Barker’s in Utero Hypothesis
The developmental origins of adult disease, often called as the ‘Barker hypothesis’ states that adverse influences early in development, particularly during the intrauterine life, can result in permanent changes in the physiology and metabolism of adults Such changes could result in increased disease risk in adulthood. This hypothesis originally evolved from observations made in some regions of England which had the highest rates of infant mortality in the early twentieth century. Follow-up of adults from the region decades later revealed that a number of them suffered from highest rates of mortality from coronary heart diseases. As the most commonly registered cause of infant death at the start of the twentieth century was low birth weight, these observations led to the hypothesis that low birth weight babies who survived infancy and childhood might be at increased risk of coronary heart disease later in life. These results have since been replicated in other studies from many different countries, some of them specifically focused on women.
In the 1980s, the ‘foetal origins of adult disease’ hypothesis got a new impetus when a link between the low birth weight and the incidence of cardiovascular disease was noted in many middle-aged men and women of U.K. Following this there has been an emerging body of evidence from physiological, clinical and epidemiological studies. They support the ‘Barker Hypothesis’ that what happens during foetal development may be as important as the genetic makeup in determining the health of the infant. This evidence has led to the understanding that malnutrition in utero carries a far reaching impact on the future health of the newborn.
The Barker hypothesis outlines a mechanism by which the undernourished foetus adapts to its environment by undergoing changes in the body’s structure, metabolism, hormonal sensitivity and physiology. While it thereby ensures the continued survival and growth of the foetus, there is also a compromise in the process. The disturbance in the nutrient balance results in intrauterine growth retardation (IUGR). In developing countries, the major determinants of IUGR are identified as:
(i) Inadequate nutritional status of the mother before conception;
(ii) Short stature of mothers indicating under-nutrition and infection during childhood;
(iii)Low gestational weight of the foetus/child primarily due to inadequate diet of the mother particularly during the pregnancy period.
The causes of IUGR are also attributed to:
(i) Deep rooted causes related to status of women in society;
(ii) Access to quality health care;
(iii) Sanitation;
(iv) Household food security;
(v) Education;
(vi) Poverty.
The foetal origin of disease theory has thus major implications on how nutritional interventions targeting towards specifically identified women should be approached. Investment in intervention to improve foetal growth and development not only will decrease the prevalence of IUGR, but will also prevent negative health outcomes throughout the life cycle. However, the intergenerational and intra-generational effects of longstanding poverty and nutritional deprivation on maternal and foetal health cannot be addressed by narrowly focussing on single nutritional interventions during a few months in pregnancy. It needs a strategy that comprehensively addresses targeting at different points in the life cycle.