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Exposure to Smoke During Development: Fetal Programming of Adult Disease

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Exposure to Smoke During Development: Fetal Programming of Adult Disease TOBACCO INDUCED DISEASES Vol. 3, No. 2:5-16 (2006) © PTID Society Exposure to Smoke During Development: Fetal Programming of Adult Disease Hugo T. Bergen Dept. of Human Anatomy & Cell Science, University of Manitoba, ABSTRACT: It is well established that smoking has potent effects on a number of parameters including food intake, body weight, metabolism, and blood pressure. For example, it is well documented that 1) there is an inverse relationship between smoking and body weight, and 2) smoking cessation is associated with weight gain. However, there is increasing evidence that smoking can exert deleterious effects on energy balance through maternal exposure during fetal development. Specifically, there appears to be an increased incidence of metabolic disease (including obesity), and cardiovascular disease in children and adults that were exposed to smoke during fetal development. The present review will examine the relationship between maternal smoke and adult disease in offspring. The epidemiological studies highlighting this relationship will be reviewed as well as the experimental animal models that point to potential mechanisms underlying this relationship. A better understanding of how smoking effects changes in energy balance may lead to treatments to ameliorate the long-lasting effects of perinatal exposure to smoke as well as increasing the health benefits associated with smoking cessation. Smoking And The Fetal Origins Of and newborn growth and the subsequent Disease development of obesity is a commonly cited example of this phenomenon (7; 8). I. Introduction - Fetal Programming of The epidemiological studies that reported Adult Disease this association led to the formulation of the “thrifty phenotype hypothesis” (9). Recently there has been increased This hypothesis stated that a poor attention paid to the hypothesis that some nutritional environment for the fetus, diseases that have been considered to be brought on by either malnutrition or diseases of adulthood (e.g., obesity, type II placental dysfunction, can induce an diabetes, cardiovascular disease, adaptive response that will optimize hypertension, and some cancers) may have growth and development later in life. The their origins in fetal development. This is adaptive response (which may include most commonly referred to as either the changes in circulating hormones, receptor “developmental origins of disease” or the sensitivity, regulatory enzymes, central “fetal origins of disease” (1-7). The nervous system changes), would lead to hypothesis states that the susceptibility to potential increased survival of the adult develop some diseases is determined in individual under conditions of marginal part by the intrauterine and early postnatal nutritional supply. However, under environment, i.e., perturbations to the conditions of nutritional abundance the early environment (e.g., nutritional result will be maladaptive with increased deficits) can significantly increase incidence of obesity, hyperlipidemia, susceptibility to develop disease later in hypertension and type II diabetes in life. The association between poor fetal adulthood. 6 Bergen H One of the first and best documented One of the first epidemiological studies examples of this phenomenon was the that examined the effect of maternal development of obesity in individuals 20 smoking on the subsequent development years after they were born during the of obesity was a birth cohort study of over Dutch famine of 1944-1945. Individuals 17,000 births and these individuals were were at greater risk of developing obesity tracked at 16 and 33 years of age (20). following exposure to under-nutrition This study identified a significant effect of during late gestation and early post-natal maternal smoking on the subsequent periods (10). The last 30 years has seen development of non-diabetic obesity, as numerous epidemiological studies well as an effect on diabetes (see below). outlining a relationship between In the offspring of mothers that smoked gestational nutrition together with birth during pregnancy, there was significant weight (as a marker of impaired fetal increase in the incidence of obesity (at 33 growth) and subsequent diseases such as years of age) and the magnitude of the obesity, type II diabetes, hypertension and effect was greater in the offspring of heavy cardiovascular disease to name a few (1; 5; smokers than the offspring of medium 11-15) Epidemiological studies have now smokers. Similar results were obtained in been bolstered by an increasing number of a study of over 6,000 children (21). experimental studies demonstrating a Specifically, there was a dose dependent relationship between perinatal nutrition association between maternal smoking and/or birth weight, and adult disease (2; during pregnancy and childhood obesity 7; 16-19). The mechanism(s) responsible (5-7 yrs. of age) that was independent of a for translating fetal effects into adult variety of lifestyle confounders or other disease are not well understood but several risk factors for obesity. However, it is candidates include imprinting through also known that maternal smoking can epigenetic programming. significantly impair fetal growth (22; 23) and that low birth weight is itself Most of the research, with respect to early associated with increased incidence of programming of adult disease, has focused obesity later in life (24). In this clinical on nutritional challenges (under- and over- scenario, i.e., obesity in individuals born nutrition) on the subsequent development small for gestational age, the post-natal of adult diseases. However, there is and early developmental period is increasing evidence that long-lived effects characterized by a phenomenon referred to of perinatal perturbations may not be as “catch-up growth”(22; 24-26). limited to nutritional influences but may Therefore, obesity due to maternal also include other influences such as smoking may be secondary to the effects maternal smoking. The present review of maternal smoking on fetal growth; i.e., will focus on the effects of maternal maternal smoking produces smaller babies smoking on the subsequent development and smaller babies are more susceptible to of diseases in the offspring. It should be develop a variety of adult diseases. noted that cigarette smoke contains However, it should be noted that the numerous components that are relationship between maternal smoking biologically active. Although nicotine is a during pregnancy and overweight in dominant factor in this regard, other children is a complex one. Specifically, a components of smoke may also be more recent epidemiological study involved in mediating the detrimental reported that the likelihood of being effects of smoke on fetal development and overweight at 4.5 years was almost the subsequent promotion of disease into doubled as a result of maternal smoking adulthood. during pregnancy. Interestingly, the effect of maternal smoking on overweight was II. Smoking and Obesity seen in normal birth weight children that Exposure To Smoke During Development: Fetal Programming Of Adult Disease 7 had the greatest weight gain in the first note that the effect was independent of few months of life as well as in high birth birth weight (and mother’s pre-pregnancy weight children that had the least amount weight). Given that smoking has also of weight gain after birth (27). This been linked to low birth weight and that suggests that maternal smoking may low birth weight has been linked to increase susceptibility to develop obesity; the dissociation between these overweight and this can occur in normal two variables in this study indicates that birth weight as well as high birth weight the effect of smoking is not simply children. through an effect on birth weight (32; 33). However, although catch-up growth may An important issue regarding the effect of be a factor in the subsequent development maternal smoke on fetal development and of obesity, studies also suggest that the subsequent health effects is determining effect of maternal smoking on obesity in the sensitivity of the fetus to the offspring can occur independently of detrimental effects of smoke. From a catch-up growth (21). It was reported that public health perspective, it is vital to infants exposed to maternal smoke had know whether smoking is harmful to the lighter birth weights but as they grew into fetus in the first trimester when women adolescence they tended to have greater who smoke and do not know that they are body mass index and this tendency pregnant, will be unintentionally exposing increased with age (28). Importantly, their fetuses to the harmful effects of studies have reported that the association smoke. In a recent study it was reported between maternal smoking on obesity that there was no difference in the effect of remains even when adjusted for birth maternal smoking between mothers that weight; i.e, maternal smoking exerts an smoked throughout pregnancy and those influence independent of its effects on that smoked only during the first trimester fetal growth (21; 28; 29). In a subsequent on subsequent development of obesity study it was also reported that the effects (34). These results could not be explained of maternal smoke on development of by other potentially confounding factors obesity was observed in children 5-7 years such as breastfeeding, watching television, of age and that if mothers that otherwise playing video games, and parental obesity. smoked, abstained during pregnancy and This suggests that during
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