Psychoses, especially schizophrenia, are often preceded by cognitive deficits and psychosis risk states. Altered metabolic profiles have been found in schizophrenia. However, the associations between metabolic profiles and poorer cognitive performance and psychosis risk in the population remain to be determined.

Detailed molecular profiles were measured for up to 8976 individuals from two general population-based prospective birth cohorts: the Northern Finland Birth Cohort 1986 (NFBC 1986) and the Avon Longitudinal Study of Parents and Children (ALSPAC). A high-throughput nuclear magnetic resonance spectroscopy platform was used to quantify 70 metabolic measures at age 15–16 years in the NFBC 1986 and at ages 15 and 17 years in ALSPAC. Psychosis risk was assessed using the PROD-screen questionnaire at age 15–16 years in the NFBC 1986 or the psychotic-like symptoms assessment at age 17 years in ALSPAC. Cognitive measures included academic performance at age 16 years in both cohorts and general intelligence and executive function in ALSPAC. Logistic regression measured cross-sectional and longitudinal associations between metabolic measures and psychosis risk and cognitive performance, controlling for important covariates.

Seven metabolic measures, primarily fatty acid (FA) measures, showed cross-sectional associations with general cognitive performance, four across both cohorts (low density lipoprotein diameter, monounsaturated FA ratio, omega-3 ratio and docosahexaenoic acid ratio), even after controlling for important mental and physical health covariates. Psychosis risk showed minimal metabolic associations.

FA ratios may be important in marking risk for cognitive deficits in adolescence. Further research is needed to clarify whether these biomarkers could be causal and thereby possible targets for intervention.

To consider how physical activity interacts with diet to modify lipoprotein metabolism and comment on implications for human health.

An overview of lipoprotein metabolism is followed by a summary of the main effects of physical activity on lipoprotein metabolism. Interactions with dietary practice and the disposition of dietary lipid are reviewed, with comment on links with body fatness.

Literature is reviewed in relation to the risk of atherosclerotic disease.

Although some data are presented on athletic groups, evidence relating to individuals with normal physical activity habits is mainly discussed.

Physical inactivity is a risk factor for cardiovascular disease and one mechanism may involve changes to lipoprotein metabolism. The consensus is that aerobic activity involving an expenditure of >= 8 MJ · week-1 results in an increase in HDL cholesterol and probably decreases in fasting triacylglycerol. These changes occur despite the spontaneous increase in the proportion of dietary energy from carbohydrate which accompanies increased exercise. For this reason, exercise may be a means of reducing the hypertriglyceridaemic and HDL-lowering effects of low fat (high carbohydrate) diets. Decreases in total and low density lipoprotein cholesterol are sometimes, but not always, reported in sedentary individuals beginning exercise. One mechanism linking all these changes may be alterations to the dynamics of triacylglycerol-rich particles, particularly in the fed state.

The expenditure of considerable amounts of energy through regular, frequent physical activity increases the turnover of lipid substrates, with effects on their transport and disposition which may reduce the progression of atherosclerosis.