Could your child be preordained to be an overweight couch potato? New Zealand physiologists are proposing that the well-known association between obesity, metabolic syndrome, sedentary behaviour, and overeating might have a common biological cause.
Obesity is an increasingly prevalent, costly, and important health problem worldwide. In Western societies, such as the US, the incidence of obesity is approximately 32 per cent of the adult population, and the prevalence in children has risen by approximately 40 per cent in the last 16 years.
It is also rising rapidly in developing countries such as India and China as Western diets and lifestyle are adopted. Although the causes of obesity are multifactorial, these recent increases have been too sudden to be explained by genetic factors.
Population studies conducted in the last decade suggest that environmental factors active during embryonic and fetal development are of substantial consequence for the risk of developing metabolic and cardiovascular disorders in adulthood.
The biological basis underlying this concept of 'foetal programming' remains speculative but may involve permanent alterations in gene expression that may in turn modify tissue differentiation and hormonal and metabolic regulation.
Some members of the scientific community believe that the foetus adapts to adverse environmental cues while in the womb with permanent readjustments in homoeostatic systems to aid survival. However, if these adaptations are inconsistent with the environment encountered after birth, these adaptations may lead to an increased risk of disease.
Obesity is one disease associated with impaired foetal development, as children of low birth weight have been shown to develop this disorder in their adult life. But many reports relating the foetal environment to metabolic disease and adult obesity are confounded as lifestyle influences obscure the linkage between metabolic predisposition and maturity-onset obesity.
Past research has shown that a maternal malnutrition throughout pregnancy in the rat model results in obesity, hypertension, and excessive insulin in the blood in the offspring when they reach adulthood.
The authors of a new study note that the onset of the abnormal eating behaviors occurred before puberty, thus preceding the development of obesity. This observation led to a hypothesis that prenatal maternal environment might also affect other components of behaviour associated with an individual's metabolic behavior.
The animal study from New Zealand investigated the effect of the prenatal environment on programming of voluntary locomotor behavior in postnatal life. The authors of "Sedentary Behavior During Postnatal Life is Determined by the Prenatal Environment and Exacerbated by Postnatal Hypercaloric Nutrition" are M. H. Vickers, B. H. Breier, D. McCarthy, and P. D. Gluckman, all from the Liggins Institute faculty of medical and health sciences, University of Auckland, Auckland, New Zealand. Their findings are published in the July 2003 edition of the American Journal of Physiology-Regulatory, Integrative and Comparative Physiology.
For the study, Virgin Wistar rats (age three months) were mated and included in an animal model of foetal programming using maternal undernutrition. Animals were assigned to one of two nutritional groups, with 15 per group: undernutrition of a standard diet throughout gestation (undernourished group) or a complete standard diet throughout gestation (ad libitum-fed group).
Food intake and maternal weights were recorded daily until birth. After birth, pups were weighed, and litter size was recorded. After weaning, male offspring from ad libitum-fed and undernourished mothers were divided into two balanced postnatal groups to be fed either a standard diet or a hypercaloric diet. The mineral and vitamin content in the two diets was identical and in accordance with the requirements for standard rat diets.
Two separate studies were undertaken. In the first study, voluntary locomotor activity was assessed in the offspring (six per group of each gender) near puberty and in adulthood (145 days). Food intake was also measured over a five-day period from day 140 to day 145.
In a second study an identical manipulation was used prenatally, but all rats (eight per group of each gender) were maintained on a normal diet after weaning, and their behavior was studied at 14 months of age.
The researchers found that in the first study, offspring that were undernourished in the womb were significantly more sedentary in postnatal life than those born of mothers with a standard diet for all parameters measured, and independent of postnatal diet.
Analysis of ingestive behaviour revealed overeating in mature offspring that had been exposed to maternal undernutrition. This was independent of postnatal diet, although sedentary behaviour was exacerbated by hypercaloric nutrition.
Importantly, in the animals tested at a peripubertal age, diminished locomotor activity was already present before the development of maturity-onset obesity and was significantly reduced in males compared with females.
In the second trial, offspring of undernourished mothers at 14 months of age were shown to be significantly less active than offspring of normally fed mothers. A gender difference occurred, with males significantly less active than females, but the prenatal effect was significant in each gender. This second study confirms, write the scientists, that the sedentary effect is persistent through life, is solely related to prenatal maternal diet, and occurs in both genders.
They conclude that the prenatal environment can lead to the development of both abnormal eating and exercise behaviours, adding to previous research findings that the environment in the womb can influence physiological features of the metabolic syndrome.
This research raises the intriguing possibility, the researchers continue, that some behaviours and lifestyle choices that exacerbate the metabolic syndrome in humans are an inherent part of the syndrome and may have a prenatal origin.
The implications of this hypothesis are profound, write the scientists. If sedentary behaviour and overeating are determined during prenatal development, this may explain why public health attempts to improve exercise and to reduce food intake in adults with hypertension, insulin resistance, and hyperlipidaemia are often ineffective.