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1.  Genetic Markers of Adult Obesity Risk Are Associated with Greater Early Infancy Weight Gain and Growth 
PLoS Medicine  2010;7(5):e1000284.
Ken Ong and colleagues genotyped children from the ALSPAC birth cohort and showed an association between greater early infancy gains in weight and length and genetic markers for adult obesity risk.
Genome-wide studies have identified several common genetic variants that are robustly associated with adult obesity risk. Exploration of these genotype associations in children may provide insights into the timing of weight changes leading to adult obesity.
Methods and Findings
Children from the Avon Longitudinal Study of Parents and Children (ALSPAC) birth cohort were genotyped for ten genetic variants previously associated with adult BMI. Eight variants that showed individual associations with childhood BMI (in/near: FTO, MC4R, TMEM18, GNPDA2, KCTD15, NEGR1, BDNF, and ETV5) were used to derive an “obesity-risk-allele score” comprising the total number of risk alleles (range: 2–15 alleles) in each child with complete genotype data (n = 7,146). Repeated measurements of weight, length/height, and body mass index from birth to age 11 years were expressed as standard deviation scores (SDS). Early infancy was defined as birth to age 6 weeks, and early infancy failure to thrive was defined as weight gain between below the 5th centile, adjusted for birth weight. The obesity-risk-allele score showed little association with birth weight (regression coefficient: 0.01 SDS per allele; 95% CI 0.00–0.02), but had an apparently much larger positive effect on early infancy weight gain (0.119 SDS/allele/year; 0.023–0.216) than on subsequent childhood weight gain (0.004 SDS/allele/year; 0.004–0.005). The obesity-risk-allele score was also positively associated with early infancy length gain (0.158 SDS/allele/year; 0.032–0.284) and with reduced risk of early infancy failure to thrive (odds ratio  = 0.92 per allele; 0.86–0.98; p = 0.009).
The use of robust genetic markers identified greater early infancy gains in weight and length as being on the pathway to adult obesity risk in a contemporary birth cohort.
Please see later in the article for the Editors' Summary
Editors' Summary
The proportion of overweight and obese children is increasing across the globe. In the US, the Surgeon General estimates that, compared with 1980, twice as many children and three times the number of adolescents are now overweight. Worldwide, 22 million children under five years old are considered by the World Health Organization to be overweight.
Being overweight or obese in childhood is associated with poor physical and mental health. In addition, childhood obesity is considered a major risk factor for adult obesity, which is itself a major risk factor for cancer, heart disease, diabetes, osteoarthritis, and other chronic conditions.
The most commonly used measure of whether an adult is a healthy weight is body mass index (BMI), defined as weight in kilograms/(height in metres)2. However, adult categories of obese (>30) and overweight (>25) BMI are not directly applicable to children, whose BMI naturally varies as they grow. BMI can be used to screen children for being overweight and or obese but a diagnosis requires further information.
Why Was This Study Done?
As the numbers of obese and overweight children increase, a corresponding rise in future numbers of overweight and obese adults is also expected. This in turn is expected to lead to an increasing incidence of poor health. As a result, there is great interest among health professionals in possible pathways between childhood and adult obesity. It has been proposed that certain periods in childhood may be critical for the development of obesity.
In the last few years, ten genetic variants have been found to be more common in overweight or obese adults. Eight of these have also been linked to childhood BMI and/or obesity. The authors wanted to identify the timing of childhood weight changes that may be associated with adult obesity. Knowledge of obesity risk genetic variants gave them an opportunity to do so now, without following a set of children to adulthood.
What Did the Researchers Do and Find?
The authors analysed data gathered from a subset of 7,146 singleton white European children enrolled in the Avon Longitudinal Study of Parents and Children (ALSPAC) study, which is investigating associations between genetics, lifestyle, and health outcomes for a group of children in Bristol whose due date of birth fell between April 1991 and December 1992. They used knowledge of the children's genetic makeup to find associations between an obesity risk allele score—a measure of how many of the obesity risk genetic variants a child possessed—and the children's weight, height, BMI, levels of body fat (at nine years old), and rate of weight gain, up to age 11 years.
They found that, at birth, children with a higher obesity risk allele score were not any heavier, but in the immediate postnatal period they were less likely to be in the bottom 5% of the population for weight gain (adjusted for birthweight), often termed “failure to thrive.” At six weeks of age, children with a higher obesity risk allele score tended to be longer and heavier, even allowing for weight at birth.
After six weeks of age, the obesity risk allele score was not associated with any further increase in length/height, but it was associated with a more rapid weight gain between birth and age 11 years. BMI is derived from height and weight measurements, and the association between the obesity risk allele score and BMI was weak between birth and age three-and-a-half years, but after that age the association with BMI increased rapidly. By age nine, children with a higher obesity risk allele score tended to be heavier and taller, with more fat on their bodies.
What Do These Findings Mean?
The combined obesity allele risk score is associated with higher rates of weight gain and adult obesity, and so the authors conclude that weight gain and growth even in the first few weeks after birth may be the beginning of a pathway of greater adult obesity risk.
A study that tracks a population over time can find associations but it cannot show cause and effect. In addition, only a relatively small proportion (1.7%) of the variation in BMI at nine years of age is explained by the obesity risk allele score.
The authors' method of finding associations between childhood events and adult outcomes via genetic markers of risk of disease as an adult has a significant advantage: the authors did not have to follow the children themselves to adulthood, so their findings are more likely to be relevant to current populations. Despite this, this research does not yield advice for parents how to reduce their children's obesity risk. It does suggest that “failure to thrive” in the first six weeks of life is not simply due to a lack of provision of food by the baby's caregiver but that genetic factors also contribute to early weight gain and growth.
The study looked at the combined obesity risk allele score and the authors did not attempt to identify which individual alleles have greater or weaker associations with weight gain and overweight or obesity. This would require further research based on far larger numbers of babies and children. The findings may also not be relevant to children in other types of setting because of the effects of different nutrition and lifestyles.
Additional Information
Please access these Web sites via the online version of this summary at
Further information is available on the ALSPAC study
The UK National Health Service and other partners provide guidance on establishing a healthy lifestyle for children and families in their Change4Life programme
The International Obesity Taskforce is a global network of expertise and the advocacy arm of the International Association for the Study of Obesity. It works with the World Health Organization, other NGOs, and stakeholders and provides information on overweight and obesity
The Centers for Disease Control and Prevention (CDC) in the US provide guidance and tips on maintaining a healthy weight, including BMI calculators in both metric and Imperial measurements for both adults and children. They also provide BMI growth charts for boys and girls showing how healthy ranges vary for each sex at with age
The Royal College of Paediatrics and Child Health provides growth charts for weight and length/height from birth to age 4 years that are based on WHO 2006 growth standards and have been adapted for use in the UK
The CDC Web site provides information on overweight and obesity in adults and children, including definitions, causes, and data
The CDC also provide information on the role of genes in causing obesity.
The World Health Organization publishes a fact sheet on obesity, overweight and weight management, including links to childhood overweight and obesity
Wikipedia includes an article on childhood obesity (note that Wikipedia is a free online encyclopedia that anyone can edit; available in several languages)
PMCID: PMC2876048  PMID: 20520848
2.  Earlier Mother's Age at Menarche Predicts Rapid Infancy Growth and Childhood Obesity 
PLoS Medicine  2007;4(4):e132.
Early menarche tends to be preceded by rapid infancy weight gain and is associated with increased childhood and adult obesity risk. As age at menarche is a heritable trait, we hypothesised that age at menarche in the mother may in turn predict her children's early growth and obesity risk.
Methods and Findings
We tested associations between mother's age at menarche, mother's adult body size and obesity risk, and her children's growth and obesity risk in 6,009 children from the UK population-based Avon Longitudinal Study of Parents and Children (ALSPAC) birth cohort who had growth and fat mass at age 9 y measured by dual-energy X-ray absorptiometry. A subgroup of 914 children also had detailed infancy and childhood growth data. In the mothers, earlier menarche was associated with shorter adult height (by 0.64 cm/y), increased weight (0.92 kg/y), and body mass index (BMI, 0.51 kg/m2/y; all p < 0.001). In contrast, in her children, earlier mother's menarche predicted taller height at 9 y (by 0.41 cm/y) and greater weight (0.80 kg/y), BMI (0.29 kg/m2/y), and fat mass index (0.22 kg/m2/year; all p < 0.001). Children in the earliest mother's menarche quintile (≤11 y) were more obese than the oldest quintile (≥15 y) (OR, 2.15, 95% CI 1.46 to 3.17; p < 0.001, adjusted for mother's education and BMI). In the subgroup, children in the earliest quintile showed faster gains in weight (p < 0.001) and height (p < 0.001) only from birth to 2 y, but not from 2 to 9 y (p = 0.3–0.8).
Earlier age at menarche may be a transgenerational marker of a faster growth tempo, characterised by rapid weight gain and growth, particularly during infancy, and leading to taller childhood stature, but likely earlier maturation and therefore shorter adult stature. This growth pattern confers increased childhood and adult obesity risks.
Earlier age at menarche may be a transgenerational marker of faster growth, particularly during infancy, leading to taller childhood stature but earlier maturation and hence shorter adult stature.
Editors' Summary
Childhood obesity is a rapidly growing problem. Twenty-five years ago, overweight children were rare. Now, 155 million of the world's children are overweight and 30–45 million are obese. Overweight and obese children—those having a higher than average body mass index (BMI; weight divided by height squared) for their age and sex—are at increased risk of becoming obese adults. Such people are more likely to develop heart disease, diabetes, and other health problems than lean people. Many factors are involved in the burgeoning size of children. Parental obesity, for example, predisposes children to being overweight. In part, this is because parents influence the eating habits of their offspring and the amount of exercise they do. In addition, though, children inherit genetic factors from their parents that make them more likely to put on weight.
Why Was This Study Done?
To prevent childhood obesity, health care professionals need ways to predict which infants are likely to become obese so that they can give parents advice on controlling their children's weight. In girls, early menarche (the start of menstruation) is associated with an increased risk of childhood and adult obesity and tends to be preceded by rapid weight gain in the first two years of life. Because age at menarche is inherited, the researchers in this study have investigated whether mothers' age at menarche predicts rapid growth in infancy and childhood obesity in their offspring using data from the Avon Longitudinal Study of Parents and Children (ALSPAC). In 1991–1992, this study recruited nearly 14,000 children born in Bristol, UK. Since then, the children have been regularly examined to investigate how their environment and genetic inheritance interact to affect their health.
What Did the Researchers Do and Find?
The researchers measured the growth and fat mass of 6,009 children from ALSPAC at 9 years of age. For 914 of these children, the researchers had detailed data on their growth during infancy and early childhood. They then looked for any associations between the mother's age at menarche (as recalled during pregnancy), mother's adult body size, and the children's growth and obesity risk. In the mothers, earlier menarche was associated with shorter adult height and increased weight and BMI. In the children, those whose mothers had earlier menarche were taller and heavier than those whose mothers had a later menarche. They also had a higher BMI and more body fat. The children whose mothers had their first period before they were 11 were twice as likely to be obese as those whose mothers did not menstruate until they were 15 or older. Finally, for the children with detailed early growth data, those whose mothers had the earliest menarche had faster weight and height gains in the first two years of life (but not in the next seven years) than those whose mothers had the latest menarche.
What Do These Findings Mean?
These findings indicate that earlier mother's menarche predicts a faster growth tempo (the speed at which an individual reaches their adult height) in their offspring, which is characterized by rapid weight and height gain during infancy. This faster growth tempo leads to taller childhood stature, earlier sexual maturity, and—because age at puberty determines adult height—shorter adult stature. An inherited growth pattern like this, the researchers write, confers an increased risk of childhood and adult obesity. As with all studies that look for associations between different measurements, these findings will be affected by the accuracy of the measurements—for example, how well the mothers recalled their age at menarche. Furthermore, because puberty, particularly in girls, is associated with an increase in body fat, a high BMI at age nine might indicate imminent puberty rather than a risk of long-standing obesity—further follow-up studies will clarify this point. Nevertheless, the current findings provide a new factor—earlier mother's menarche—that could help health care professionals identify which infants require early growth monitoring to avoid later obesity.
Additional Information.
Please access these Web sites via the online version of this summary at
The Avon Longitudinal Study of Parents and Children has a description of the study and results to date
The US Centers for Disease Control and Prevention provides information on overweight and obesity (in English and Spanish)
US Department of Health and Human Services's program, Smallstep Kids, is an interactive site for children about healthy eating (in English and Spanish)
The International Obesity Taskforce has information on obesity and its prevention
The World Heart Federation's Global Prevention Alliance provides details of international efforts to halt the obesity epidemic and its associated chronic diseases
The Child Growth Foundation has information on childhood growth and its measurement
PMCID: PMC1876410  PMID: 17455989
3.  Early growth and coronary heart disease in later life: longitudinal study 
BMJ : British Medical Journal  2001;322(7292):949-953.
To determine how growth during infancy and childhood modifies the increased risk of coronary heart disease associated with small body size at birth.
Longitudinal study.
Helsinki, Finland.
4630 men who were born in the Helsinki University Hospital during 1934-44 and who attended child welfare clinics in the city. Each man had on average 18.0 (SD 9.5) measurements of height and weight between birth and age 12 years.
Main outcome measures
Hospital admission or death from coronary heart disease.
Low birth weight and low ponderal index (birth weight/length3) were associated with increased risk of coronary heart disease. Low height, weight, and body mass index (weight/height2) at age 1 year also increased the risk. Hazard ratios fell progressively from 1.83 (95% confidence interval 1.28 to 2.60) in men whose body mass index at age 1 year was below 16 kg/m2 to 1.00 in those whose body mass index was >19 (P for trend=0.0004). After age 1 year, rapid gain in weight and body mass index increased the risk of coronary heart disease. This effect was confined, however, to men with a ponderal index <26 at birth. In these men the hazard ratio associated with a one unit increase in standard deviation score for body mass index between ages 1 and 12 years was 1.27 (1.10 to 1.47; P=0.001).
Irrespective of size at birth, low weight gain during infancy is associated with increased risk of coronary heart disease. After age 1 year, rapid weight gain is associated with further increase in risk, but only among boys who were thin at birth. In these boys the adverse effects of rapid weight gain on later coronary heart disease are already apparent at age 3 years. Improvements in fetal, infant, and child growth could lead to substantial reductions in the incidence of coronary heart disease.
What is already known on this topicCoronary heart disease is associated with low birth weightOne study has shown that irrespective of size at birth, low weight gain in infancy is also associated with increased risk of the disease among menRapid weight gain after age 6 years is associated with further increase in riskWhat this study addsThe association with low weight gain in infancy is confirmedThe adverse effects of rapid childhood weight gain on risk of coronary heart disease are already apparent at age 3 years and occur only in boys who were thin at birth
PMCID: PMC31033  PMID: 11312225
4.  Pregnancy Weight Gain and Childhood Body Weight: A Within-Family Comparison 
PLoS Medicine  2013;10(10):e1001521.
David Ludwig and colleagues examine the within-family relationship between pregnancy weight gain and the offspring's childhood weight gain, thereby reducing the influence of genes and environment.
Please see later in the article for the Editors' Summary
Excessive pregnancy weight gain is associated with obesity in the offspring, but this relationship may be confounded by genetic and other shared influences. We aimed to examine the association of pregnancy weight gain with body mass index (BMI) in the offspring, using a within-family design to minimize confounding.
Methods and Findings
In this population-based cohort study, we matched records of all live births in Arkansas with state-mandated data on childhood BMI collected in public schools (from August 18, 2003 to June 2, 2011). The cohort included 42,133 women who had more than one singleton pregnancy and their 91,045 offspring. We examined how differences in weight gain that occurred during two or more pregnancies for each woman predicted her children's BMI and odds ratio (OR) of being overweight or obese (BMI≥85th percentile) at a mean age of 11.9 years, using a within-family design. For every additional kg of pregnancy weight gain, childhood BMI increased by 0.0220 (95% CI 0.0134–0.0306, p<0.0001) and the OR of overweight/obesity increased by 1.007 (CI 1.003–1.012, p = 0.0008). Variations in pregnancy weight gain accounted for a 0.43 kg/m2 difference in childhood BMI. After adjustment for birth weight, the association of pregnancy weight gain with childhood BMI was attenuated but remained statistically significant (0.0143 kg/m2 per kg of pregnancy weight gain, CI 0.0057–0.0229, p = 0.0007).
High pregnancy weight gain is associated with increased body weight of the offspring in childhood, and this effect is only partially mediated through higher birth weight. Translation of these findings to public health obesity prevention requires additional study.
Please see later in the article for the Editors' Summary
Editors' Summary
Childhood obesity has become a worldwide epidemic. For example, in the United States, the number of obese children has more than doubled in the past 30 years. 7% of American children aged 6–11 years were obese in 1980, compared to nearly 18% in 2010. Because of the rising levels of obesity, the current generation of children may have a shorter life span than their parents for the first time in 200 years.
Childhood obesity has both immediate and long-term effects on health. The initial problems are usually psychological. Obese children often experience discrimination, leading to low self-esteem and depression. Their physical health also suffers. They are more likely to be at risk of cardiovascular disease from high cholesterol and high blood pressure. They may also develop pre-diabetes or diabetes type II. In the long-term, obese children tend to become obese adults, putting them at risk of premature death from stroke, heart disease, or cancer.
There are many factors that lead to childhood obesity and they often act in combination. A major risk factor, especially for younger children, is having at least one obese parent. The challenge lies in unravelling the complex links between the genetic and environmental factors that are likely to be involved.
Why Was This Study Done?
Several studies have shown that a child's weight is influenced by his/her mother's weight before pregnancy and her weight gain during pregnancy. An obese mother, or a mother who puts on more pregnancy weight than average, is more likely to have an obese child.
One explanation for the effects of pregnancy weight gain is that the mother's overeating directly affects the baby's development. It may change the baby's brain and metabolism in such a way as to increase the child's long-term risk of obesity. Animal studies have confirmed that the offspring of overfed rats show these kinds of physiological changes. However, another possible explanation is that mother and baby share a similar genetic make-up and environment so that a child becomes obese from inheriting genetic risk factors, and growing up in a household where being overweight is the norm.
The studies in humans that have been carried out to date have not been able to distinguish between these explanations. Some have given conflicting results. The aim of this study was therefore to look for evidence of links between pregnancy weight gain and children's weight, using an approach that would separate the impact of genetic and environmental factors from a direct effect on the developing baby.
What Did the Researchers Do and Find?
The researchers examined data from the population of the US state of Arkansas recorded between 2003 and 2011. They looked at the health records of over 42,000 women who had given birth to more than one child during this period. This gave them information about how much weight the women had gained during each of their pregnancies. The researchers also looked at the school records of the children, over 91,000 in total, which included the children's body mass index (BMI, which factors in both height and weight). They analyzed the data to see if there was a link between the mothers' pregnancy weight gain and the child's BMI at around 12 years of age. Most importantly, they looked at these links within families, comparing children born to the same mother. The rationale for this approach was that these children would share a similar genetic make-up and would have grown up in similar environments. By taking genetics and environment into account in this manner, any remaining evidence of an impact of pregnancy weight gain on the children's BMI would have to be explained by other factors.
The results showed that the amount of weight each mother gained in pregnancy predicted her children's BMI and the likelihood of her children being overweight or obese. For every additional kg the mother gained during pregnancy, the children's BMI increased by 0.022. The children of mothers who put on the most weight had a BMI that was on average 0.43 higher than the children whose mothers had put on the least weight.
The study leaves some questions unanswered, including whether the mother's weight before pregnancy makes a difference to their children's BMI. The researchers were not able to obtain these measurements, nor the weight of the fathers. There may have also been other factors that weren't measured that might explain the links that were found.
What Do These Findings Mean?
This study shows that mothers who gain excessive weight during pregnancy increase the risk of their child becoming obese. This appears to be partly due to a direct effect on the developing baby.
These results represent a significant public health concern, even though the impact on an individual basis is relatively small. They could contribute to several hundred thousand cases of childhood obesity worldwide. Importantly, they also suggest that some cases could be prevented by measures to limit excessive weight gain during pregnancy. Such an approach could prove effective, as most mothers will not want to damage their child's health, and might therefore be highly motivated to change their behavior. However, because inadequate weight gain during pregnancy can also adversely affect the developing fetus, it will be essential for women to receive clear information about what constitutes optimal weight gain during pregnancy.
Additional Information
Please access these websites via the online version of this summary at
The US Centers for Disease Control and Prevention provide Childhood Obesity Facts
The UK National Health Service article “How much weight will I put on during my pregnancy?” provides information on pregnancy and weight gain and links to related resources
PMCID: PMC3794857  PMID: 24130460
5.  Follow-up Study of Physical Growth of Children Who Had Excessive Weight Gain in First Six Months of Life 
British Medical Journal  1970;2(5701):74-76.
The aim of this study was to determine whether excessive weight gain in the first six weeks, three months, or six months of life was correlated. with overweight and obesity at the age of 6 to 8 years. One hundred and thirty eight infants with excessive weight gain in the first six months of life, 53 children with slow weight gain, and 33 children with an average weight gain were re-examined at the age of 6, 7, or 8 years.
The mean height and weight of children who had gained weight rapidly in infancy were significantly higher than those of children who had gained weight slowly; those of infants whose weight gain had been average fell in between. The number of obese children in the rapid-weight-gain group was significantly higher than that of the combined average and slow-weight-gain groups. The rapidity of weight gain in infancy was a better guide to the risk of overweight in later childhood than the weight of the parents.
PMCID: PMC1699929  PMID: 5420235
6.  Is infant weight associated with childhood blood pressure? Analysis of the Promotion of Breastfeeding Intervention Trial (PROBIT) cohort 
Background Weight gain during infancy may programme later health outcomes, but examination of this hypothesis requires appropriate lifecourse methods and detailed weight gain measures during childhood. We examined associations between weight gain in infancy and early childhood and blood pressure at the age of 6.5 years in healthy children born at term.
Methods We carried out an observational analysis of data from a cluster-randomized breastfeeding promotion trial in Belarus. Of 17 046 infants enrolled between June 1996 and December 1997, 13 889 (81.5%) had systolic and diastolic blood pressure measured at 6.5 years; 10 495 children with complete data were analysed. A random-effects linear spline model with three knot points was used to estimate each individual's birthweight and weight gain from birth to 3 months, 3 months to 1 year and 1–5 years. Path analysis was used to separate direct effects from those mediated through subsequent weight gain.
Results In boys, after controlling for confounders and prior weight gain, the change in systolic blood pressure per z-score increase in weight gain was 0.09 mmHg [95% confidence interval (95% CI) −0.14 to 0.31] for birthweight; 0.41 mmHg (95% CI 0.19–0.64) for birth to 3 months; 0.69 mmHg (95% CI 0.47–0.92) for 3 months to 1 year and 0.82 mmHg (95% CI 0.58–1.06) for 1–5 years. Most of the associations between weight gain and blood pressure were mediated through weight at the age of 6.5 years. Findings for girls and diastolic blood pressure were similar.
Conclusions Children who gained weight faster than their peers, particularly at later ages, had higher blood pressure at the age of 6.5 years, with no association between birthweight and blood pressure.
PMCID: PMC3383097  PMID: 22039193
Birthweight; blood pressure; lifetime; multi-level model; path analysis; weight gain
7.  Describing differences in weight and length growth trajectories between white and Pakistani infants in the UK: analysis of the Born in Bradford birth cohort study using multilevel linear spline models 
Archives of Disease in Childhood  2013;98(4):274-279.
To describe the growth pattern from birth to 2 years of UK-born white British and Pakistani infants.
Birth cohort.
Bradford, UK.
314 white British boys, 383 Pakistani boys, 328 white British girls and 409 Pakistani girls.
Main outcome measures
Weight and length trajectories based on repeat measurements from birth to 2 years.
Linear spline multilevel models for weight and length with knot points at 4 and 9 months fitted the data well. At birth Pakistani boys were 210 g lighter (95% CI −290 to −120) and 0.5 cm shorter (−1.04 to 0.02) and Pakistani girls were 180 g lighter (−260 to −100) and 0.5 cm shorter (−0.91 to −0.03) than white British boys and girls, respectively. Pakistani infants gained length faster than white British infants between 0 and 4 months (+0.3 cm/month (0.1 to 0.5) for boys and +0.4 cm/month (0.2 to 0.6) for girls) and gained more weight per month between 9 and 24 months (+10 g/month (0 to 30) for boys and +30 g/month (20 to 40) for girls). Adjustment for maternal height attenuated ethnic differences in weight and length at birth, but not in postnatal growth. Adjustment for other confounders did not explain differences in any outcomes.
Pakistani infants were lighter and had shorter predicted mean length at birth than white British infants, but gained weight and length quicker in infancy. By age 2 years both ethnic groups had similar weight, but Pakistani infants were on average taller than white British infants.
PMCID: PMC3858016  PMID: 23418036
Growth; Ethnicity; Child; Born in Bradford; Multilevel Models
8.  Preterm infant linear growth and adiposity gain: tradeoffs for later weight status, and IQ 
The Journal of pediatrics  2013;163(6):10.1016/j.jpeds.2013.06.032.
Among preterm infants, to examine tradeoffs between cognitive outcome and overweight/obesity at school age and in young adulthood in relation to infancy weight gain and linear growth.
Study design
We studied 945 participants in the Infant Health and Development Program, an 8-center study of preterm (≤37 weeks), low birth weight (≤2500 grams) infants from birth to 18 years. Adjusting for maternal and child factors in logistic regression, we estimated the odds of overweight/obesity (BMI ≥85th percentile at age 8 or ≥25 kg/m2 at age 18) and in separate models, low IQ (<85) per z-score change in infant length and BMI from term to 4 months, 4-12 months, and 12-18 months.
More rapid linear growth from term to 4 months was associated with lower odds of IQ<85 at age 8 (OR 0.82, 95% CI 0.70, 0.96), but a higher odds of overweight/obesity (OR 1.27, 95% CI 1.05, 1.53). More rapid BMI gain in all 3 infant time intervals was also associated with a higher odds of overweight/obesity, and from 4-12 months with a lower odds of IQ <85 at age 8. Results at age 18 were similar.
In preterm, low birth weight infants born in the 1980’s, faster linear growth soon after term was associated with better cognition but also with a higher risk of overweight/obesity at 8 and 18 years of age. BMI gain over the entire 18 months after term was associated with later risk of overweight/obesity, with less evidence for a benefit to IQ.
PMCID: PMC3834090  PMID: 23910982
9.  Adipose and Height Growth Through Childhood and Blood Pressure Status in a Large Prospective Cohort Study 
Hypertension  2012;59(5):919-925.
Raised blood pressure (BP) is the world’s leading mortality risk factor. Childhood BP substantially predicts adult levels, and although both prenatal and postnatal growth influence it, their relative importance is debated. In a longitudinal study (Avon Longitudinal Study of Parents and Children) of 12 962 healthy children, we aimed to assess the relative contribution of different growth periods and of standardized measures of height versus weight-for-height (an adiposity marker) to BP at age 10 years. Conditional growth modeling was used in the 3230 boys and 3346 girls with BP measurements. Systolic BP was inversely associated with birth weight and weight-for-height but not length (−0.33, −0.27, and −0.12 mm Hg · SD−1; P=0.003, 0.035, and 0.35, respectively). In infancy, weight, weight-for-height, and height gains were all positively associated with systolic BP (0.90, 0.41, and 0.82 mm Hg · SD−1, respectively; all P<0.001). After infancy, all of the growth modalities were positively associated with systolic BP (weight, 1.91; weight-for-height, 1.56; height, 1.20 mm Hg · SD−1; all P<0.001). Similar but weaker associations were found with diastolic BP. Although BP at 10 years was associated with both prenatal and early postnatal growth, their influence was small compared with that of later growth. Because BP ranking relative to the population is substantially determined in the first decade of life, a focus on strategies to reduce the development of adiposity from infancy onward, rather than an emphasis on the nutrition and weight of mothers and infants, should bring greater reductions in population BP.
PMCID: PMC3428923  PMID: 22493074
blood pressure; childhood growth; hypertension; obesity; population
10.  Associations between Infant Feeding Practice Prior to Six Months and Body Mass Index at Six Years of Age 
Nutrients  2014;6(4):1608-1617.
Rapid growth during infancy is associated with increased risk of overweight and obesity and differences in weight gain are at least partly explained by means of infant feeding. The aim was to assess the associations between infant feeding practice in early infancy and body mass index (BMI) at 6 years of age. Icelandic infants (n = 154) were prospectively followed from birth to 12 months and again at age 6 years. Birth weight and length were gathered from maternity wards, and healthcare centers provided the measurements made during infancy up to 18 months of age. Information on breastfeeding practices was documented 0–12 months and a 24-h dietary record was collected at 5 months. Changes in infant weight gain were calculated from birth to 18 months. Linear regression analyses were performed to examine associations between infant feeding practice at 5 months and body mass index (BMI) at 6 years. Infants who were formula-fed at 5 months of age grew faster, particularly between 2 and 6 months, compared to exclusively breastfed infants. At age 6 years, BMI was on average 1.1 kg/m2 (95% CI 0.2, 2.0) higher among infants who were formula fed and also receiving solid foods at 5 months of age compared to those exclusively breastfed. In a high-income country such as Iceland, early introduction of solid foods seems to further increase the risk of high childhood BMI among formula fed infants compared with exclusively breastfed infants, although further studies with greater power are needed.
PMCID: PMC4011054  PMID: 24747694
MeSH terms; growth; infant; breastfeeding; weaning; overweight; child
11.  Associations of postnatal weight and length/height gain with wheeze, asthma and atopy: The PROBIT Study 
It has been hypothesised that postnatal weight and length/height gain are variously related to wheeze, asthma and atopy, however supporting evidence is limited and inconsistent.
Weights and lengths/heights of 12,171 term-infants were measured from birth to 12 months and at 6.5 years, and extracted from polyclinic records prospectively obtained between 12 and 60 months. Atopic phenotypes were ascertained at 6.5 years with the International Study of Asthma and Allergy in Childhood questionnaire and skin-prick tests. Logistic regression models investigated whether rates of weight and length/height gain from infancy to mid-childhood were associated with atopy phenotypes that have occurred ever or in the last 12 months.
After controlling for confounders and prior weight and length/height gain, all weight gain variables except birthweight were positively associated with ever having wheezed (p<0.1). A one SD increase in weight gain rate between 0–3 months was associated with a 12% increase (2%–23%) in allergic rhinitis ever. No other consistent patterns of association were found for weight gain or length/height gain rate between 0–60 months with atopic outcomes at 6.5 years. In contrast, all atopy outcomes except for ever having asthma were associated with current weight and height, even after controlling for prior growth.
Current height and weight are more strongly associated with the development of atopic phenotypes in childhood than patterns of infant and early childhood growth, which may well reflect reverse causality (atopy effects on growth) or residual confounding by an unknown common cause of growth and atopy.
PMCID: PMC3711479  PMID: 23374010
wheeze; asthma; atopy; postnatal growth; weight gain; length gain
12.  Relationship of weight gain in infancy to subcutaneous fat and relative weight at 10 1/2 years of age. 
In a representative sample of 895 schoolchildren, aged between 9 years 10 months and 11 years 2 months, the risk of being overweight or obese was compared between those who had gained weight rapidly during infancy and those whose weight gain had been normal. A substantially increased risk ratio was found only in boys for whom a correlation analysis showed that the total weight gain during the first year of life was associated with the total body mass in relation to height, more or less independently of the degree of fatness at 10 1/2 years of age. In girls, a direct but very weak association was found between weight gain in infancy and the degree of fatness at 10 1/2 years. The implications of these findings with respect to aetiology and the possibilities of prevention are briefly discussed.
PMCID: PMC478973  PMID: 1009275
13.  Birth weight and growth from infancy to late adolescence in relation to fat and lean mass in early old age: findings from the MRC National Survey of Health and Development 
High birth weight and greater weight gain in infancy have been associated with increased risk of obesity as assessed using body mass index, but few studies have examined associations with direct measures of fat and lean mass. This study examined associations of birth weight and weight and height gain in infancy, childhood and adolescence with fat and lean mass in early old age.
A total of 746 men and 812 women in England, Scotland and Wales from the MRC National Survey of Health and Development whose heights and weights had been prospectively ascertained across childhood and adolescence and who had dual energy X-ray absorptiometry measures at age 60–64 years.
Associations of birth weight and standardised weight and height (0–2 (weight only), 2–4, 4–7, 7–11, 11–15, 15–20 years) gain velocities with outcome measures were examined.
Higher birth weight was associated with higher lean mass and lower android/gynoid ratio at age 60–64 years. For example, the mean difference in lean mass per 1 standard deviation increase in birth weight was 1.54 kg in males (95% confidence interval=1.04, 2.03) and 0.78 kg in females (0.41, 1.14). Greater weight gain in infancy was associated with higher lean mass, whereas greater gains in weight in later childhood and adolescence were associated with higher fat and lean mass, and fat/lean and android/gynoid ratios. Across growth intervals greater height gain was associated with higher lean but not fat mass, and with lower fat/lean and android/gynoid ratios.
Findings suggest that growth in early life may have lasting effects on fat and lean mass. Greater weight gain before birth and in infancy may be beneficial by leading to higher lean mass, whereas greater weight gain in later childhood and adolescence may be detrimental by leading to higher fat/lean and android/gynoid ratios.
PMCID: PMC3884138  PMID: 23779050
abdominal obesity; growth; birth weight; body composition; muscle mass
14.  Leisure Time Physical Activity of Moderate to Vigorous Intensity and Mortality: A Large Pooled Cohort Analysis 
PLoS Medicine  2012;9(11):e1001335.
Analyzing data from over 650,000 individuals, Dr. Steven Moore and colleagues report that greater amounts of leisure-time physical activity were associated with higher life expectancy across a wide range of activity levels and body mass index groups.
Leisure time physical activity reduces the risk of premature mortality, but the years of life expectancy gained at different levels remains unclear. Our objective was to determine the years of life gained after age 40 associated with various levels of physical activity, both overall and according to body mass index (BMI) groups, in a large pooled analysis.
Methods and Findings
We examined the association of leisure time physical activity with mortality during follow-up in pooled data from six prospective cohort studies in the National Cancer Institute Cohort Consortium, comprising 654,827 individuals, 21–90 y of age. Physical activity was categorized by metabolic equivalent hours per week (MET-h/wk). Life expectancies and years of life gained/lost were calculated using direct adjusted survival curves (for participants 40+ years of age), with 95% confidence intervals (CIs) derived by bootstrap. The study includes a median 10 y of follow-up and 82,465 deaths. A physical activity level of 0.1–3.74 MET-h/wk, equivalent to brisk walking for up to 75 min/wk, was associated with a gain of 1.8 (95% CI: 1.6–2.0) y in life expectancy relative to no leisure time activity (0 MET-h/wk). Higher levels of physical activity were associated with greater gains in life expectancy, with a gain of 4.5 (95% CI: 4.3–4.7) y at the highest level (22.5+ MET-h/wk, equivalent to brisk walking for 450+ min/wk). Substantial gains were also observed in each BMI group. In joint analyses, being active (7.5+ MET-h/wk) and normal weight (BMI 18.5–24.9) was associated with a gain of 7.2 (95% CI: 6.5–7.9) y of life compared to being inactive (0 MET-h/wk) and obese (BMI 35.0+). A limitation was that physical activity and BMI were ascertained by self report.
More leisure time physical activity was associated with longer life expectancy across a range of activity levels and BMI groups.
Please see later in the article for the Editors' Summary
Editors' Summary
Regular physical activity is essential for human health. It helps to maintain a healthy body weight and prevents or delays heart disease, type 2 diabetes, and some cancers. It also makes people feel better and increases life expectancy. The World Health Organization (WHO) currently recommends that adults do at least 150 minutes of moderate- to vigorous-intensity physical activity every week. Moderate-intensity physical activities (for example, brisk walking and gardening) require a moderate amount of effort and noticeably increase the heart rate; vigorous-intensity physical activities (for example, running or fast swimming) require a large amount of effort and cause rapid breathing and a substantial heart rate increase. Worryingly, people in both developed and developing countries are becoming increasingly physically inactive. People are sitting at desks all day instead of doing manual labor; they are driving to work in cars instead of walking or cycling; and they are participating in fewer leisure time physical activities.
Why Was This Study Done?
Although various studies suggest that physical activity increases life expectancy, few have quantified the years of life gained at distinct levels of physical activity. Moreover, the difference in life expectancy between active, overweight individuals and inactive, normal weight individuals has not been quantified. Thus, it is hard to develop a simple public health message to maximize the population benefits of physical activity. In this pooled prospective cohort analysis, the researchers determine the association between levels of leisure time physical activities, such as recreational walking, and years of life gained after age 40, both overall and within body mass index (BMI) groups. A pooled prospective cohort analysis analyzes the combined data from multiple studies that have followed groups of people to investigate associations between baseline characteristics and outcomes such as death. BMI is a ratio of weight to height, calculated by dividing a person's weight by their height squared; normal weight is defined as a BMI of 18.5–24.9 kg/m2, obesity (excessive body fat) is defined as a BMI of more than 30 kg/m2.
What Did the Researchers Do and Find?
The researchers pooled self-reported data on leisure time physical activities and BMIs from nearly 650,000 individuals over the age of 40 years enrolled in one Swedish and five US prospective cohort studies, most of which were investigating associations between lifestyle factors and disease risk. They used these and other data to calculate the gain in life expectancy associated with specific levels of physical activity. A physical activity level equivalent to brisk walking for up to 75 minutes per week was associated with a gain of 1.8 years in life expectancy relative to no leisure time activity. Being active—having a physical activity level at or above the WHO-recommended minimum of 150 minutes of brisk walking per week—was associated with an overall gain of life expectancy of 3.4–4.5 years. Gains in life expectancy were seen also for black individuals and former smokers, groups for whom relatively few data had been previously available. The physical activity and life expectancy association was also evident at all BMI levels. Being active and normal weight was associated with a gain of 7.2 years of life compared to being inactive and class II+ obese (having a BMI of more than 35.0 kg/m2). However, being inactive but normal weight was associated with 3.1 fewer years of life compared to being active but class I obese (having a BMI of 30–34.9 kg/m2).
What Do These Findings Mean?
These findings suggest that participation in leisure time physical activity, even below the recommended level, is associated with a reduced risk of mortality compared to participation in no leisure time physical activity. This result may help convince currently inactive people that a modest physical activity program may have health benefits, even if it does not result in weight loss. The findings also suggest that physical activity at recommended levels or higher may increase longevity further, and that a lack of leisure time physical activity may markedly reduce life expectancy when combined with obesity. Although the accuracy and generalizability of these findings may be limited by certain aspects of the study's design (for example, some study participants may have overestimated their leisure time physical activity), these findings reinforce the public health message that both a physically active lifestyle and a normal body weight are important for increasing longevity.
Additional Information
Please access these websites via the online version of this summary at
The World Health Organization provides information about physical activity and health (in several languages); its 2010 Global Recommendations on Physical Activity for Health is available in several languages
The US Centers for Disease Control and Prevention provides information on physical activity for different age groups; its Physical Activity for Everyone webpages include guidelines, instructional videos, and personal success stories
The UK National Health Service information source NHS Choices also explains the benefits of regular physical activity and includes physical activity guidelines, tips for exercising, and some personal stories
MedlinePlus has links to other resources about exercise and physical fitness (in English and Spanish)
PMCID: PMC3491006  PMID: 23139642
15.  Associations of Intrauterine and Postnatal Weight and Length Gains With Adolescent Body Composition: Prospective Birth Cohort Study From Brazil 
The Journal of Adolescent Health  2012;51(6):S58-S64.
Early growth patterns have been associated with subsequent obesity risk. However, findings from middle-income populations suggest that early infant growth may benefit lean mass and height rather than adiposity. We tested the hypothesis that rapid weight or length gain in different growth periods would be associated with size and body composition in adolescence, in a prospective birth cohort from southern Brazil.
Body composition was assessed in 425 adolescents (52.2% male) at 14 years. Exposures were birth weight z-score and conditional growth in weight or length for the periods 0–6, 6–12 and 12–48 months. Differences in anthropometric and body composition outcomes between tertiles of growth in each period were tested by one-way analysis of variance.
Size at birth and conditional weight and length at 6 months were associated with later height. The effect of infant weight gain on lean mass was greater for males than females, and effect on fat mass greater for females than males. By early childhood, rapid weight gain generated relatively similar effects on both tissue masses in both sexes. Rapid length gain had stronger effects on outcomes in males than females at each time point, and benefited lean mass more than adiposity. All effects were substantially attenuated after adjusting for current height. Early weight gain was more important than length gain at influencing body composition outcomes in adolescence.
Rapid infant weight and length gains were primarily associated with larger size in adolescence rather than increased adiposity. From one year onwards, associations between rapid weight gain and fat and lean masses remained after adjustment for height.
PMCID: PMC3508414  PMID: 23283163
Body composition; Growth; Obesity; Nutritional programming
16.  Birth Weight, Early Weight Gain and Pubertal Maturation: a Longitudinal Study 
Pediatric Obesity  2012;7(2):101-109.
To investigate the effect of birth weight and early weight gain on the timing of various measures of puberty in both girls and boys.
A total of 856 newborns enrolled in the North Carolina Infant Feeding Study were followed to age 5 years, with 600 children followed up at adolescence. Birth weight was obtained from medical records and children were weighed at study visits until age 5 years; gains in standardized weights were calculated over four early age intervals: 0–6 months, 6–12 months, 1–2 years, and 2–5 years. Age at menarche in girls and age at advanced Tanner stages in both girls and boys were reported by adolescents and their parents. Survival models were used to analyze the effects of birth weight and early weight gain on these outcomes.
Girls with higher birth weight and greater weight gains during the four early age intervals were younger when they reached menarche and advanced Tanner stages; boys with greater early weight gains also were younger when they reached advanced Tanner stages, but few of these effects were statistically significant.
Higher birth weights and greater weight gains during infancy and early childhood can lead to earlier sexual maturation in girls.
PMCID: PMC3313082  PMID: 22434749
Age at menarche; Birth weight; Puberty; Tanner stage; Weight gain
17.  Adiposity, insulin resistance and cardiovascular risk factors in 9–10-year-old Indian children: relationships with birth size and postnatal growth 
Lower birthweight, and rapid childhood weight gain predict elevated cardiovascular risk factors in children. We examined associations between serial, detailed, anthropometric measurements from birth to 9.5 years of age and cardiovascular risk markers in Indian children. Children (n = 663) born at the Holdsworth Memorial Hospital, Mysore, India were measured at birth and 6–12 monthly thereafter. At 9.5 years, 539 (255 boys) underwent a 2-h oral glucose tolerance test, and blood pressure (BP) and fasting lipid concentrations were measured. Insulin resistance was calculated using the HOMA equation. These outcomes were examined in relation to birth measurements and changes in measurements (growth) during infancy (0–2 years), 2–5 years and 5–9.5 years using conditional s.d. scores. Larger current weight, height and skinfold thickness were associated with higher risk markers at 9.5 years (P<0.05). Lower weight, smaller length and mid-arm circumference at birth were associated with higher fasting glucose concentrations at 9.5 years (P≤0.01). After adjusting for current weight/height, there were inverse associations between birthweight and/or length and insulin concentrations, HOMA, systolic and diastolic BP and plasma triglycerides (P<0.05). Increases in conditional weight and height between 0–2, 2–5 and 5–9.5 years were associated with higher insulin concentrations, HOMA and systolic BP. In conclusion, in 9–10-year-old Indian children, as in other studies, cardiovascular risk factors were highest in children who were light or short at birth but heavy or tall at 9 years. Greater infant and childhood weight and height gain were associated with higher risk markers.
PMCID: PMC3272429  PMID: 22318657
birthweight; infancy; insulin resistance; postnatal growth
18.  Determinants of rapid weight gain during infancy: baseline results from the NOURISH randomised controlled trial 
BMC Pediatrics  2011;11:99.
Rapid weight gain in infancy is an important predictor of obesity in later childhood. Our aim was to determine which modifiable variables are associated with rapid weight gain in early life.
Subjects were healthy infants enrolled in NOURISH, a randomised, controlled trial evaluating an intervention to promote positive early feeding practices. This analysis used the birth and baseline data for NOURISH. Birthweight was collected from hospital records and infants were also weighed at baseline assessment when they were aged 4-7 months and before randomisation. Infant feeding practices and demographic variables were collected from the mother using a self administered questionnaire. Rapid weight gain was defined as an increase in weight-for-age Z-score (using WHO standards) above 0.67 SD from birth to baseline assessment, which is interpreted clinically as crossing centile lines on a growth chart. Variables associated with rapid weight gain were evaluated using a multivariable logistic regression model.
Complete data were available for 612 infants (88% of the total sample recruited) with a mean (SD) age of 4.3 (1.0) months at baseline assessment. After adjusting for mother's age, smoking in pregnancy, BMI, and education and infant birthweight, age, gender and introduction of solid foods, the only two modifiable factors associated with rapid weight gain to attain statistical significance were formula feeding [OR = 1.72 (95%CI 1.01-2.94), P = 0.047] and feeding on schedule [OR = 2.29 (95%CI 1.14-4.61), P = 0.020]. Male gender and lower birthweight were non-modifiable factors associated with rapid weight gain.
This analysis supports the contention that there is an association between formula feeding, feeding to schedule and weight gain in the first months of life. Mechanisms may include the actual content of formula milk (e.g. higher protein intake) or differences in feeding styles, such as feeding to schedule, which increase the risk of overfeeding.
Trial Registration
Australian Clinical Trials Registry ACTRN12608000056392
PMCID: PMC3226648  PMID: 22054415
19.  Rapid weight gain in early infancy is associated with adult body fat percentage in young women 
Although rapid childhood weight gain has been suggested to be a risk factor for lifetime obesity and other chronic diseases, few studies have been conducted in Asian populations. The aim of this study was, therefore, to ascertain whether rapid childhood weight gain is associated with indices of obesity in adulthood and, if so, which period in early development provides the greatest predictive value of future obesity in young Japanese women.
A total of 86 female university students aged 18–21 years old participated in this study. Current height, weight, body fat percentage (BFP) as evaluated by bioelectrical impedance analysis, and BMI were measured. Body weight at birth, 3 and 6 months, and 1.5 and 3 years of age was obtained from the maternity record book (Boshi-techo), and body weight at 6 years was obtained from school health records. We assessed infant weight gain by the weight change Z-score.
Current BFP was found to be significantly correlated with weight change between 0 and 3 months (r = 0.26, P = 0.034) and between 3 and 6 months of age (r = −0.28, P = 0.031). However, none of the physical activity indices correlated with BMI and BFP.
Rapid weight gain in early infancy positively associates with BFP in young Japanese women.
PMCID: PMC2955903  PMID: 21432570
Body fat; Japanese; Infants; Rapid weight gain; Young women
20.  Adult Metabolic Syndrome and Impaired Glucose Tolerance Are Associated With Different Patterns of BMI Gain During Infancy 
Diabetes Care  2008;31(12):2349-2356.
OBJECTIVE—The purpose of this study was to describe patterns of infant, childhood, and adolescent BMI and weight associated with adult metabolic risk factors for cardiovascular disease.
RESEARCH DESIGN AND METHODS—We measured waist circumference, blood pressure, glucose, insulin and lipid concentrations, and the prevalence of metabolic syndrome (National Cholesterol Education Program Adult Treatment Panel III definition) in 1,492 men and women aged 26–32 years in Delhi, India, whose weight and height were recorded every 6 months throughout infancy (0–2 years), childhood (2–11 years), and adolescence (11 years–adult).
RESULTS—Men and women with metabolic syndrome (29% overall), any of its component features, or higher (greater than upper quartile) insulin resistance (homeostasis model assessment) had more rapid BMI or weight gain than the rest of the cohort throughout infancy, childhood, and adolescence. Glucose intolerance (impaired glucose tolerance or diabetes) was, like metabolic syndrome, associated with rapid BMI gain in childhood and adolescence but with lower BMI in infancy.
CONCLUSIONS—In this Indian population, patterns of infant BMI and weight gain differed for individuals who developed metabolic syndrome (rapid gain) compared with those who developed glucose intolerance (low infant BMI). Rapid BMI gain during childhood and adolescence was a risk factor for both disorders.
PMCID: PMC2584194  PMID: 18835958
21.  Longitudinal Analyses of Childhood Growth: Evidence From Project Koshu 
Journal of Epidemiology  2015;25(1):2-7.
Recently, it has been suggested that fetal and infant environments are associated with childhood and adulthood health status, specifically regarding presence of obesity and chronic diseases. This concept is known as the “Developmental Origins of Health and Disease (DOHaD) hypothesis.” Thus, it is necessary to collect information about the fetal and infancy periods in order to examine the association between fetal and infancy exposures and later growth. Based on the DOHaD hypothesis, childhood growth trajectories, which were described by multilevel analysis, might be important in examining the effects of early-life environment on later-life health. The author and colleagues examined the association between maternal smoking during pregnancy and fetal/childhood growth, specifically risk of childhood obesity, by using the dataset from an ongoing prospective cohort study called “Project Koshu,” which enrolled pregnant women and their children from a rural area of Japan. Children born to smoking mothers were likely to have lower birth weights and, thereafter, to show an increase in body mass index compared to children of non-smoking mothers. Differences in pubertal growth patterns by gender and childhood weight status were then examined. Growth rate and height gain trajectories were similar between genders, although pubertal growth spurts were observed earlier in girls than in boys. The overweight/obese children grew faster than did the non-overweight children in the early pubertal stages, and the non-overweight children caught up and showed greater height gains at older ages. Because Project Koshu is ongoing, further studies examining new research questions will be conducted with larger sample sizes.
PMCID: PMC4275431
smoking; pregnancy; fetal growth; childhood growth; multilevel analysis
22.  Socioeconomic status and weight gain in early infancy 
The association between low socioeconomic status (SES) and childhood obesity foreshadows life-long inequalities in health. Insight into the causal mechanisms linking childhood adversity to long-term health could be provided by discovering when the negative SES gradient in weight emerges, and what early life experiences are associated with it.
To examine SES differences in infant weight gain in the first three months of life, and assess contributions of parental BMI, maternal smoking, and feeding method to this association.
Observational study using longitudinal weight data from 2402 families taking part in the Gemini study; a twin birth cohort recruited from all twin births between March and December 2007 in England and Wales.
Outcome Measures
Infant weights at birth and three months converted to standard deviation scores (SDS), change in weight SDS, and rapid growth. SES was indexed by occupation and maternal education.
There were no SES differences in birth weight, but lower SES was associated with higher three-month weight, greater change in weight, and a higher prevalence of rapid growth (all p<0.01); with graded associations across levels of SES. Including parental overweight or smoking in pregnancy in the regression model did not affect the association between SES and weight gain, but including feeding method attenuated the SES effect on weight gain by at least 62% and rendered it non-significant.
The foundations for lifelong socioeconomic inequalities in obesity risk may be laid in early infancy, with infant feeding practices playing a part in the diverging weight trajectories.
PMCID: PMC3145137  PMID: 21540830
Socioeconomic status; Obesity; Birth cohort; Weight Gain; Infancy; breastfeeding
23.  Relation of birth weight and childhood respiratory infection to adult lung function and death from chronic obstructive airways disease. 
BMJ : British Medical Journal  1991;303(6804):671-675.
OBJECTIVE--To examine whether birth weight, infant weight, and childhood respiratory infection are associated with adult lung function and death from chronic obstructive airways disease. DESIGN--Follow up study of men born during 1911-30 whose birth weights, weights at 1 year, and childhood illnesses were recorded at the time by health visitors. SETTING--Hertfordshire, England. SUBJECTS--5718 men born in the county during 1911-30 and a subgroup of 825 men born in the county during 1920-30 and still living there. MAIN OUTCOME MEASURES--Death from chronic obstructive airways disease, mean forced expiratory volume in one second (FEV1) and forced vital capacity (FVC), and respiratory symptoms. RESULTS--55 men died of chronic obstructive airways disease. Death rates fell with increasing birth weight and weight at 1 year. Mean FEV1 at age 59 to 70 years, adjusted for height and age, rose by 0.06 litre (95% confidence interval 0.02 to 0.09) with each pound (450 g) increase in birth weight, independently of smoking habit and social class. Bronchitis or pneumonia in infancy was associated with a 0.17 litre (0.02 to 0.32) reduction in adult FEV1 and with an increased odds ratio of wheezing and persistent sputum production in adult life independently of birth weight, smoking habit, and social class. Whooping cough in infancy was associated with a 0.22 litre (0.02 to 0.42) reduction in adult FEV1. CONCLUSIONS--Lower birth weight was associated with worse adult lung function. Intrauterine influences which retard fetal weight gain may irrecoverably constrain the growth of the airways. Bronchitis, pneumonia, or whooping cough in infancy further reduced adult lung function. They also retarded infant weight gain. Consistent with this, death from chronic obstructive airways disease in adult life was associated with lower birth weight and weight at 1 year. Promoting lung growth in fetuses and infants and reducing the incidence of lower respiratory tract infection in infancy may reduce the incidence of chronic obstructive airways disease in the next generation.
PMCID: PMC1670943  PMID: 1912913
24.  Change in the Body Mass Index Distribution for Women: Analysis of Surveys from 37 Low- and Middle-Income Countries 
PLoS Medicine  2013;10(1):e1001367.
Using cross-sectional surveys, Fahad Razak and colleagues investigate how the BMI (body mass index) distribution is changing for women in low- and middle-income countries.
There are well-documented global increases in mean body mass index (BMI) and prevalence of overweight (BMI≥25.0 kg/m2) and obese (BMI≥30.0 kg/m2). Previous analyses, however, have failed to report whether this weight gain is shared equally across the population. We examined the change in BMI across all segments of the BMI distribution in a wide range of countries, and assessed whether the BMI distribution is changing between cross-sectional surveys conducted at different time points.
Methods and Findings
We used nationally representative surveys of women between 1991–2008, in 37 low- and middle-income countries from the Demographic Health Surveys ([DHS] n = 732,784). There were a total of 96 country-survey cycles, and the number of survey cycles per country varied between two (21/37) and five (1/37). Using multilevel regression models, between countries and within countries over survey cycles, the change in mean BMI was used to predict the standard deviation of BMI, the prevalence of underweight, overweight, and obese. Changes in median BMI were used to predict the 5th and 95th percentile of the BMI distribution. Quantile-quantile plots were used to examine the change in the BMI distribution between surveys conducted at different times within countries. At the population level, increasing mean BMI is related to increasing standard deviation of BMI, with the BMI at the 95th percentile rising at approximately 2.5 times the rate of the 5th percentile. Similarly, there is an approximately 60% excess increase in prevalence of overweight and 40% excess in obese, relative to the decline in prevalence of underweight. Quantile-quantile plots demonstrate a consistent pattern of unequal weight gain across percentiles of the BMI distribution as mean BMI increases, with increased weight gain at high percentiles of the BMI distribution and little change at low percentiles. Major limitations of these results are that repeated population surveys cannot examine weight gain within an individual over time, most of the countries only had data from two surveys and the study sample only contains women in low- and middle-income countries, potentially limiting generalizability of findings.
Mean changes in BMI, or in single parameters such as percent overweight, do not capture the divergence in the degree of weight gain occurring between BMI at low and high percentiles. Population weight gain is occurring disproportionately among groups with already high baseline BMI levels. Studies that characterize population change should examine patterns of change across the entire distribution and not just average trends or single parameters.
Please see later in the article for the Editors' Summary
Editors' Summary
The number of obese people (individuals who have an excessive amount of body fat) is rapidly increasing in many countries. Globally, there were about 200 million obese adults in 1995; by 2010, 475 million adults were obese and another billion were classified as overweight. Obesity is defined as having a body mass index (BMI, an indicator of body fat calculated by dividing a person's weight in kilograms by their height in meters squared) of more than 30.0 kg/m2. Compared to people with a healthy weight (a BMI between 18.5 and 24.9 kg/m2), obese individuals and overweight individuals (who have a BMI between 25.0 and 29.9 kg/m2) have an increased risk of developing diabetes, heart disease and stroke, and tend to die younger. At the same time in many developing countries substantial numbers of people are underweight (BMI <18.5 kg/m2) or have chronic energy deficiency (BMI <16.0 kg/m2) and are at risk of increased risk of dying due to infectious disease or respiratory problems.
Why Was This Study Done?
The global obesity epidemic is usually described in terms of increases in the average BMI or in the prevalence of obesity (the proportion of the population whose BMI is above 30.0 kg/m2). Such descriptions assume that the BMIs of fat and thin people are increasing at the same rate and that the shape of the population's BMI distribution curve remains constant. However, as average BMI and the prevalence of obesity can increase it is unclear how the prevalence of underweight changes. This is potentially important for the health of the population because underweight individuals, like obese individuals, tend to die younger than healthy weight individuals, particularly in low-income countries. In this study, the researchers use repeated cross-sectional survey data collected from low- and middle-income countries in the Demographic and Health Surveys (DHS) to examine changes in BMI in women across the BMI distribution between 1991 and 2008. Repeated cross-sectional surveys collect data from a population at multiple time points from different individuals drawn from the same population, DHS are a data collection and surveillance project that help developing countries track health and population trends.
What Did the Researchers Do and Find?
The researchers used statistical models to analyze data from DHS surveys of more than 730,000 women living in 37 low- and middle-income countries (two to five surveys per country). Increasing average BMI was associated with an increase in the standard deviation of BMI (a measure of the dispersion of BMI in the population) both across and within countries over time. With increasing average BMI, the BMI at both the 5th and 95th percentile increased; 90% of the BMIs in a population lie between these percentiles so these BMI values indicate the spread of the BMI distribution. However, the BMI at the 95th percentile increased about 2.5 times faster than the BMI at the 5th percentile. Moreover, with increasing average BMI, the prevalence of overweight and obesity increased faster than the decline in the prevalence of underweight. Finally, quantile-quantile plots for each country (a graphical method that compares two distributions) revealed a consistent pattern of unequal weight gain across the BMI distribution as average BMI increased, with pronounced weight gains at the obese end of the distribution and little change at the underweight end.
What Do These Findings Mean?
These findings show that increases in average BMI are associated with an increased spread of BMI across and within populations. Consequently, changes in average BMI or single measurements such as the prevalence of overweight do not capture the divergence in the degree of weight gain occurring between that part of the population that has a low BMI and that part that has a high BMI. In other words, at least for the low- and middle-income countries included in this study, population weight gain is occurring disproportionately among groups with high baseline BMI levels. The researchers suggest, therefore, that the characterization of the BMI of populations over time should examine the patterns of change across the whole BMI distribution. Moreover, rather than a single broad population strategy for weight control, optimum health outcomes, they suggest, might be achieved by a strategy that includes targeted interventions to reduce weight in high BMI segments of the population and to increase weight in low BMI segments.
Additional Information
Please access these Web sites via the online version of this summary at
The US Centers for Disease Control and Prevention provides information on all aspects of overweight and obesity (in English and Spanish)
The World Health Organization provides information on obesity (in several languages); Malri's story describes the health risks faced by an obese child
The UK National Health Service Choices website also provides detailed information about obesity and a link to a personal story about losing weight
The International Obesity Taskforce provides information about the global obesity epidemic
The US Department of Agriculture's website provides a personal healthy eating plan; the Weight-control Information Network is an information service provided for the general public and health professionals by the US National Institute of Diabetes and Digestive and Kidney Diseases (in English and Spanish)
MedlinePlus has links to further information about obesity (in English and Spanish)
PMCID: PMC3545870  PMID: 23335861
25.  Weight gain in infancy and early childhood is associated with school age body mass index but not intelligence and blood pressure in very low birth weight children 
Rates of weight gain in infancy and early childhood can influence later neurocognitive, metabolic, and cardiovascular health. We studied the relationship of weight gain during infancy and early childhood to intelligence quotient (IQ), blood pressure (BP), and body mass index (BMI) at age 9 in children born with very low birth weight (VLBW). Sixty-five children born prematurely with VLBW were followed longitudinally and at 9 years IQ, BP, and BMI were measured. The mean weight z scores at birth, neonatal intensive care discharge, 1 year corrected for prematurity, 5, and 9 years were −0.17, −2.09, −1.3, −0.68, 0.06, respectively. Weight gain during infancy (discharge to 1 year corrected for prematurity) and early childhood (1 year corrected age to 5 years) was expressed as rate of change in weight, rate of change in weight z score, and interval change in weight z score. In multiple regression analyses that adjusted for race, gender, maternal education, antenatal steroids, birth weight z score, major intracranial lesions on ultrasound, and chronic lung disease, rates of weight gain in infancy and early childhood were predictive of BMI z score at 9 years, regression coefficients (95% confidence intervals); 0.19 (0.02, 0.36) and 0.37 (0.11, 0.63), respectively, expressed as change in BMI z score per 10 g/week weight increase. Rates of weight gain were not predictive of systolic BP z score, Verbal IQ or Performance IQ. In VLBW infants, more rapid weight gain during infancy, and especially early childhood, is associated with higher BMI at school age.
PMCID: PMC3434458  PMID: 22962630
prematurity; growth; follow-up; outcomes

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