What is fetal origin of adult heart disease?

What is fetal origin of adult heart disease?

Fetal origins of adult disease is popularly known as Barker’s hypothesis. The concept was proposed by David Barker in 1990 and was noted in his book “Fetal and Infant Origins of Adult Disease”, published in 1992. The hypothesis proposed that adverse nutrition in early life as measured by birth weight increased susceptibility to adult diseases like metabolic syndrome with risk for coronary artery disease and stroke. Coronary artery disease is the disease of blood vessels of the heart, often leading to heart attack. Metabolic syndrome is characterized by excess fat deposits over the waist region, high blood pressure, high blood sugar and abnormalities in blood fat levels.

An article by Barker DJ et al in 2009 mentioned that malnutrition during fetal life, infancy and early childhood permanently change the structure and function of the body by ‘programming’. Fetal life is life before birth, within the mother’s womb.

They reviewed the findings of the Helsinki Birth Cohort which had over thirteen thousand persons born during 1934 to 1944. There was an older cohort of over seven thousand persons born between 1924 to 1933. It was found that children who develop coronary artery disease and diabetes later grow slowly during fetal life and infancy. Thereafter their body mass indices increase rapidly.

Those who develop stroke later was found to grow slowly in fetal life, infancy and childhood. The authors also reviewed how the growth of girls during infancy, childhood and at puberty influences long term disease in the next generation.

Calkins K and associates who reviewed the concept in 2019 noted that clues to the fetal origin of adult disease concept originally arose from large 20th century European studies. They mention that large diverse human studies and various animal models have extensively confirmed these original observations. They considered that the implications were beyond the low birth weight population and include babies exposed to nutritional and non-nutritional stress during critical periods of development. Several diseases other than heart and blood vessel disease also come under the purview of this concept.

The so-called ‘catch-up growth’ of low birth weight children may not be that ideal though caregivers often consider it as comforting. Catch-up growth reflects body’s natural response to nutrient deprivation. But this exponential childhood growth increases the risk for metabolic syndrome characterized by overweight, insulin resistance, abnormal blood fat levels and high blood pressure.

The thrifty phenotype hypothesis proposes that poor nutrition in early life produces permanent changes in glucose-insulin metabolism. This is considered as the reason for associations between poor fetal growth and later development of type 2 diabetes and metabolic syndrome. There is reduced capacity to secrete insulin and resistance of the cells to the action of insulin. These combined with effects of obesity, ageing and physical inactivity are the most important factors determining the development of type 2 diabetes.