Hispanic white vs. not); primary caregiver weight status (overweight, defined as BMI > 25 vs. not); and family income-to-needs ratio. Mean child BMI z-score was 0.88 (SD = 1.03). Mean cortisol AUC was 6.11 μg/dL/min (SD = 10.44). In the fully adjusted model, for each 1-standard deviation unit decrease in cortisol AUC, the child's BMI z-score increased by 0.17 (SE 0.07) standard deviation units (p <.02). A blunted cortisol response to stress, as is often seen following chronic stress exposure, is associated with increased BMI z-score in very young children. Further work is needed to understand how associations between stress, cortisol, and elevated body mass index may develop very early in the lifespan.

BackgroundIn areas of declining malaria transmission such as in The Gambia, the identification of malaria infected individuals becomes increasingly harder. School surveys may be used to identify foci of malaria transmission in the community.MethodsThe survey was carried out in May–June 2011, before the beginning of the malaria transmission season. Thirty two schools in the Upper River Region of The Gambia were selected with probability proportional to size; in each school approximately 100 children were randomly chosen for inclusion in the study. Each child had a finger prick blood sample collected for the determination of antimalarial antibodies by ELISA, malaria infection by microscopy and PCR, and for haemoglobin measurement. In addition, a simple questionnaire on socio-demographic variables and the use of insecticide-treated bed nets was completed. The cut-off for positivity for antimalarial antibodies was obtained using finite mixture models. The clustered nature of the data was taken into account in the analyses.ResultsA total of 3,277 children were included in the survey. The mean age was 10 years (SD = 2.7) [range 4–21], with males and females evenly distributed. The prevalence of malaria infection as determined by PCR was 13.6% (426/3124) [95% CI = 12.2–16.3] with marked variation between schools (range 3–25%, p<0.001), while the seroprevalence was 7.8% (234/2994) [95%CI = 6.4–9.8] for MSP119, 11.6% (364/2997) [95%CI = 9.4–14.5] for MSP2, and 20.0% (593/2973) [95% CI = 16.5–23.2) for AMA1. The prevalence of all the three antimalarial antibodies positive was 2.7% (79/2920).ConclusionsThis survey shows that malaria prevalence and seroprevalence before the transmission season were highly heterogeneous.

In England and Wales between 1951 and 1980 233

Platelet monoamine oxidase (MAO) activity was compared in four age and sex-matched groups: monozygotic (MZ) twins discordant for schizophrenia, normal MZ twins, normal dizygotic (DZ) twins and unrelated individuals. Among the twin groups, schizophrenic and normal there was a remarkably consistent degree of genetic control amounting to 70-80 per cent of the variation in activity. The mean platelet MAO activity of the schizophrenic twins was significantly lower than that of controls, but not than that of their psychiatrically well, neuroleptic-free cotwins; indeed the correlation for the MZ twins discordant for schizophrenia was almost exactly the same as that for the normal MZs. Thus, lower platelet MAO activity in schizophrenia, where it is found, is genetically modulated and not the result of the illness or its treatment.