80
views
0
recommends
+1 Recommend
0 collections
    0
    shares
      • Record: found
      • Abstract: not found
      • Article: not found

      Fetal origins of adult disease: strength of effects and biological basis

      , , ,
      International Journal of Epidemiology
      Oxford University Press (OUP)

      Read this article at

      ScienceOpenPublisherPubMed
      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          Low birthweight has been consistently shown to be associated with coronary heart disease (CHD) and its biological risk factors. The effects of low birthweight are increased by slow infant growth and rapid weight gain in childhood. To quantify the importance of developmental processes in the genesis of CHD it is necessary to establish the impact of fetal, infant and childhood growth on major pathological events in later life-death, hospital treatment and the need for medication. Longitudinal study of 13 517 men and women who were born in Helsinki University Hospital during 1924-1944, whose body sizes at birth and during childhood were recorded, and in whom deaths, hospital admissions, and prescription of medication for chronic disease are documented. The combination of small size at birth and during infancy, followed by accelerated weight gain from age 3 to 11 years, predicts large differences in the cumulative incidence of CHD, type 2 diabetes and hypertension. Coronary heart disease and type 2 diabetes may originate through two widespread biological phenomena-developmental plasticity and compensatory growth.

          Related collections

          Most cited references19

          • Record: found
          • Abstract: not found
          • Article: not found

          Phenotypic Plasticity and the Origins of Diversity

            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            Fetal and childhood growth and hypertension in adult life.

            The association between low birth weight and raised blood pressure has been extensively replicated. Little is known about the way childhood growth modifies the effects of low birth weight. We report on the fetal and childhood growth of 1958 men and women who received treatment for hypertension and belong to a cohort of 7086 people born in Helsinki, Finland, during 1924-1933. As expected, the men and women who developed hypertension had low birth weight (P=0.002). They were also shorter in body length at birth (P=0.02). After birth they experienced accelerated growth, so that by 7 years their heights and weights were approximately average. In a simultaneous regression, both birth length and tall height had statistically significant although opposing effects on hypertension (P=0.003 for birth length and 0.009 for height at 7 years). Accelerated postnatal growth was associated with better childhood living conditions. Children who later developed both hypertension and type 2 diabetes, rather than hypertension alone, had small placental size as well as small body size at birth, and their accelerated postnatal growth continued beyond 7 years. We suggest that hypertension may originate through retarded growth in utero followed by accelerated postnatal growth as a result of good living conditions. Retarded fetal growth leads to permanently reduced cell numbers in the kidney and other tissues, and subsequent accelerated growth may lead to excessive metabolic demand on this limited cell mass.
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              The relation of small head circumference and thinness at birth to death from cardiovascular disease in adult life.

              To determine how fetal growth is related to death from cardiovascular disease in adult life. A follow up study of men born during 1907-24 whose birth weights, head circumferences, and other body measurements were recorded at birth. Sheffield, England. 1586 Men born in the Jessop Hospital. Death from cardiovascular disease. Standardised mortality ratios for cardiovascular disease fell from 119 in men who weighed 5.5 pounds (2495 g) or less at birth to 74 in men who weighed more than 8.5 pounds (3856 g). The fall was significant for premature cardiovascular deaths up to 65 years of age (chi 2 = 5.0, p = 0.02). Standardised mortality ratios also fell with increasing head circumference (chi 2 = 4.6, p = 0.03) and increasing ponderal index (weight/length3) (chi 2 = 3.8, p = 0.05; for premature deaths chi 2 = 6.0, p = 0.01). They were not related to the duration of gestation. Among men for whom the ratio of placental weight to birth weight was in the highest fifths the standardised mortality ratio was 137. These findings show that reduced fetal growth is followed by increased mortality from cardiovascular disease. They suggest that reduction in growth begins early in gestation. They are further evidence that cardiovascular disease originates through programming of the body's structure, physiology, and metabolism by the environment during fetal life. Maternal nutrition may have an important influence on programming.
                Bookmark

                Author and article information

                Journal
                International Journal of Epidemiology
                Oxford University Press (OUP)
                1464-3685
                0300-5771
                December 2002
                December 01 2002
                December 2002
                December 2002
                December 01 2002
                December 2002
                : 31
                : 6
                : 1235-1239
                Article
                10.1093/ije/31.6.1235
                12540728
                8e4b2687-92db-496e-acc6-ba8d8ac377de
                © 2002
                History

                Comments

                Comment on this article