Metabolic Syndrome In Later Life Research Articles

A lifecourse study of risk for hyperinsulinaemia, dyslipidaemia and obesity (the central metabolic syndrome) at age 49-51 years.

Suboptimal maternal nutrition and catch-up growth in early childhood predispose to insulin resistance and other components of metabolic syndrome in later life. A central metabolic syndrome (CMS) has been identified comprising obesity, dyslipidaemia and insulin resistance. This study was designed to investigate determinants of risk for CMS. Persons born in Newcastle in May and June 1947 (n = 358) were followed to 1996-1998. A lifecourse approach was used to estimate the proportion of variance in a summary measure of CMS at age 49-51 years accounted for by factors operating at different stages of life. After adjustment for other early life variables, childhood catch-up growth in men accounted for significant variation in the CMS score independent of adult lifestyle. In adulthood, exercise level in men and smoking in both genders were independently associated with CMS. Over two-thirds of explained variation in the CMS score in women, and almost half in men, was accounted for exclusively by factors measured in adulthood. While risk for CMS in men is compounded by early life disadvantage, promotion of a healthier adult lifestyle and a reduction in the number of people taking up smoking would appear to be the public health interventions most likely to reduce the prevalence of CMS in middle age.

Growth and growth hormone in children born small for gestational age

Growth hormone has an important role in childhood growth, but growth hormone is also detectable from early gestation, suggesting a role in fetal development and metabolism. In early postnatal life, infants who have been growth restricted in utero have abnormal patterns of growth hormone secretion with what appears to be evidence of growth hormone resistance, whereas in later childhood, growth hormone deficiency is often observed. Recent studies using high doses of growth hormone in short small for gestational age children have demonstrated increases in growth rate whether or not these children have classical growth hormone deficiency. The benefits are in terms not only of height but also of body composition and psychosocial function. However, the risk of side effects and long-term complications, such as increased insulin resistance, need to be assessed carefully, especially in people who have a family history of type 2 diabetes or the metabolic syndrome in later life.

Will feeding mothers prevent the Asian metabolic syndrome epidemic?

Evolutionary pressures have probably amplified the mechanisms for minimizing the impact of environmental factors through compensatory maternal mechanisms. Nevertheless, experimentally there are clear long-term programming effects of manipulations to the maternal diet on the likelihood of neural-tube defects associated with folate deficiency The fat/lean ratios of the newborn, and subsequent development, seem to be linked to amino acid or folate supply. An altered balance in the hypothalamic-pituitary-adrenal axis, which experimentally has profound effects on brain development, is induced by low-protein maternal diets. Such diets are linked to a reduced pancreatic capacity for insulin production and to an altered hepatic architecture, with a change in the control of glucose metabolism. Human studies suggest that what happens in pregnancy is modified by the child's diet in the first months of life. Low birthweight is linked to early stunting, and predisposes to abdominal obesity and metabolic syndrome in later life. Metabolic syndrome amplifies the risks of diabetes, hypertension, coronary heart disease and probably some cancers. Mothers with gestational diabetes are themselves prone to early type 2 diabetes and produce heavier babies prone to childhood obesity and adolescent type 2 diabetes. There is increasing evidence of an intergenerational effect, with big babies being prone to excess weight gain, which then, in girls, predisposes them to diabetes in pregnancy, which, in turn, promotes an accelerating cycle of early diabetes in subsequent generations. Essential fatty acids and fat soluble vitamins are important, but we need early interventions and monitoring systems to justify coherent policies.