According to an author writing in the London Times , Roger Dobson, the time spent in the womb may influence whether folks suffer, years later, from cancer, obesity or heart disease. A research program working under the “fetal origins of disease” hypothesis suggests that diseases may originate through fetal adaptations to under-nutrition, over-nutrition or unbalanced nutrition, or to other environmental changes. According to Dobson, the debate now is not so much about the validity of the theory, as to how strong its effects are, and how they can be changed. This does not seem to be accurate, however, because there are fatal statistcal problems with these kinds of analyses, say other scientists.
The theory, first put forward by researchers at Southampton University, is that the fetus responds to an adverse environment by re-setting its growth plans to prepare for a life in a deprived environment. But if that environment turns out not to be deprived it is not best equipped to survive. Fearing that life outside the womb is going to be as deprived as it is inside, the fetus may, for example, create a level of insulin resistance that allows survival in times of famine through efficient storage of fat in rare times of plenty. But in a postnatal world of constant plenty, that set-up would lead to a greater risk of obesity, diabetes and heart disease. Research shows that babies conceived during the Dutch famine (1944-1945) were more prone to heart disease and obesity.
Most human disease is the result of the interaction of genetic susceptibility and environmental factors. While most research has looked at environmental effects after birth, studies at Southampton University and elsewhere claim that the 266 or so days from conception to birth is the time when much of what will happen during the decades ahead is determined. The mother’s diet, hormonal changes, changes in the placenta, maternal exposure to disease and toxins and the general weight, fitness and lifestyle of the mother are all said to contribute.
Wednesday, March 15, 2006
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