Early origins of mental disorder - risk factors in the perinatal and infant period

BACKGROUND: There is increasing understanding of the significance of early neurodevelopment in establishing risk for the range of mental disorders. Models of the early aetiology of mental disorders are complex with a range of potential factors from genetic and epigenetic to environmental influencing neurological and psychological development. Whilst the mechanisms are not fully understood, this paper provides an overview of potential biological and neurobiological factors that might be involved. METHOD: An aetiological model is presented and discussed. The discussion includes a range of risk factors for mental disorder. Maternal anxiety disorder is presented and reviewed as an example of the interaction of placental, epigenetic and early parenting factors elevating risk of poor neonatal outcome. RESULTS: Available evidence points to the importance of in-utero influences as well as the role of early attachment and emotional care. Transgenerational mechanisms such as the impact of maternal mental disorder on foetal development are important models for examination of early risk. Maternal anxiety, as an example, is a significant risk factor for compromised mental health. CONCLUSIONS: Development of models for understanding the early origins of mental disorder is an important step in elaborating risk reduction strategies. Comprehensive early identification of risk raises the possibility of preventive interventions.

Establishing reference values for central blood pressure and its amplification in a general healthy population and according to cardiovascular risk factors

AIMS: Estimated central systolic blood pressure (cSBP) and amplification (Brachial SBP-cSBP) are non-invasive measures potentially prognostic of cardiovascular (CV) disease. No worldwide, multiple-device reference values are available. We aimed to establish reference values for a worldwide general population standardizing between the different available methods of measurement. How these values were significantly altered by cardiovascular risk factors (CVRFs) was then investigated. METHODS AND RESULTS: Existing data from population surveys and clinical trials were combined, whether published or not. Reference values of cSBP and amplification were calculated as percentiles for 'Normal' (no CVRFs) and 'Reference' (any CVRFs) populations. We included 45,436 subjects out of 82,930 that were gathered from 77 studies of 53 centres. Included subjects were apparently healthy, not treated for hypertension or dyslipidaemia, and free from overt CV disease and diabetes. Values of cSBP and amplification were stratified by brachial blood pressure categories and age decade in turn, both being stratified by sex. Amplification decreased with age and more so in males than in females. Sex was the most powerful factor associated with amplification with 6.6 mmHg (5.8-7.4) higher amplification in males than in females. Amplification was marginally but significantly influenced by CVRFs, with smoking and dyslipidaemia decreasing amplification, but increased with increasing levels of blood glucose. CONCLUSION: Typical values of cSBP and amplification in a healthy population and a population free of traditional CVRFs are now available according to age, sex, and brachial BP, providing values included from different devices with a wide geographical representation. Amplification is significantly influenced by CVRFs, but differently in men and women.

Is the health burden associated with obesity changing?

Prioritization of obesity prevention and management policy is based on one's understanding of the health risks associated with increasing body weight. However, there is evidence that the magnitude of these health risks may be changing over time. Here, the authors analyze the theoretical drivers of these changes and then examine whether there is empirical evidence to support the theory. They conclude that, although the mortality risks associated with increasing body weight may be decreasing over time, the overall health burden appears likely to increase.

Review : regular brisk walking improves cardiovascular risk factors in healthy sedentary adults

QUESTION In healthy sedentary adults, does regular brisk walking improve cardiovascular risk factors?

METHODS Data sources: Medline and Web of Science (1971 to September 2004) and reference lists.Study selection and assessment:English-language, randomised controlled trials (RCTs) with duration ⩾4 weeks that assessed the effects of walking as the only intervention on changes in cardiovascular risk factors in sedentary, but otherwise healthy, adults. 24 RCTs (n = 1128, mean age 52 y, 83% women) met the selection criteria. The mean length of the walking programmes was 35 weeks (range 8–104 wk). On average, walking was done 4.4 days/week for 38 minutes per session. The mean intensity of the walking interventions was 70% of predicted maximum heart rate or 56% of VO2 max. Quality of individual studies was assessed based on allocation concealment. Outcomes: cardiovascular fitness (VO2 max), body weight, percent body fat, body mass index, and systolic and diastolic blood pressure (BP).

MAIN RESULTS Brisk walking increased cardiovascular fitness and reduced body weight, body mass index, body fat composition, and diastolic BP more than the control condition (table). No effect on systolic BP was observed (table).

CONCLUSION In healthy sedentary adults, regular brisk walking improves cardiovascular fitness, body composition, and diastolic blood pressure.