Animal models for probing the developmental basis of disease and dysfunction paradigm.
There is a major paradigm shift taking place in science that while simple is profound. The new paradigm suggests that susceptibility to disease is set in utero or neonatally as a result of the influences of nutrition and exposures to environmental stressors/toxicants. In utero nutrition and/or in utero or neonatal exposures to environmental toxicants alter susceptibility to disease later in life as a result of their ability to affect the programming of tissue function that occurs during development. This concept, which is still a hypothesis undergoing scientific testing and scrutiny, is called the developmental basis of health and disease. If true, then it says that the focus on disease prevention and intervention must change from the time of disease onset to perhaps decades prior: during the in utero and neonatal period. Perhaps the reason it has been so difficult to link environmental exposure to disease susceptibility is that scientists have been looking at the wrong time! Certainly, not all exposures that result in increased disease or dysfunction occur during development. This paradigm shift just suggests that this is a sensitive window of exposure that should be examined more thoroughly. This overview focuses on animal models for the assessment of this new scientific paradigm and the animal data that now supports it.
Heindel
Jerrold J
JJ
Division of Extramural Research and Training, National Institute of Environmental Health Sciences, National Institutes of Health, Department of Health and Human Services, Research Triangle Park, NC 27709, USA. heindelj@niehs.nih.gov
D000230:Adenocarcinoma / Q000139:chemically induced; D000818:Animals; D002908:Chronic Disease; D004781:Environmental Exposure / Q000009:adverse effects*; D004785:Environmental Pollutants / Q000633:toxicity; D044127:Epigenesis, Genetic; D005260:Female; D005298:Fertility / Q000187:drug effects; D015870:Gene Expression / Q000187:drug effects; D006801:Humans; D007889:Leiomyoma / Q000139:chemically induced; D008431:Maternal-Fetal Exchange; D023421:Models, Animal; D009369:Neoplasms / Q000139:chemically induced; D009765:Obesity / Q000209:etiology; D010302:Parkinson Disease, Secondary / Q000139:chemically induced; D010795:Phthalic Acids / Q000633:toxicity; D011247:Pregnancy; D011297:Prenatal Exposure Delayed Effects; D013076:Sperm Count
D004785:Environmental Pollutants; D010795:Phthalic Acids