'Thrifty Phenotype' Hypothesis Gains Ground. (Implications Of Fetal Growth Restriction).
The Barker hypothesis, also commonly known as the 'thrifty phenotype hypothesis, holds that fetal growth restriction is an important cause of some of the most common, costly, and disabling medical disorders of later life: coronary heart disease, stroke, diabetes, hypertension, impaired glucose metabolism, and the metabolic syndrome X.
Dr. David J. Barker, professor of medicine at the University of Southampton (England), first put forth his hypothesis 15 years ago. Since then dozens of largescale studies conducted in Europe, the United States, and elsewhere have convincingly demonstrated a powerful link between fetal growth restriction as reflected in low birth weight and increased risk of developing these chronic medical disorders decades later. "It's a significant body of literature that physicians should be made aware of," commented Dr. Philipps, professor and chair of pediatrics at the University of California, Davis.
The mechanisms involved haven't been corroborated in detail. But in broad outline, the thrifty phenotype hypothesis holds that in periods of nutritional deprivation, the fetus adopts two strategies to ensure survival: It preferentially shunts blood to the brain from key bodily organs; and during a critical window of intrauterine development it engages in programming of organ structure and function so as to maintain long-term metabolic thriftiness later in life under conditions of poor postnatal nutrition.
These fetal adaptations may well have had survival value 20,000 or 50,000 years ago, when starvation was a constant threat. But they probably don't today in the developed world, where circulatory problems secondary to uteroplacental dysfunction are vastly more common than maternal malnutrition as a cause of fetal malnutrition and intrauterine growth restriction (IUGR). Today these IUGR fetuses typically enter a world of relative plenty in which their thrifty phenotype causes bodily harm, Dr. Philipps explained at the conference, jointly sponsored by Symposia Medicus and Stanford University.
The implications for obstetric diagnosis include a likely need to replace current circulatory assessments, such as echocardiographic measurement of end diastolic flow, with measures that provide physicians with an idea of how many nutrients are actually reaching the fetus. This might be ascertained via measurement of fetal cerebral and placental villous blood flo.
Older fetal growth assessment measures, such as abdominal circumference, may give way to more sophisticated modalities, including 3-D ultrasound assessment of fetal body weight and liver volume, the pediatrician said.
In the realm of obstetric therapeutics, the Barker hypothesis implies that timing of delivery is an issue worthy of reconsideration. It may actually be better to deliver some IUCR fetuses early, before "thrifty" programming of the liver, kidney and pancreatic islet cells is completed, provided it can be shown that early delivery and catch-up growth in the first year helps reduce disease later in life.
There is also considerable research interest in finding ways to identify and interrupt fetal malnutrition in an effort to reduce the incidence of common chronic diseases later in life. Intervention might take the form of pharmacotherapy targeted at uterine and/or placental blood flow abnormalities.
Another possibility is fetal rescue via delivery of nutrients to the undernourished fetus, although Dr. Philipps believes this approach is fraught with hazard.
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|Publication:||OB GYN News|
|Date:||Oct 15, 2001|
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