C Osmond1. 1. MRC Environmental Epidemiology Unit (University of Southampton), Southampton General Hospital.
Abstract
BACKGROUND: The 'programming' hypothesis for the causation of heart disease suggests that there are critical periods of development in early life during which a stimulus or insult has permanent effects on the subject's organ or tissue structure and physiology. Exposure to such effects might be expected to be linked to year of birth and produce cohort (generation) effects in heart disease death rates. Evidence is sought for such effects in data from England and Wales. METHODS: The age- and period-specific heart disease death rates for men and women aged 30-69 in England and Wales have declined recently in both men and women. The trends have two components. The first is described by a peak in rates during 1977-1981 that applies to both sexes and all age-groups. This is consistent with risk conferred by adult diet and lifestyle. The second component required to explain the trends also applies to both sexes and is described by a risk that is lower in each successive year of birth. This is consistent with risk linked to poor growth in early life. CONCLUSION: Poor early growth has become less common as maternal health, physique and nutritional status have improved through the century. The trends are therefore consistent with the'programming' hypothesis for the causation of coronary heart disease.
BACKGROUND: The 'programming' hypothesis for the causation of heart disease suggests that there are critical periods of development in early life during which a stimulus or insult has permanent effects on the subject's organ or tissue structure and physiology. Exposure to such effects might be expected to be linked to year of birth and produce cohort (generation) effects in heart disease death rates. Evidence is sought for such effects in data from England and Wales. METHODS: The age- and period-specific heart disease death rates for men and women aged 30-69 in England and Wales have declined recently in both men and women. The trends have two components. The first is described by a peak in rates during 1977-1981 that applies to both sexes and all age-groups. This is consistent with risk conferred by adult diet and lifestyle. The second component required to explain the trends also applies to both sexes and is described by a risk that is lower in each successive year of birth. This is consistent with risk linked to poor growth in early life. CONCLUSION: Poor early growth has become less common as maternal health, physique and nutritional status have improved through the century. The trends are therefore consistent with the'programming' hypothesis for the causation of coronary heart disease.