Developmental Origins of Adult Disease

Towards the end of the Second World War, the German military blocked shipments of food and suplies to a region of Holland, resulting in pregnant women having access to about 800-1200 Kcal per day.

Later research determined that men who were born during the famine period had higher risks for specific chronic diseases, such as hypertension or Type 2 diabetes, depending upon the specific period of gestation in which their mothers were malnourished.  In the mid-1990s, epidemiological reports suggested that adults who were growth retarded as children were also at a higher risk for chronic diseases.  This research is part of a body of research called the “Developmental Origins of Adult Health and Disease”.

The main focus of our research in “developmental origins” is to better understand the relationship between poor growth early in life and metabolic adaptations that may predispose people to chronic diseases.  In 2000, we were the first to publish findings that stunted children oxidize fat at a lower rate compared to normal height children, a risk factor for fat gain over a long period of time.  Later, we reported that children who were born small for gestational age, as well as stunted children, deposit more fat in the abdominal region, a marker for increased visceral adipose tissues, further increasing their risk for metabolic diseases.

Presently, we are extending these studies to better understand the mechanisms behind these adaptations.

We have just recently completed a study on metabolic differences in growth retarded children born in North Korea compared to normal height children born in South Korea (results are still being analyzed and will be available later this year). One of the more interesting findings of this study was that children who were conceived in North Korea, but born in China, were taller than those children who were born and grew up in North Korea, but still shorter than those who were born and grew up in South Korea.  This observation is a reflection of the interaction between in utero and early childhood environments on growth.

In addition, we are collaborating with scientists at the University of Health Sciences of Porto Alegre, Brazil  (http://www.ufcspa.edu.br) on a longitudinal study of children born in 2002 who have had frequent measurements of height, weight, and other parameters of health.  One of the major results from this study, still considered preliminary as we’re revising our statistical analyses to confirm findings, is that children who are stunted at age 1 year are more likely to have unhealthy lipid profiles as young as 7 years of age.  If confirmed, these will be the first evidence the poor growth is associated with cardiovascular risk factors in childhood, well before any disease has manifested.

Finally, a new project is underway in Sao Paulo, in collaboration with the Federal University of Sao Paulo, where we are studying changes in body composition during recovery from undernutrition, especially between those children who recover height and those who do not recover height.  In physiological terms, recovery from malnutrition is a dynamic process stimulated by available energy and hormonal regulation of weight.  Given sufficient calories and nutrients, almost all children rapidly recover body weight, yet not all recover height at the same rate as linear growth is a more complicated biochemical and physical process.  Thus, there is interest to determine if the composition of the weight gained by those who recover height or not is similar or  if different, how so.

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