Birth weight

How Early Should Obesity Prevention Start?

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Obesity has pervaded the United States and is spreading throughout the world. Following in its wake is type 2 diabetes, which will affect at least half a billion people worldwide by 2030. A majority of U.S. women of childbearing age are overweight or obese (as defined by a body-mass index [BMI, the weight in kilograms divided by the square of the height in meters] >25). These women are likely to gain excessive weight when they’re pregnant, making it harder for them to return to their prepregnancy weight after delivery. Postpartum weight retention not only portends increased lifelong risks for obesity-related complications but also an increased BMI at the inception of future pregnancies. During pregnancy, excessive weight gain, along with other risk factors such as gestational diabetes, can alter fetal growth and metabolism, leading to higher adiposity in the offspring. If the child is female, grows up obese, and becomes pregnant, the cycle begins again. It is time to interrupt this vicious cycle to prevent obesity and chronic diseases in mothers and children.

Once obesity is present, it is challenging to treat because of multiple physiological, behavioral, and cultural feedback loops. The good news is that the prenatal period and the first postnatal year hold critical clues that may lead to interventions to reduce obesity in women and prevent it in children. In a range of animal models (from rodents to nonhuman primates), dietary, hormonal, mechanical, and other perturbations that occur prenatally and during infancy induce lifelong, often irreversible derangements in the offspring’s adiposity and metabolism. These changes involve the environmental alteration of genetic expression, in part through epigenetic mechanisms, rather than changes in the genome itself. Thus, timely intervention during the early, plastic phases of development — unlike corrective efforts made later in life — may lead to improved lifelong health trajectories.

Because of challenges in measuring fetal exposures and the long latency between initial determinants and salient health outcomes, however, it is difficult to translate such proofs of principle in animals to human populations. The first generation of developmental-origins studies in humans linked birth weight to adult obesity-related morbidity and mortality. We now recognize that birth weight and each of its components, gestational duration and fetal growth, are low-resolution, momentary markers for myriad prenatal and perinatal influences. In the past decade, many such influences have been identified and quantified in epidemiologic studies that have involved the period before birth, used modern methods to mitigate confounding, and incorporated biomarkers. These studies have identified prenatal risk factors for obesity ranging from lifestyle factors such as the mother’s smoking status to psychosocial factors including antepartum depression, medical conditions such as gestational diabetes, physiological stress as reflected by fetal exposure to glucocorticoids, and epigenetic markers such as gene-specific DNA methylation levels in umbilical-cord tissue.

After birth, rapid weight gain in the first 3 to 6 months of life is a potent predictor of later obesity and cardiometabolic risk. Lactation cannot be the entire explanation, because breast-fed babies tend to gain more weight than formula-fed babies in the first few months of life. The perinatal hormonal milieu may very well be a contributing factor. In one study, higher leptin levels in umbilical-cord blood, chiefly reflecting placental production, were associated with slower gain in infant weight-for-length and lower adiposity at the ages of 3 years and 7 years. In contrast, higher leptin levels at 3 years of age were associated with faster gains in BMI from 3 to 7 years, suggesting that leptin resistance develops between birth and 3 years of age.1 These findings are consistent with studies in animals showing a critical period of perinatal leptin exposure that allows normal maturation of appetite-regulating neurons in the hypothalamus. Features of infant feeding other than breast versus bottle may also play a role. Among formula-fed infants, the introduction of solids before 4 months was associated with a sixfold increase in the odds of obesity 3 years later.2

Emerging risk factors for obesity include exposure to endocrine disruptors, which appear to do the most damage during times of maximum developmental plasticity, and the gut microbiota. Our bodies contain about 1013 cells but as many as 1014 microorganisms. Certain modifications in the number and type of microorganisms during infancy are associated with excess weight gain, at least in rodents. The infant gut is normally colonized during transit through the birth canal, which could be one reason why children delivered by cesarean section appear to be at elevated risk for obesity.3

Given obesity’s numerous developmental determinants, it is logical that effective prevention would target multiple modifiable factors. In combination, two well-studied prenatal risk factors, excessive gestational weight gain and maternal smoking during pregnancy, and two postnatal factors, fewer months of breast-feeding and a shorter duration of daily sleep during infancy, are associated with wide variation in childhood obesity. In one study, preschool-age children whose mothers did not smoke or gain excessive weight during pregnancy and who were breast-fed for at least 12 months and slept for at least 12 hours per day during infancy had a predicted obesity prevalence of 6%, as compared with 29% among children for whom the opposite was true for all four risk factors4; the rates were similar (4% and 28%, respectively) when the children reached 7 to 10 years of age (see graphPredicted Probability of Obesity at 7 to 10 Years of Age for 16 Combinations of Four Modifiable Prenatal and Postnatal Risk Factors.). These observational data raise the possibility that avoiding some or all of these risk factors could substantially reduce the proportion of childhood obesity.

Preventing racial and ethnic disparities in obesity risk will also require a developmental approach. By school age, rates of obesity among black and Hispanic children in the United States are higher than the rates among white children, even after adjustment for socioeconomic circumstances. Many of the risk factors during pregnancy and early childhood are more prevalent among nonwhite persons, and they explain a substantial proportion of racial and ethnic differences in obesity in mid-childhood.5

Several features of pregnancy and infancy make the prenatal and postnatal periods conducive to behavior change to reduce the risk of obesity and its complications. First, women appear especially willing to modify their behavior during these periods to benefit their children. Second, since pregnant women and infants receive frequent routine medical care, interventions involving improved health care delivery have great potential. Third, these periods are relatively brief, and we know that behavior-change interventions are typically most successful in the short term. Fourth, if effective interventions begun during pregnancy are maintained after birth, they will reduce the risk of maternal obesity for future pregnancies and thus help to interrupt the intergenerational cycle.

Ongoing intervention studies promise to inform medical practice and public health. Many current trials target excessive gestational weight gain, including seven randomized, controlled trials funded by the National Institutes of Health that will together include more than 1000 overweight or obese women and follow infants through at least 1 year of age. It remains to be proven, however, that reducing gestational weight gain reduces the obesity risk in offspring. An alternative approach focuses on dietary quality, independent of calorie content, to ameliorate maternal insulin resistance and excessive placental nutrient transfer. Pilot studies have suggested that a multiple-risk-factor approach during infancy, targeting mothers as conduits for changes in their infants, can improve sleep duration and delay the introduction of solid foods.

But even as we await the results of obesity-prevention trials, some recommendations are warranted because of their beneficial effects on other health outcomes. Pregnant women should not smoke. Treatment of gestational diabetes reduces macrosomia at birth, although such treatment hasn’t been proven to prevent obesity. U.S. rates of elective cesarean sections have apparently leveled off, but reducing these rates, especially of cesarean sections performed before 39 weeks of gestation, is a public health goal. Simple sleep-hygiene measures are worth trying, even in early infancy. The ideal age, in terms of allergy prevention, for introducing solid foods appears to be 4 to 6 months, and further research may show that the same is true in terms of obesity prevention.

 

Source: NEJM

The dangers of being born too small or too soon.

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Birth is dangerous, especially for infants born too small or too soon. Although much is known about the mortality risk for such infants in high-income countries, little is known about the risk in poorer countries. In The Lancet, Joanne Katz and colleagues begin to fill in the gap on just how dangerous it is to be born too small or too soon in a low-income or middle-income country.1 The investigators analysed more than 2 million birth outcomes from resource-poor countries in Asia, Africa, and Latin America and calculated the regional risk of neonatal and post-neonatal mortality associated with being born preterm, small-for-gestational age (SGA), or both.

Using data from 20 cohorts in 13 countries, Katz and colleagues show that being born SGA increased the risk of neonatal mortality by two to five times across the three regions, but being born preterm (<37 completed weeks of gestation) raised the risk by six to 26 times. When children were born both SGA and preterm, neonatal mortality was ten to 39 times higher than in otherwise normal neonates. These findings provide the first solid estimates of the excess risk of dying for infants in these categories of births for countries where 135 million babies are born every year.

Katz and colleagues’ findings advance our knowledge by going beyond the use of low birthweight (<2500 g) as a means of identifying infants in danger. The low birthweight category includes both premature and growth-restricted infants. It excludes newborn babies heavier than 2500 g who might also be premature or have restricted growth and therefore still have an increased risk of dying. As a result of these findings, the sources of neonatal mortality are now better known in the regions studied and appropriate interventions to prevent early deaths can be developed.

Katz and colleagues are also the first to document the high proportion of Asian and African newborn babies (21% and 16%, respectively) who are SGA (defined as the lowest tenth percentile of the growth reference) but neither preterm nor low birthweight. In view of the surprisingly high proportion of such infants, it is disappointing that the authors did not provide the associated mortality risk. Term-SGA infants had about three times higher risk of death (across all regions) during the early and late neonatal as well as the postneonatal periods, but these included a high proportion of low-birthweight (LBW) infants. The investigators state that the large group of infants who are SGA but not preterm or LBW have a higher mortality risk than term, appropriate weight-for-gestational-age infants, but we are left to wonder: how much higher?

The high prevalence of term SGA births and their excess risk of death throughout infancy suggest that there is more to know about these babies than just their weight-for-gestational age. They could also be shorter, as documented in Guatemala,2where linear growth failure was detectable as early as 15 weeks of gestation, and infants tend to be born “short and round”.3 Infants of HIV-infected mothers on antiretroviral therapy in Haiti and Zambia were also born small, largely because of shortness at birth rather than thinness.4, 5 There has been much discussion about the causes and consequences of proportional (ie, short and round) versus disproportional (long and thin) phenotypes of SGA babies, with some evidence that thin SGA babies are at higher risk of adverse outcomes.6, 7 Elucidation of the differences in mortality risk among types of SGA infants will require datasets that include infant length at birth, but such data are rare.

Katz and colleagues’ findings present important methodological challenges. The investigators included cohorts on the basis of completeness and quality of their data. Nonetheless, in six of the cohorts, they imputed some birthweights because some data were missing or measured too late. Some of the variability in birthweight might have resulted from the 72 h observation window used (during which breastfed neonates can lose up to 10% of their weight8). Unfortunately, the preferred reference dataset for calculating birthweight-for-gestational age (the Alexander reference9) provides data at only the tenth percentile, so the authors used a different reference dataset to identify infants below the third percentile.10 Both references are from large US populations, with data obtained in 1972—76 and 1991, respectively. The appropriateness of these reference populations, especially for the cohorts from South Asia, is unknown and might be among the factors that account for the high proportions of SGA births seen. Again, not knowing the excess mortality associated with the SGA babies who were term and not LBW, we wonder whether the use of the tenth percentile of the Alexander reference put too many babies in this risk category.

The analysis presented by Katz and colleagues is a substantial contribution, and points the way to further advances. Most of the cohort studies included were not representative of the country where they were done, and the studies included in a given region were also not representative of that region—eg, the vast majority of data from Latin America was from Chile. More representative data are surely needed. Also, many low-income or middle-income countries are in eastern Europe and central Asia, regions not represented in these analyses. The scarcity of data from these regions, however, is because of a dearth of global resources and attention rather than a product of poor study design. We hope that this important study can serve as a catalyst for the development of stronger datasets that require fewer assumptions and include additional essential information, including length at birth.

Source: Lancet

 

Teenage pregnancy increased risk for obesity .

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 According to data from the National Health and Nutrition Examination Survey, researchers have determined that teenage mothers are more likely to develop obesity later in life.

“For the first time, we’ve identified our youngest moms as a high-risk group for obesity, which we know to be one of the most debilitating, long-term health issues we face,”Tammy Chang, MD, MPH, MS, clinical lecturer at the University of Michigan Medical School and a Robert Wood Johnson Foundation Clinical Scholar, said in a press release.

Chang and colleagues used the 2001-2010NHANES to investigate associations between overweight and obesity and teenage births among women aged 20 to 59 years. The patients were included if they had at least one live birth, were not pregnant at the time of the survey or recently pregnant (unweighted, n=5,220; weighted, n=48.4 million), researchers wrote.

After performing bivariate analyses, the researchers found that women with a teen birth were significantly more likely to become overweight (RR=1.61; 95% CI, 1.37-1.90) or obese (RR=1.84; 1.56-2.16) compared with women who did not have a teen birth. Adjusted data indicate women with a teen birth continued to be more susceptible for becoming overweight (aRR=1.33; 95% CI, 1.10-1.62) or obese (aRR=1.32, 95% CI, 1.09-1.61) compared with women without a teen birth, they wrote.

“We know that teen pregnancy is tied to certain immediate risks, such as babies having low birth weight and mothers struggling to complete high school — and now we know that it is also associated with poor long-term health outcomes,” Chang said. “Obesity is a prevalent, expensive health problem with detrimental health consequences and it’s difficult to reverse, which is why it’s incredibly important to identify at-risk groups early so that we can intervene.”

The researchers suggest further studies on modifiable physiologic and sociomedical reasons behind early pregnancy and subsequent risk forobesity.

 

PERSPECTIVE

 

  • This study is unique in that it  investigates whether teen pregnancy could be a risk factor for obesity later in life. The researchers looked at data on about 5200  women aged 20 to 59.

The investigators  sought to examine the difference in the prevalence of obesity or overweight status in women who gave birth between ages 13 and 19 years  vs. those who gave birth at age 20 or later. They found that women who gave birth during their teen years were 32% more likely to be obese compared to women who gave birth at or after age 20

Clearly, this study establishes teen pregnancy as a risk factor for obesity later in life. However, we’ve  to recognize that this is an association study and it doesn’t necessarily suggest cause-and-effect link between teen pregnancy and development of obesity in later life.

The findings are not necessarily surprising because there are common sociographic factors that predispose patients to teen pregnancy as well as obesity (i.e., lower socioeconomic status, school and home environments with limited access to healthy  to healthy foods, limited places to exercise, poor understanding of health in general, or poor access to health care).

The researchers also point out that avoiding teen pregnancy might be one of the ways we can  decrease development of  obesity in adults. We often think about teen pregnancy and short-term consequences such as interruption in  education of the mother and poor access to health care and adequate resourcesbut this study  highlights a long term health risk teen pregnancy may have has on these  teens later in life.

 

Source: Endocrine Today

 

 

Association between maternal serum 25-hydroxyvitamin D level and pregnancy and neonatal outcomes: systematic review and meta-analysis of observational studies.

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Abstract

Objective To assess the effect of 25-hydroxyvitamin D (25-OHD) levels on pregnancy outcomes and birth variables.

Design Systematic review and meta-analysis.

Data sources Medline (1966 to August 2012), PubMed (2008 to August 2012), Embase (1980 to August 2012), CINAHL (1981 to August 2012), the Cochrane database of systematic reviews, and the Cochrane database of registered clinical trials.

Study selection Studies reporting on the association between serum 25-OHD levels during pregnancy and the outcomes of interest (pre-eclampsia, gestational diabetes, bacterial vaginosis, caesarean section, small for gestational age infants, birth weight, birth length, and head circumference).

Data extraction Two authors independently extracted data from original research articles, including key indicators of study quality. We pooled the most adjusted odds ratios and weighted mean differences. Associations were tested in subgroups representing different patient characteristics and study quality.

Results 3357 studies were identified and reviewed for eligibility. 31 eligible studies were included in the final analysis. Insufficient serum levels of 25-OHD were associated with gestational diabetes (pooled odds ratio 1.49, 95% confidence interval 1.18 to 1.89), pre-eclampsia (1.79, 1.25 to 2.58), and small for gestational age infants (1.85, 1.52 to 2.26). Pregnant women with low serum 25-OHD levels had an increased risk of bacterial vaginosis and low birthweight infants but not delivery by caesarean section.

Conclusion Vitamin D insufficiency is associated with an increased risk of gestational diabetes, pre-eclampsia, and small for gestational age infants. Pregnant women with low 25-OHD levels had an increased risk of bacterial vaginosis and lower birth weight infants, but not delivery by caesarean section.

 

Source: BMJ