title: Is body size at birth related to circadian salivary cortisol levels in adulthood? Results from a longitudinal cohort study.
abstract: BACKGROUND
  The hypothesis of fetal origins of adult disease has during the last decades received interest as an explanation of chronic, e.g. cardiovascular, disease in adulthood stemming from fetal environmental conditions. Early programming and enduring dysregulations of the hypothalamic-pituitary-adrenal (HPA axis), with cortisol as its end product, has been proposed as a possible mechanism by which birth weight influence later health status. However, the fetal origin of the adult cortisol regulation has been insufficiently studied. The present study aims to examine if body size at birth is related to circadian cortisol levels at 43 years.
  
  
  METHODS
  Participants were drawn from a prospective cohort study (n = 752, 74.5%). Salivary cortisol samples were collected at four times during one day at 43 years, and information on birth size was collected retrospectively from delivery records. Information on body mass during adolescence and adulthood and on health behavior, medication and medical conditions at 43 years was collected prospectively by questionnaire and examined as potential confounders. Participants born preterm or < 2500 g were excluded from the main analyses.
  
  
  RESULTS
  Across the normal spectrum, size at birth (birth weight and ponderal index) was positively related to total (area under the curve, AUC) and bedtime cortisol levels in the total sample. Results were more consistent in men than in women. Descriptively, participants born preterm or < 2500 g also seemed to display elevated evening and total cortisol levels. No associations were found for birth length or for the cortisol awakening response (CAR).
  
  
  CONCLUSIONS
  These results are contradictory to previously reported negative associations between birth weight and adult cortisol levels, and thus tentatively question the assumption that only low birth weight predicts future physiological dysregulations.
authors.affiliation: Dept of Public Health and Clinical Medicine, Family Medicine, Umeå University, Umeå, Sweden. Per.E.Gustafsson@fammed.umu.se
authors.forename: Per E
authors.initials: PE
authors.lastname: Gustafsson
authors.forename: Urban
authors.initials: U
authors.lastname: Janlert
authors.forename: Töres
authors.initials: T
authors.lastname: Theorell
authors.forename: Anne
authors.initials: A
authors.lastname: Hammarström
mesh_terms: D000293:Adolescent; D000328:Adult; D019540:Area Under Curve; D001724:Birth Weight / Q000502:physiology*; D049628:Body Size / Q000502:physiology*; D002940:Circadian Rhythm / Q000502:physiology*; D015331:Cohort Studies; D005260:Female; D005500:Follow-Up Studies; D006305:Health Status Indicators; D006801:Humans; D006854:Hydrocortisone / Q000032:analysis* / Q000502:physiology; D007030:Hypothalamo-Hypophyseal System; D008297:Male; D010913:Pituitary-Adrenal System; D012463:Saliva / Q000737:chemistry*; D017678:Sex Distribution; D012959:Socioeconomic Factors; D013548:Sweden
chemical_list: D006854:Hydrocortisone