The Barker hypothesis Barker 2003

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The ''thrifty phenotype'' was popularized by Professor Barker in Southampton, England (Cheung et al., 2004). From large epidemiological studies it has been recognized that IUGR children have an increased risk of developing some types of adult-onset disease. Diabetes, hypertension, myocardial events and stroke are all increased in IUGR infants when they become adults. The ''Barker hypothesis" is that fetal programming in-utero, which leads to an IUGR infant, causes the resetting of normal physiological and biochemical development in the fetus as a survival technique. This is beneficial in the relatively hostile intra-uterine environment during pre-eclampsia, but becomes a problem when the child encounters different nutritional circumstances after birth. The concept of a ''thrifty phenotype'' child describes a child who will ''hoard'' fat when available in case of subsequent ''famine''. The initial observations by Barker were from data collected on English men born at the start of the twentieth century. As they became adults prosperity increased and nutrition improved. It could be that these later effects of IUGR are more apparent as a population moves from relative poverty to prosperity. Fetal growth restriction is often seen in the developing world secondary to small maternal size from previous poor nutrition. As countries such as India become more prosperous the Barker hypothesis suggests that the small children born at present (average birth weight in India is 2700 g) will become obese adults with increased risk of certain diseases. There has been an increase in the incidence of diseases such as type 2 diabetes in India. Better nutrition in childhood will counter the effect of maternal size causing small babies, but this will take one generation to take effect. In PIH maternal size is not an important factor in the development of IUGR. The reduced placental function causes IUGR as the fetus reacts with an anti-insulin response, and some of the long-term detrimental effects likely result from their increased insulin resistance in adult life. It has also been noted that in IUGR premature newborns there is increased arterial ''stiffness'' when measured at 8years of age (Verder et al., 1999). This is not present in appropriately grown premature infants, although it is not clear that this represents a definite risk for later development of hypertension.

• Long-term follow up is essential for high-risk newborns.

• Significant handicap can occur without cerebral palsy.

• Visual and hearing handicap must be screened for in children with PVH and PVL.

Short stature resulting from IUGR is avoidable.

• Learning problems often only become apparent with increasing age.

• Fetal programming is now accepted as a cause of adult-onset disease.

REFERENCES

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Cheung, Y.F., Wong, K.Y., Lam, B.C.C. and Tsoi, N.S. (2004). Relation of arterial stiffness with gestational age and birth weight. Arch. Dis. Child., 89, 217-21.

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Schreiber, M., Gin-Mestan, K., Marks, J.D., Huo, D., Lee, G. and Srisuparp, P. (2003). Inhaled nitric oxide in premature infants with the respiratory distress syndrome. N. Engl. J. Med., 349, 2099-107.

Stoll, B. J., Hansen, N., Fanaroff, A. A., et al. (2002). Late-onset sepsis in very low birth weight neonates: the experience of the NICHD neonatal research network. Pediatrics, 110, 285-91.

Verder, H., Albertsen, P., Ebbesen, F., et al. (1999). Nasal continuous positive airway pressure and early surfactant therapy for respiratory distress syndrome in newborns of less than 30 weeks gestation. Pediatrics, 103(2), E24.

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