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SUPPLEMENT ARTICLE |
* Obesity Research Center, St Luke’s Hospital, Columbia University, New York, New York
Institute of Human Nutrition, Columbia University, New York, New York
Shape Up America!, Portage, Wisconsin
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ABSTRACT |
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 TOP ABSTRACT OBESITY ORIGINS IN FETAL...WHAT ARE INFANTS AND...TRANSITIONING TO SOLID FOODS...LONGITUDINAL PERSPECTIVE ON...REFERENCES |
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Methodology. A meeting was convened of experts in areas that bear on prevention of obesity development during intrauterine life, infancy, and very early childhood. They presented recent data and their interpretations of the stage of our current knowledge in related areas. They also proposed possible useful interventions and future directions for research.
Findings. The speakers’ talks indicated that (1) breastfeeding as currently practiced seems to be significantly (albeit weakly) protective against obesity and should be encouraged as the preferred method of feeding infants for as long a duration as practical during the first year of life; (2) infant-feeding practices are changing in a way that may predispose to obesity (eg, soda and french fries are being fed to infants as young as 7 months of age), possibly altering taste preferences for foods and beverages that are energy dense and nutrient poor; (3) although little is known about parenting styles (eg, authoritative versus permissive), parenting style is likely to be a fruitful area of current research into childhood obesity etiology; and (4) the pattern of weight changes in the first few years of life may contribute to later risk of obesity.
Conclusions. Children’s obesity will continue to be a growing problem unless we improve understanding of the key factors likely to be operative during intrauterine life, infancy, and very early childhood, identify those in whom intervention would have the greatest effect, design and evaluate preventive interventions, and promote those that are successful.
Key Words: obesity • pediatrics • prevention • infant feeding • birth weight • activity • dietary choices • maternal weight • feeding styles
Abbreviations: IOM, Institute of Medicine • SES, socioeconomic status • BMI, body mass index • NCHS, National Center for Health Statistics • LGA, large for gestational age • SGA, small for gestational age • NHANES, National Health and Nutrition Examination Survey • WIC, Special Supplemental Nutrition Program for Women, Infants, and Children • OR, odds ratio • CI, confidence interval • FITS, Feeding Infants and Toddlers Study • IFSQ, Infant Feeding Style Questionnaire • ALSPAC, Avon Longitudinal Study of Parents and Children
In late 2001, Congress allocated monies to fund a study to be conducted by the Institute of Medicine (IOM), to develop an action plan to prevent obesity in children and youth. According to Senate Report 107-84, the study "should assess the primary factors responsible for the increasing prevalence of childhood obesity and identify the most promising methods for prevention."1(p92) Accordingly, the IOM appointed a Committee on Prevention of Obesity in Children and Youth, which is charged with assessing the nature of obesity among children and youths in the United States and developing a prevention-oriented action plan to reduce its prevalence.
In February 2003, Dr B. J. Moore was appointed to the IOM committee, with 17 other individuals from throughout the United States. In August and September 2003, as a result of informal discussions among committee members, the idea was born of developing a conference to focus on very early critical periods of development that might predispose individuals to obesity. Dr Moore secured the necessary funding for the conference through her affiliation with Shape Up America!, a nonprofit 501(c)3 educational organization. The Gerber Product Company agreed to provide funding for the conference venue, food, audiovisual support, speaker travel, and honoraria. Although it was not an IOM event, this Shape Up America! conference was designed in consultation with the members of the IOM committee.
The focus of the conference was on the earliest critical periods considered important for the development of childhood obesity, namely, conception, intrauterine life, infancy, the postweaning period, and the preschool period. Certain members of the committee were particularly generous with their time and ideas in identifying topics and speakers. In that regard, we wish to acknowledge the contributions of Dr Robert Whitaker of Mathematica Policy Research, Dr Leann Birch of Pennsylvania State University, Dr Tom Robinson of Stanford University, Dr Shiriki Kumanyika of the University of Pennsylvania, Dr Dennis Bier of the Baylor College of Medicine, Dr Russell Pate of the University of South Carolina, and Dr Ross Brownson of St. Louis University.
Dr Sally Lederman was selected by Dr Moore because of her expertise in the fields of nutrition, obesity, growth, pregnancy, and lactation. She directed the development of the conference summary and drafted the editors’ overview, in collaboration with Dr Moore and Dr Sharon Akabas, who was selected as coauthor because of her background in nutrition education and her interest in the role of activity in preventing obesity among children.
The conference was held at the Marriott Metro Center Hotel in Washington, DC, on December 8, 2003. It included research-based presentations by 7 session speakers, Dr M. Gillman, Dr M. Kramer, Dr B. Devaney, Dr J. Mennella, Dr J. Wardle, Dr M. Bentley, and Dr A. Ness. In their invitations to speak at the conference, the speakers were asked to address, to the extent possible, a set of questions whose answers might guide future approaches to preventing childhood obesity and inform subsequent research efforts. Different speakers undertook to answer different selections of the questions posed, on the basis of their expertise and research findings, and focused on different broad areas, as indicated by the session titles in this summary. Several speakers included materials from the peer-reviewed literature and used that information to bridge gaps or suggest relationships that could be helpful in decision-making. New research findings, both their own and those of others, obtained through personal communications, were also included, which made for a stimulating, exciting, and challenging conference. The conference summary presented here is a detailed summary of the presentations, derived from a transcript of the proceedings. Each speaker reviewed the summary of his or her presentation for accuracy.
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OBESITY ORIGINS IN FETAL DEVELOPMENT AND THE FIRST 6 MONTHS OF LIFE |
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TOPABSTRACTOBESITY ORIGINS IN FETAL...WHAT ARE INFANTS AND...TRANSITIONING TO SOLID FOODS...LONGITUDINAL PERSPECTIVE ON...REFERENCES |
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Many factors, operating from preconception through childhood and adolescence, may affect obesity risk. Maternal prepregnancy body mass index (BMI) may determine pregnancy glucose and insulin levels in the mother and fetus, with high levels increasing newborn weight. Postnatally, the feeding of the newborn, infant, and child can determine the rate of growth and influence the timing and magnitude of the adiposity rebound seen in childhood, with subsequent dietary and activity patterns contributing to later BMI, adiposity, and a fat distribution characterized by central obesity. Such factors then contribute to morbid outcomes, including insulin resistance, cardiovascular disease, and type 2 diabetes mellitus.
The increasing importance of obesity development among children was illustrated with data on the changing prevalence of obesity among children 6 to 11 and 12 to 19 years of age.2,3 The data showed that, between 1976–1980 and 1999–2000, obesity rates more than doubled among children 6 to 11 years of age and more than tripled among those 12 to 19 years of age, although there had been little change in the prevalence between 1963 and 1976. Additional data from Kim et al4 were used to develop a linear model of weight changes among children 0 to 71 months of age, controlling for age, gender, race/ethnicity, Medicaid status, and clinic site. The data showed an 83% increase in overweight (>95th percentile) and a 27% increase in the risk of overweight (>85th to 95th percentile). Data reported by Mokdad et al5 showed changes in obesity prevalence according to state during the past decade. In 1991, only 5 states exhibited obesity prevalences of >15%; by 2001, all states exceeded this value and most demonstrated obesity prevalences of 20% to 24%, with Mississippi having even higher levels.
Dr Gillman then addressed the following question: Does obesity begin in the womb? To explore this question, >20 studies that considered birth weight and later BMI, taken from various sources, were reviewed. These studies were limited in being mostly from Europe, North America, and Australia, rarely having data on gestational age, socioeconomic status (SES), or parental height or weight, and mostly covering childhood, with only a few covering adulthood. The findings were of interest, however, because almost all showed a direct relationship between birth weight and later BMI and none showed an inverse relationship. The few with null findings were smaller studies that might have lacked the power needed.
Dr Gillman presented several examples of such data, examining the relationship of birth weight to later BMI or obesity development over a broad age range. Data reported by Bavdekar et al6 related birth weight, in 250-g groupings between 2 kg and >3.25 kg, to BMI at 8 years of age (Fig 1). Mean BMI increased linearly from 
13 to 14.1 across these birth-weight groups. Gillman et al,7 in a study of >14 000 children 9 to 14 years of age (the Growing Up Today Study), showed an increase in the odds of adolescent overweight of 30% to 50%, depending on the factors controlled, with a 1-kg increase in birth weight (3-5% increase in the odds ratio [OR] per 100-g increase in birth weight) (Table 1). Data reported by Sorenson et al,8 which adjusted for gestational age, birth length, and maternal factors, showed a similar linear increase in BMI among Danish conscripts at 18 to 26 years of age, as their birth weight, grouped in 500-g categories, increased from <2.5 kg to >4.5 kg (Fig 2). The largest increase in BMI was among those who exceeded 4.5 kg at birth. Mean BMI ranged from 22.7 in the lowest-birth-weight group to 24.8 in the highest-birth-weight group.
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Independent of the potential contributions of such factors, direct effects may result from alterations in the fetal environment, including the transfer of fatty acids, leptin, and other hormones, fetal hyperinsulinemia, and the functioning of the fetal/placental unit. Supporting this view are data showing the growth patterns of children of diabetic mothers from birth to 8 years of age.9 These children had a higher weight for length at birth and at every year after age 1, relative to a National Center for Health Statistics (NCHS) reference. Data from a later report10 showed that this higher weight persisted through 14 to 17 years of age.
A within-family study indicated that family genetic factors and environment did not account for the relationship between birth weight and later weight among infants of diabetic mothers (Fig 3).11 The authors studied Pima Indian siblings in cases in which only 1 sibling was exposed to maternal diabetes mellitus in utero. Individuals exposed in utero exhibited BMI values 5 units higher than those of the unexposed siblings, measured either in late childhood or through age 24. A recent report,7 based on data from the Growing Up Today Study, examined obesity risk among 14 000 children according to maternal diabetes status during pregnancy (Table 2). The results showed a weaker association between gestational diabetes and offspring obesity, perhaps because of less severe gestational diabetes or better diabetes treatment.
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Because birth weight may be related to later obesity risk, it is relevant that the proportion of infants born large for gestational age (LGA; >90th percentile of weight for gestational age) in the United States has increased since 1990, particularly among whites (E. Oken, MD, verbal communication, 2003). Changes in the prevalence of factors that influence birth weight might have contributed to this increase. For example, the rate of diabetes mellitus during pregnancy increased from 2.2% to 3.2%, the rates of maternal smoking and adolescent pregnancy decreased, and the level of maternal education and first-trimester prenatal care increased. Changes in maternal BMI were not available, but increases in BMI could also increase birth weight. However, increases in birth weight resulting from these factors might be attenuated by other factors that tend to reduce birth weight, including decreased rates of postterm delivery because of more frequent labor induction, increased maternal age and rates of hypertension, increased numbers of births to unwed mothers, and increased numbers of preterm deliveries because of multiple births. (Dr Kramer later presented an analysis of data from 1 hospital that estimated the magnitude of the effects, in a Canadian population, of several factors known to affect birth weight.)
In addition to the effects of high birth weight on later BMI, the effects of low birth weight warrant review. Of particular concern is the effect of restricted fetal growth on central obesity. Central obesity, assessed as the waist-to-hip ratio or as skinfold measurements, is associated with insulin resistance and the metabolic syndrome, which is manifested as hypertension, hypertriglyceridemia, and glucose intolerance or frank type 2 diabetes, with an increased risk of cardiovascular disease. Several studies showed an inverse relationship of birth weight to central obesity, adjusted for attained BMI (Table 3),6,15–17 as well as to various measures of insulin resistance (Table 4). 6,18,19 Two studies17,20 reported an inverse relationship between birth weight and measures of the insulin resistance syndrome, also with adjustment for attained BMI. Data from the Nurses’ Health Study21–23 showed linear decreases in the risks of coronary heart disease, stroke, hypertension, and type 2 diabetes as birth weight increased from <5 to >10 lb, with adjustment for attained BMI (Fig 4). These various results, with adjustment for attained BMI, indicate that, at any given adult BMI, individuals with higher birth weights have lower risks of these outcomes, compared with those with lower birth weights.
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What are the implications for pregnancy interventions of the findings on the effects of intrauterine life? Although there are valid epidemiologic links between birth weight and adult health, clear etiologic factors have not been identified or quantified. Because lower birth weight is related to worse cardiovascular outcomes, some workers have recommended increasing efforts to raise birth weights, even in the developed world. However, Dr Gillman cautioned that such efforts could be harmful because of their possible effects in increasing obesity, which could increase the risk of type 2 diabetes and other diseases.
In a study of insulin resistance at 8 years of age among children in India, birth weight and insulin resistance (on HOMA, the homeostatic model assessment scale) were divided into tertiles.6 The highest risk for insulin resistance was among individuals in the lowest birth-weight tertile who were in the highest weight tertile at age 8. In a study of adolescents from the Philippines, blood pressure increased with increased BMI tertile but decreased across birth-weight tertiles.27 That is, with division of birth weight and adolescent blood pressure into 3 groups, blood pressure was highest for individuals born at the lowest weights and attaining the highest weights. Within the group with highest adolescent BMI values, higher birth weight was protective. Similarly, among white and Mexican American adults, those who were in the highest birth-weight tertile and remained thin showed no insulin resistance syndrome, whereas those who were born small and were in the highest BMI tertile in adulthood demonstrated a 25% prevalence of insulin resistance syndrome, the highest rate.28 It is clear that high adult BMI increases the risk at all birth weights, but the risk in all BMI tertiles is lowest for those with higher birth weight. In a cohort of 1256 Welsh men 45 to 59 years of age, the expected inverse relationship between birth weight and coronary disease was observed, with the lowest birth weight being related to more coronary disease than the highest birth weight.29 High birth weight was protective; all of the risk seemed to be related to having a high BMI in adulthood, with birth weight in the lower 2 tertiles.
Studies in rats suggest that prenatal conditions may determine postnatal behaviors that influence body weight, suggesting a prenatal origin for the "couch potato" syndrome.30 Rat mothers were either fed normally or restricted in energy during pregnancy. The pups were cross-fostered after birth, to either a normal-nutrition condition or overnutrition induced by a high-fat diet. This model provided adult rats with only prenatal undernutrition or undernutrition followed by postnatal overnutrition. Measurements showed increased energy intake and decreased physical activity (monitored as distance traveled) in the postnatally overnourished groups, compared with the normally nourished comparison groups, whether they were well nourished or energy-restricted during pregnancy. Increased mass of the retroperitoneal fat pad in the postnatally overnourished rats indicated the development of a relative central adiposity; this was accompanied by a decrease in total muscle mass, with an increase in systolic BP and insulin resistance. Postnatal overnutrition increased BP, compared with a normal state, but the effect was greatest when combined with prenatal undernutrition. These findings suggest that fetuses in a growth-restricted environment are not prepared to live with a surfeit of energy postnatally. The combination of restricted fetal growth and excess energy postnatally yields the worst outcomes.
We have noted that the interaction of lower birth weight with higher adult BMI yields the highest risk for cardiovascular disease outcomes. This combination of conditions is characteristic of the developing world undergoing the epidemiologic nutritional transition. In South Korea between 1938 and the middle 1990s, for example, the rates of deaths resulting from circulatory system diseases and malignancies increased from 1% to 28% and 22%, respectively, whereas the rate of deaths resulting from infections and parasitic diseases decreased from 18.5% to 2.4% and that of deaths resulting from respiratory system diseases decreased from 22% to 5%.31 In such settings, preventing the development of obesity is increasingly important.
The early postnatal level of nutrition appears able to influence later obesity. Therefore, it is logical to consider whether breastfeeding plays a role in preventing later obesity. Possible mechanisms include metabolic programming from the breast milk itself. Earlier studies suggested that breast milk and formula produce different insulin responses.32,33 Newer data suggest that there is a difference in leptin concentrations among breastfed versus bottle-fed infants.34,35 Another possibility is that breastfeeding leads to more internal control of energy intake by the child, whereas there might be more parental control over formula feeding. Whatever the relationship of feeding method to outcomes, there are problems in assuming that the observed associations are causal, because the social and cultural determinants of breastfeeding may also be related to later development of obesity.
Dr Gillman presented data he had collected from a brief literature review of reports since 1999 that dealt with breastfeeding and later overweight. All except 1 of the studies were cross-sectional and included populations of >2000 subjects; most were from the developed world. The collated results suggested a possible effect of breastfeeding duration, but results were mixed. The study by Gillman et al36 showed that the risk of overweight in adolescence declined monotonically with increased duration of breastfeeding in infancy (Fig 5). In the combined set of studies, when breastfeeding was considered dichotomously (yes or no), there was a consistent mean reduction in the prevalence of later obesity (variously defined), although the finding was not always statistically significant (Fig 6). 25,26,36–41 For example, Bergmann et al40 examined children 9 times between birth and 6 years of age and compared the findings for subjects who were breastfed for >3 months or <3 months. In both BMI and triceps skinfold measurements, breastfed infants began diverging from bottle-fed infants at 3 to 4 years of age, with, for example, a smaller proportion above the 90th percentile of BMI (Fig 7).
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Some preliminary results were presented from Project Viva, a cohort study exploring behavioral mechanisms of the breastfeeding effect and including >2000 deliveries. Three-year follow-up studies are now in progress. Interview data, biological samples, and dietary information were collected in this study. To examine the association of breastfeeding with behavioral factors that might affect the weight of the child, the effect of maternal restriction of feeding was examined, because this factor has been correlated with obesity among toddlers and preschool-aged children.42 The mother’s level of agreement with the statement "I have to be careful not to feed my infant too much" was used as the measure of this factor. Data on prenatal concerns about the child eating too much or not enough or becoming overweight or underweight were also collected. This allowed a preliminary examination of breastfeeding duration and maternal feeding restriction at 12 months, controlling for infant gender.
For each additional 1 month of breastfeeding, there was an 11% decrease in the odds of the mother agreeing or strongly agreeing with the statement quoted above. Results were similar when demographic characteristics, mother’s preexisting attitudes, and infant birth weight or 6-month weight for length were controlled, suggesting that, if breastfeeding protects against later obesity, then there might be a behavioral mechanism for the protection. Nevertheless, because the many other benefits of breastfeeding for the mother and child are well established, little harm would come from promoting breastfeeding to prevent obesity development.
Michael S. Kramer, MD, McGill University, Montreal, Quebec
Dr Kramer began by presenting data on the temporal trend in obesity, which demonstrated that, like the United States, Canada is experiencing an epidemic of obesity. Obesity prevalence has increased progressively since 1985, with most provinces exceeding 15% by 1998. The Maritime Provinces, the Northwest Territories, and the new territory in Canada, Nunavut, exhibited the highest prevalences of obesity (
20%) in the most recent data. There is a major problem with obesity in the aboriginal population. The 2 provinces with the lowest rates of obesity (10–14%) are British Columbia in the west and the province of Quebec in the east. It is probably not an accident that these 2 provinces both have mountains and an outdoor lifestyle.
Data from the US National Health and Nutrition Examination Survey (NHANES) for children show increasing obesity not only among 6- to 17-year-old individuals but even in the toddler and preschool periods.3 Recent surveys show exponentially increasing rates of obesity among children in the United States, but there are no comparable data for Canada.
The relationship of birth weight to weight in childhood has been explored with data from the Special Supplemental Nutrition Program for Women, Infants, and Children (WIC) in Tennessee.43 The birth weights of WIC participants were obtained from birth certificates and linked to their weights and heights through age 5 in WIC. The z scores of weight for age, height for age, and weight for height were examined for 8 birth-weight groupings of 500 g, ranging from 1.0 to 1.5 kg through 4.5 to 5.0 kg. A z score of 0 indicates the NCHS reference mean weight-for-age z score. The 3.0- to 3.5-kg birth-weight grouping most closely approximated that value at 5 years of age. The lightest infants (1.0–1.5 kg) and the heaviest infants (4.5–5.0 kg) had the most extreme weight-for-age and height-for-age z scores initially but moved to less extreme values within 12 months, attaining z scores of approximately –1 and +1, respectively (ie, 1 SD from the mean). Differences in weight-for-height z scores in the most extreme birth-weight groups did not decrease with age.
A study based on data from NHANES III (also linked to birth certificates) examined weight-for-age z scores for children born LGA (>90th percentile) and for those born small for gestational age (SGA; <10th percentile).44 There was some catch-up growth by the SGA infants and "catch down" by the LGA infants, reaching z scores of 0.5 below or above the mean, respectively, by the first year and remaining largely at those levels through 3 to 4 years of age.
Data from the Collaborative Perinatal Project, a large US study from the early 1960s, were recently used to examine the joint relationship of birth weight and early child weight gain (in the first 4 months) to overweight status at 7 years of age, considered as 95th percentile of BMI with the use of current NCHS standards for age 7.45 Birth weight and rate of weight gain during the first 4 months of life were both divided into quintiles. Within each early weight gain quintile, overweight status at 7 years of age tended to increase as birth weight increased, with the greatest increase in prevalence in the highest birth-weight quintile (3.61–5.56 kg). Within any birth-weight quintile, there was also an increased prevalence of overweight with increased rate of gain in the first 4 months, with a particularly large increase in the highest quintile of weight gain. Therefore, weight gain and birth weight had independent effects that persisted through at least age 7. (A table from this publication showed the OR for overweight status as 1.38 and 1.17 [2 models] for each 100-g increment in the rate of weight gain per month and 1.06 and 1.02 for each 100 g of birth weight.)
Data from a small study from Canada46 considered this issue at later ages, to show the lasting effects of low birth weight for gestational age on later fat content. SGA infants were matched, with respect to SES and other factors, with infants who were born between the 25th and 75th percentiles of weight for gestational age. In the subjects’ teenage years, there was no significant difference in subscapular skinfold measurements, but significantly lower triceps skinfold measurements were recorded for those who were SGA, compared with those who were appropriate weight for gestational age. This finding may support relatively increased central adiposity among individuals born SGA, although the small sample size suggests the need for cautious interpretation. In a study of Swedish children monitored from birth through 18 years of age,47 BMI at birth was correlated with BMI at 18 years of age (Spearman correlation coefficient: 0.15). As might be expected, the correlation of current BMI with BMI at 18 years increased with increasing age.
A study of Finnish twin pairs examined the relationship of the intratwin difference in ponderal index at birth and the intratwin difference in BMI at 16 years of age.48 For the 637 monozygotic twin pairs, there was a very weak, although highly statistically significant, correlation between the differences in ponderal index at birth and the differences in BMI at age 16 (Pearson r: 0.05). The much stronger correlation among the same-sex dizygotic twins (r = 0.15) suggests that environmental factors played a much larger role than genetics in the degree to which these twins exhibited similar BMI values at age 16.
A Swedish study examined women’s weight in early pregnancy and their own birth weights, with the use of a national birth register that included data on mothers’ BMI values and could be linked to the mothers’ earlier birth records.49 Women who were born SGA (z scores of less than –2) had a slightly reduced (not statistically significant) chance of having a BMI of 25 when they became childbearers 20 to 30 years later, with an adjusted OR of 0.9 (95% confidence interval [CI]: 0.8-1.1). There was, however, a statistically significant increased risk (adjusted OR: 1.8; 95% CI: 1.5-2.1) of having a BMI of 25 during pregnancy among women who were born LGA (z scores of more than +2).
A study of Australian children related being SGA or LGA at birth to the risk of having a >94th percentile BMI at 5 years of age, with the use of an internal standard based on this cohort.50 Being SGA at birth reduced by one-half the risk of having a high BMI at age 5. Being LGA doubled the risk. Dr Kramer noted that these results were different from those presented by Dr Gillman. He proposed that there is no increased risk of obesity development at the low end of the birth-weight distribution; if attained BMI is not controlled, then low-birth-weight newborns are protected from obesity. He indicated that attained BMI should not be controlled, because BMI is on the causal path between fetal growth and later adiposity/obesity and "it actually artificially inflates the risk of obesity in SGA children."
The effect of high birth weight may become more important as birth-weight distributions move toward higher weights. Data for Canada and the United States are similar, but the increases in birth weight in the United States may be somewhat smaller. Canadian trends in low birth weight (<2500 g) and preterm births (births before 37 completed weeks) also differ from those in the United States. In the early 1980s, rates of both low-birth-weight and preterm births were declining very slightly in Canada (Fig 8).51 Since the middle 1980s, however, Canadian rates of preterm births have increased, as have rates in almost all developed countries and in many developing countries, primarily because of increases in obstetric interventions and in the numbers of multiple births. However, the low birth-weight rate, despite its being driven largely by preterm births, actually declined slightly. This finding suggests that the size of infants born at term is increasing, although more infants are being born early, with shorter gestations. Preterm births are more common, but birth weight is increasing, particularly for term births. The data showed that mean birth weight increased 50 g from 1981 to 1997. Accounting for the decline in gestational age that occurred during the period (more preterm births and fewer postterm births) with the use of birth-weight z scores, the birth-weight increase was 0.2 z score, or 100 g.
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9.5% in 1997. Similarly, the LGA rate increased by 25%, from 8% to 10%, during this time period. Therefore, birth weight for gestational age has increased, as would be predicted from the contrasting trends in preterm births and low birth weight. Like US birth certificates, Canadian birth certificates lack information on maternal BMI. Data from hospital records are more inclusive. Dr Kramer presented findings for an 18-year period at a maternity hospital at McGill University that enabled examination of factors that might have influenced birth-weight trends and fetal growth during the period.52 Differences in the hospital’s absolute LGA and SGA rates, compared with the contemporaneous national figures presented above, likely reflect the relative SES advantage of the population the hospital serves. Nevertheless, the general decrease in SGA rates and increase in LGA rates during the time period were similar to those occurring throughout Canada. Changes in determinants that affect birth weight or birth weight for gestational age played a role. There was a 50% decrease in the proportion of mothers smoking more than one-half of a pack of cigarettes per day (Fig 9). Furthermore, the prevalence of maternal obesity (BMI of >29) doubled and the prevalence of net maternal pregnancy weight gain of at least 0.5 kg/week (exclusive of the weight of the infant) also almost doubled, increasing steadily during this time period. The prevalence of gestational diabetes mellitus increased dramatically to nearly 5%, partly because of increased screening but probably partly reflecting a real increase.
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2.2% per year in the risk of SGA (Table 5). Increased maternal prepregnancy BMI explained approximately one seventh of the change. Reductions in maternal smoking and the other standard factors that were controlled also explained most of the decrease in the SGA rate. The LGA rate increased 2% per year. Approximately one quarter of that increase was explained by increases in BMI, but increases were also attributable to increases in the gestational diabetes rate and reductions in smoking. These analyses show that changes in maternal weight, weight gain, diabetes, smoking, age, and education largely explain the increases in birth-weight z scores and LGA rates and the decrease in SGA rates.
In the above-cited Australian study,50 maternal BMI of 95th percentile (obesity) quadrupled the risk of obesity (BMI of >95th percentile) among 5-year-old subjects, even after controlling for size for gestational age at birth. Paternal BMI of 95 percentile doubled the risk. Parental obesity is an important factor, beyond the effect of birth weight. However, the larger effect of maternal (versus paternal) BMI suggests that obesity development in the offspring is not primarily a genetic effect. The relationship to maternal BMI may be partly genetic but probably reflects maternal and family lifestyles, especially regarding eating and physical activity.
Other studies have also explored the relationship of parental weight status to the weight status of the child. An analysis based on NHANES III data37 classified maternal BMI as underweight, normal, overweight, or obese and compared the children’s weight status at 3 to 5 years of age, grouped as BMI of <85th percentile, 85th to 94th percentile (overweight), or 95th percentile (obese). The proportions of children in the 2 highest BMI categories increased monotonically as maternal weight status increased. With logistic regression analysis of these data, controlling for birth weight, race/ethnicity, gender of the child, breastfeeding, and timing of the introduction of solid foods, overweight mothers had a 54% increased risk of their children being overweight and a tripled risk of the children being obese (Table 6). Obese mothers had a tripled risk of their children being overweight and a more than quadrupled risk of their children being obese. These effects of maternal BMI may be quite long-lasting. Among African American adults, the sum of the triceps and subscapular skinfold measurements has been shown to increase with an increase in the quintile of their mothers’ prepregnancy BMI.53
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One confounder is maternal BMI. It has been shown that high maternal BMI is associated with reduced breastfeeding initiation and duration.54 Fat mothers are less likely to breastfeed and, if they try, they are less likely to be successful at it. Therefore, the higher weight status of bottle-fed infants could be attributable to selection of children of higher-weight mothers, who were both less likely to have breastfed and more likely to have higher-weight children. In addition, mothers who breastfed for at least 12 months reported lower levels of control over child feeding at 18 months.55 Highly controlling feeding practices may interfere with the child’s ability to self-regulate energy intake, an effect that may be long-lasting. Breastfeeding also may be associated with a healthier lifestyle, including increased physical activity, and with other factors that are hard to measure or often are not measured but may be responsible for part of the effect that has been attributed to breastfeeding.
Dr Kramer concluded that there is probably a protective effect of breastfeeding on child obesity but it must be a fairly small effect. The obesity epidemic developed in the United States during a 30-year period when breastfeeding initiation in hospitals increased and breastfeeding, even at 6 months, also increased.56 These increases did not prevent obesity development. However, others noted that the increase in obesity might have been even worse without the increase in breastfeeding. Furthermore, the increase in obesity might not have occurred equally, or even at all, among infants who were breastfed for a significant period, because few infants are exclusively breastfed and most are not breastfed long.
Neither birth-weight changes nor breastfeeding explains the obesity epidemic. What other factors might explain it? At this point, Dr Kramer acknowledged material provided by 2 colleagues, Dr Alison Stephen, Director of Research at the Heart and Stroke Foundation of Canada, and Dr Diane Finegood, Scientific Director of the Institute of Nutrition, Metabolism, and Diabetes of the Canadian Institutes of Health Research. Body fat is the net result of what goes in and what comes out. What goes in has to do with portion sizes, meal and snack frequencies, and the energy density of food. What comes out is basal energy expenditure, obligatory energy expenditure, adaptive thermogenesis, and physical activity.
Just 40 to 125 kJ extra every day leads to an increase in weight of 1 to 3 lb per year. The tools for measuring energy intake in the field, such as food frequency and 24-hour recall, cannot measure energy intake or energy expenditure that precisely. Consider the 8-year weight changes observed among adults between 20 and 40 years of age in 2 NHANES studies. The modal increase in weight was 10 lb, equivalent to an excess of 65 kJ per day. An excess of 210 kJ per day for 8 years would result in a gain of 40 lb, the amount gained by 10% of the subjects studied.57 Even 210 kJ per day is too small a difference to measure reliably with current methods. Typical food items have much greater energy levels (Big Mac: 2475 kJ; large order of fries: 2270 kJ; grand latte: 925 kJ; bagel: 670 kJ). On the energy expenditure side, cycling for 15 minutes requires only 315 to 630 kJ (depending on speed and resistance), using a stair climber for 15 minutes requires 650 kJ, and walking 2000 steps on a level requires 420 kJ.
Dr Kramer presented data assembled from several countries between 1900 and 2000.58–60 The data suggested that there was an increase in the percentage of energy as fat in the diet before World War II in the United States and probably in the United Kingdom, whereas there was a decrease in the 1970s and 1980s. The available data for Canada indicated a similar pattern of declining percentages of dietary fat in the past few decades. Carbohydrate intake has also decreased in the United Kingdom since values have been measured, in terms of grams per day or percentage of energy.
Dr Kramer cited an array of sources of data for the United Kingdom, including Nutrition Abstracts Review (1933 to present), the British Journal of Nutrition (1947 to present), the Journal of Human Nutrition and the European Journal of Clinical Nutrition (1947 to present), the American Journal of Clinical Nutrition, United Kingdom government publications, Medical Research Council special reports, and various medical journals. The data presented indicated that reported energy intake declined in all 3 countries, whether measured between 1972 and 1990 (Quebec and Saskatchewan) or between 1940 and 2000 (United States and United Kingdom). Use of low-energy products among US adults has skyrocketed, particularly since the middle 1980s, and there has been a concurrent increase in overweight.61 Combined results of 2 United Kingdom national surveys indicated a decrease in energy intake among children 3 to 4.5 years of age between 1950 and the early 1990s.62 Data from NHANES for US children from the 1970s to the 1990s also showed slight decreases in energy intakes among 2- to 5-year-old and 6- to 11-year-old children, with a possible slight increase in intake among teenagers in the most recent survey (1988–1994).63 The same NHANES reports indicated that the percentage of energy intake as fat has declined for all 3 age groups.63
Cross-sectional data from Nova Scotia show a decline in physical activity among both boys and girls in grades 3 through 11.64 Data on television watching among teenagers 12 to 17 years of age in the United States, taken from 2 Centers for Disease Control and Prevention surveys from the late 1960s and 1990, are consistent. Much time was spent watching television even in the 1970s, but the amount has increased in 20 years. Now, one third of teenagers say they watch 5 hours of television per day, which surely affects energy expenditure.
In conclusion, high birth weight and infant weight gain are both associated with later obesity. There has been a temporal trend toward increasing birth weight, which is attributable mostly to increases in maternal BMI, gestational weight gain, and gestational diabetes rates and a reduction in maternal smoking. Parental, and particularly maternal, BMI is associated with child obesity and subsequent adult obesity, beyond its effect on birth weight. The evidence is equivocal but perhaps suggests a protective effect of breastfeeding, although this is unlikely to be of major public health importance, in terms of its effect on adult obesity. Dr Kramer considered the evidence weak for higher energy intake being the primary factor responsible for the obesity epidemic but considered the evidence strong for decreased physical activity playing a key role.
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WHAT ARE INFANTS AND TODDLERS EATING? |
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TOPABSTRACTOBESITY ORIGINS IN FETAL...WHAT ARE INFANTS AND...TRANSITIONING TO SOLID FOODS...LONGITUDINAL PERSPECTIVE ON...REFERENCES |
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The FITS consisted of a survey of the parents and caregivers of a sample of children 4 to 24 months of age. A commercial frame, a listing judged to have the greatest coverage of all infants and toddlers, was used to draw the sample. A household survey was used to establish eligibility and recruit participants for the study. Participants answered questions on socioeconomic and demographic characteristics and were sent a food guide, a study brochure, and an incentive check. Approximately 7 to 10 days later, a 24-hour dietary recall was administered via telephone. The University of Minnesota nutrition data system was used for data collection. For statistical purposes, a second 24-hour dietary recall was administered to a random subsample of the population.
The 3022 participating children were grouped according to age, ie, 4 to 6 months, 7 to 8 months, 9 to 11 months, 12 to 14 months, 15 to 18 months, and 19 to 24 months. The ages of 4 to 6 months and 9 to 11 months were intentionally oversampled, because of the transitions in infant feeding that occur at these ages. There were 308 to 862 children in each group. The sample was reasonably representative of all US infants and toddlers, with 20% nonwhite, 12% Hispanic, 48% first-born, and 55% with working mothers (all close to national rates). Only 27%, however, participated in WIC, with lower rates for the 1- to 2-year-olds than for infants (below national rates); 80% of the sample had household incomes between $25 000 and $100 000, with 11% having lower incomes and 9% having higher incomes. This represents slightly smaller proportions at the low-income and high-income levels and a slightly greater proportion at the middle-income level, compared with national data.
The first question considered was: Are infants and toddlers overeating? The energy intakes reported in the 24-hour dietary recalls for these infants and toddlers exceeded the Estimated Energy Requirement, the new dietary reference standard for food energy that was released 1 year ago by the Macronutrient Panel.68 On average, individuals should be consuming the amount of food energy that they need in a day. In a population group, the mean intake should equal the mean energy requirement. In this population, the mean intake exceeded the mean requirement by 10% for infants 4 to 6 months of age and by 31% for children 1 to 2 years of age (Table 7). Although these intakes may represent overeating, it is also possible that the mean Estimated Energy Requirement is underestimated or that intake is overreported; all of these may contribute to the difference.
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The second question addressed was: What are infants and toddlers eating? The data showed that 29% of infants have solid foods introduced before 4 months of age, whereas introduction at 4 to 6 months is usually considered to be developmentally appropriate. Only 6 percent of the infants reach the age of 6 months before the introduction of solid foods.
The percentages of total daily energy intake attributable to 7 broad food groups were presented for each of the 6 age groupings (Fig 10). For very young infants (4–6 months and 7–8 months of age), >80% of daily energy intake is obtained from milk, either breast milk or formula. The remainder is obtained mostly from infant cereal or baby foods. A transition starts at 9 to 11 months of age and continues through the second year, as the child moves from infant feeding to baby foods and to adult foods, including table foods, cow’s milk, and other beverages. By age 2, the bulk of the food energy is obtained from table foods, including 100% juices. Other beverages, which tend to be sweetened beverages, colas and ades, account for 10% of daily energy by age 2. Cow’s milk continues to play a role up to age 2.
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20% of subjects did not consume a vegetable on the day of the recall. There are 2 interesting results related to vegetables. First, by 15 to 18 months of age, French fries or fried potatoes are the vegetables most commonly reported as being consumed. Second, 29% of the infants are consuming deep yellow vegetables at 9 to 11 months of age, when they are still consuming mostly infant foods. At 7 to 8 months, that percentage is even higher. As the children make the transition to table foods, however, the proportion consuming deep yellow vegetables decreases dramatically, to 12% at 15 to 18 months and to 8% at 19 to 24 months. During this period, the proportion of children consuming high-energy foods increases with age (Fig 11). Intakes of some common adult foods (foods that are part of the diets of older children and adults) are revealing. Candy, pizza, chicken nuggets or fried chicken, sodas, sweetened teas and ades, salty snacks (including chips, popcorns, and cheese puffs), hot dogs, sausages, and cold cuts are included in Fig 11. By 19 to 24 months of age, 1 in 10 toddlers consumed candy on the day of the recall, 23% consumed sodas or other sweetened beverages, 27% consumed salty snacks such as chips, popcorn, or cheese puffs, and 27% consumed hot dogs, sausages, or cold cuts.
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TRANSITIONING TO SOLID FOODS AND THE FAMILY TABLE: EFFECTS OF PARENTING STYLES, FEEDING PRACTICES, AND CULTURE |
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TOPABSTRACTOBESITY ORIGINS IN FETAL...WHAT ARE INFANTS AND...TRANSITIONING TO SOLID FOODS...LONGITUDINAL PERSPECTIVE ON...REFERENCES |
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In general, interventions targeted at children have failed.71 The reasons for the failure are unclear, but one primary reason might be that infants and young children eat what they like. In other words, their preferences are guided by their senses and not cognitive decisions. Taste and smell are our oldest senses; they are critical for the acceptance or rejection of food. These senses are well developed in utero but continue to change during development, such that children live in their own sensory worlds. During infancy and childhood, children learn what to like, how to eat, and when to eat. There is mounting evidence of nutritional and flavor programming early in life, but one of the gaps in our knowledge remains one of the most fundamental mysteries of human behavior, ie, why do we like the things we do?
To answer this fundamental question, Dr Mennella explored a series of questions, as follows. 1) What are the sensory capabilities and preferences of infants and children? 2) Does early exposure to salt and sweets shape preferences? 3) How do infants learn about flavors and foods? 4) Do practices early in life set the stage for lifelong food preferences? What practices facilitate later acceptance of fruits and vegetables?
Findings from developmental biology studies show that the chemical senses (taste and smell) develop in utero after tactile and vestibular capabilities but before the auditory sense. The flavor of a food includes, among other chemosensory stimuli, the oral sensation of taste (sweet, sour, salt, bitter, and umami) and the retronasal sensation of smell. The intimate connection was captured by Brillat-Savarin, who noted that ".... smell and taste are in fact but a single sense, whose laboratory is the mouth and whose chimney is the nose. ..."74 The sensory world of infants and children is different from that of adults, because their ability to detect and prefer certain tastes appears to develop after birth and is heightened during development. Within hours after birth, infants exhibit a strong preference for sweet tastes75–78 and can detect several different sugars, including lactose, glucose, and sucrose.75 In general, sweet sensation serves as a guide to foods that are rich in carbohydrates, and the heightened preference during childhood may serve the need for energy. Sweet tastes also produce a morphine-like analgesia among infants and children, and stimulation of the taste buds by the sweet taste is necessary to produce the analgesia.79–82
There is strong evidence that infants are born with a preference for sweetness, and sweetness is the predominant taste quality of breast milk. In addition to other sensory features of the mother that are preferred by the infant, such as her voice and her odor, these cues are powerful reinforcers for early learning.83,84 The heightened preference for sweet taste during early development is universal and is evident in children around the world, eg, in Brazil, France, Iraq, Israel, Mexico, the Netherlands, and North America.85 Experience can modify this preference but, in general, sweet preference decreases to adult levels during late adolescence.86,87
Bitter taste sensitivity is another critical early development among newborns. Such sensitivity protects the individual from poisoning, because most toxic plants and toxins contain bitter-tasting substances. Newborns grimace, arch their lips, and protrude their tongue in response to a bitter taste.78
Unlike the other taste sensitivities, the ability to detect salt does not develop until 4 to 6 months of age. Like sweet preference, salt preference remains heightened during later infancy and into childhood; the degree of preference is related to experience with salty foods. Salt imparts a salty flavor to food and also enhances other flavors in food.88 The most preferred level for the saltiness of food can be influenced by sodium status and dietary exposure. The sodium ion is a powerful modifier of off-tastes or bad tastes and thus enhances food palatability.88,89 Its ability to modify bitterness is enhanced during childhood, because of children’s heightened preference for salt. In addition to age-related preferences for sweetness and sodium among children, compared with adults, there are ethnic differences.
How do infants learn about flavors and foods? Dr Mennella speculated that nutrition, a key environmental influence, might act on the genome during a sensitive period in development. This influence might have long-term effects on a wide variety of metabolic, developmental, and pathologic processes in later life. The flavors associated with the foods eaten by the mother and her infant are also being programmed. Dietary experience during the first years of life is critical for the development of several aspects of food and flavor preferences72,73,90,91 (see ref 92 for review).
There is evidence that a variety of flavors are transmitted from the mother’s diet to amniotic fluid and mother’s milk. These transmitted flavors include garlic, carrot, mint, vanilla, bleu cheese, alcohol, and tobacco.93–97 One-day-old infants of mothers who consumed anise-flavored beverages or foods containing garlic during pregnancy displayed less-negative facial expressions when exposed to the odors of anise and garlic, respectively. Prenatal taste experiences dictate later preferences.98,99 Infants can detect a diversity of flavors in amniotic fluid and mother’s milk.100 They accept new foods, such as cereals, more readily if they are prepared with their mother’s milk.97 The flavor profile of human milk reflects the mother’s diet and the culture in which the infant is born and is similar to the flavor profile experience
