[Significance of prenatal exposure for long-term health effects].
A rapidly accumulating body of evidence indicates that many diseases must be understood in a life-long perspective, as trajectories that start at conception and surface upon clinical detection decades later. We know that some toxic intrauterine exposures may have life-long consequences, such as alcohol and some environmental pollutants, but it was not expected that chronic diseases such as cardiovascular disease or some cancers may have a fetal origin. Several research findings indicate that this expectation should be revised. Some studies indicate that sperm counts are declining conceiving the desired number of children. The so-called "estrogen hypothesis" states that this may be due to exposures in the intrauterine environment. About 10 years ago it was suggested that breast cancer originates in utero, which may be true also for cancer of the prostate or ovary. So far the evidence for this hypothesis is only circumstantial, but results have supported the idea. A large number of studies clearly indicate that impaired fetal growth is associated with a number of diseases. It is well known that all organs have time periods of rapid growth which may render them vulnerable to an insufficient supply of nutrition; impaired growth could alter organ structure and functioning, and the fetus could e.g. develop insulin resistance to protect itself from these "hunger" periods. "Organ programming" may be a fact we should consider when studying the etiology of e.g. cardiovascular diseases. These hypotheses--if they should hold true--are promising for new approaches to prevention. Much more work is needed however, before we can visualize these avenues of prevention, and we should make sure we develop the opportunities for doing this work now. It is high time.
Olsen
J
J
Center for epidemiologisk grundforskning, Aarhus Universitet og Statens Serum Institut. jo@soci.au.dk
D002318:Cardiovascular Diseases / Q000453:epidemiology / Q000209:etiology; D003072:Cognition Disorders / Q000453:epidemiology / Q000209:etiology; D005314:Embryonic and Fetal Development; D005260:Female; D005298:Fertility; D006304:Health Status; D006801:Humans; D008297:Male; D008431:Maternal-Fetal Exchange; D009369:Neoplasms / Q000453:epidemiology / Q000209:etiology; D011247:Pregnancy; D011297:Prenatal Exposure Delayed Effects