title: Metabolic risk in early childhood: the EarlyBird Study.
abstract: OBJECTIVE
  For a decade or more, poor nutrition during gestation, expressed as low weight at birth, was held to be the factor responsible for insulin resistance later in life. Birth weights, however, are rising and insulin-resistant states, such as diabetes, faster still. Alternative explanations are needed for insulin resistance in contemporary society. This review cites data from the EarlyBird study on the relationships of insulin resistance and metabolic disturbance in early childhood.
  
  
  METHODS
  EarlyBird is a nonintervention prospective cohort study that asks the question 'Which children develop insulin resistance, and why?' It is unique in taking serial blood samples from a young age with which to monitor the behaviour of insulin resistance and its metabolic correlates, and in its comprehensive assessment of factors known or thought to influence insulin resistance
  
  
  METHODS
  In all, 307 randomly selected healthy school children at school entry (mean age 4.9 y) and at 12 and 24 months later.
  
  
  METHODS
  In the children: Birth weight and, at each time point height, weight, body mass index (BMI, kg/m(2)), skinfolds at five sites, circumferences, resting energy expenditure, physical activity, body composition, heart rate variability, diet, HOMA-IR and HOMA-ISC, blood pressure, full blood count, haemoglobin and haematocrit, HbA1C, total cholesterol, HDL cholesterol, LDL cholesterol, triglycerides, uric acid, IGF-1, gonadotrophins and SHBG. In their parents: At baseline height, weight, BMI, waist circumference, HOMA-IR and HOMA-ISC, full blood count, haematocrit, HbA1C, total cholesterol, HDL cholesterol, calculated LDL cholesterol, triglycerides, uric acid, gonadotrophins and SHBG.
  
  
  RESULTS
  Four observations are reported here: (1) There are clear correlations in contemporary children between insulin resistance and weight at 5 y, but none with birth weight. (2) Females throughout life are intrinsically more insulin resistant than males. (3) The substantial variation of physical activity among young children is attributable to the child, and not to his environment. (4) There is dissociation in young children between fatness and insulin resistance.
  
  
  CONCLUSIONS
  There is much yet to be learned about the development of obesity and insulin resistance in children. The notions of overnutrition and underactivity alone are too simplistic.
authors.affiliation: The EarlyBird Research Centre, Peninsula Medical School, Plymouth, UK. T.Wilkin@pms.ac.uk
authors.forename: T J
authors.initials: TJ
authors.lastname: Wilkin
authors.forename: L D
authors.initials: LD
authors.lastname: Voss
authors.forename: B S
authors.initials: BS
authors.lastname: Metcalf
authors.forename: K
authors.initials: K
authors.lastname: Mallam
authors.forename: A N
authors.initials: AN
authors.lastname: Jeffery
authors.forename: S
authors.initials: S
authors.lastname: Alba
authors.forename: M J
authors.initials: MJ
authors.lastname: Murphy
mesh_terms: D000886:Anthropometry; D001724:Birth Weight; D001835:Body Weight; D002664:Child Nutritional Physiological Phenomena; D002675:Child, Preschool; D005260:Female; D006801:Humans; D007333:Insulin Resistance / Q000502:physiology*; D008297:Male; D009043:Motor Activity / Q000502:physiology; D009765:Obesity / Q000196:embryology / Q000209:etiology; D011446:Prospective Studies; D012737:Sex Factors