Drinking diet beverages during pregnancy linked to child obesity, NIH study suggests | National Institutes of Health (NIH)

  "Children born to women who had gestational diabetes and drank at least one artificially sweetened beverage per day during pregnancy were more likely to be overweight or obese at age 7, compared to children born to women who had gestational diabetes and drank water instead of artificially sweetened beverages, according to a study led by researchers at the National Institutes of Health. Childhood obesity is known to increase the risk for certain health problems later in life, such as diabetes, heart disease, stroke and some cancers. The study appears online in the International Journal of Epidemiology. "


Here's the paper :-

Maternal consumption of artificially sweetened beverages during pregnancy, and offspring growth through 7 years of age: a prospective cohort study: Int J Epidemiol 

Prenatal bisphenol A exposure weakens body's fullness cues

The new study found mice born to mothers exposed to bisphenol A were less responsive to the hormone leptin, which is sometimes called the satiety hormone. Leptin helps inhibit the appetite by reducing hunger pangs when the body does not need energy. The hormone sends signals to the hypothalamus region of the brain to suppress the appetite.
"Our findings show that bisphenol A can promote obesity in mice by altering the hypothalamic circuits in the brain that regulate feeding behavior and energy balance," said the study's senior author, Alfonso Abizaid, Ph.D., of the Department of Neuroscience at Carleton University in Ottawa, Canada. "Low level prenatal exposure to BPA delays a surge of leptin after birth that allows mice to develop the proper response to the hormone. BPA exposure permanently alters the neurobiology in the affected mice, making them prone to obesity as adults.



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Association Between Artificially Sweetened Beverage Consumption During Pregnancy and Infant Body Mass Index: JAMA Pediatrics

Importance
The consumption of artificial sweeteners has increased substantially in recent decades, including among pregnant women. Animal studies suggest that exposure to artificial sweeteners in utero may predispose offspring to develop obesity; however, to our knowledge, this has never been studied in humans.
 Objective  To determine whether maternal consumption of artificially sweetened beverages during pregnancy is associated with infant body mass index (BMI [calculated as weight in kilograms divided by height in meters squared]).
Design, Setting, and Participants  This cohort study included 3033 mother-infant dyads from the Canadian Healthy Infant Longitudinal Development (CHILD) Study, a population-based birth cohort that recruited healthy pregnant women from 2009 to 2012. Women completed dietary assessments during pregnancy, and their infants’ BMI was measured at 1 year of age (n = 2686; 89% follow-up). Statistical analysis for this study used data collected after the first year of follow-up, which was completed in October 2013. The data analysis was conducted in August 2015.
Exposures  Maternal consumption of artificially sweetened beverages and sugar-sweetened beverages during pregnancy, determined by a food frequency questionnaire.
Main Outcomes and Measures  Infant BMI z score and risk of overweight at 1 year of age, determined from objective anthropometric measurements and defined according to World Health Organization reference standards.
Results  The mean (SD) age of the 3033 pregnant women was 32.4 (4.7) years, and their mean (SD) BMI was 24.8 (5.4). The mean (SD) infant BMI z score at 1 year of age was 0.19 (1.05), and 5.1% of infants were overweight. More than a quarter of women (29.5%) consumed artificially sweetened beverages during pregnancy, including 5.1% who reported daily consumption. Compared with no consumption, daily consumption of artificially sweetened beverages was associated with a 0.20-unit increase in infant BMI z score (adjusted 95% CI, 0.02-0.38) and a 2-fold higher risk of infant overweight at 1 year of age (adjusted odds ratio, 2.19; 95% CI, 1.23-3.88). These effects were not explained by maternal BMI, diet quality, total energy intake, or other obesity risk factors. There were no comparable associations for sugar-sweetened beverages.
Conclusions and Relevance  To our knowledge, we provide the first human evidence that maternal consumption of artificial sweeteners during pregnancy may influence infant BMI. Given the current epidemic of childhood obesity and widespread use of artificial sweeteners, further research is warranted to confirm our findings and investigate the underlying biological mechanisms, with the ultimate goal of informing evidence-based dietary recommendations for pregnant women."



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Burden of disease and costs of exposure to endocrine disrupting chemicals in the European Union: an updated analysis. - PubMed - NCBI

A previous report documented that endocrine disrupting chemicals contribute substantially to certain forms of disease and disability. In the present analysis, our main objective was to update a range of health and economic costs that can be reasonably attributed to endocrine disrupting chemical exposures in the European Union, leveraging new burden and disease cost estimates of female reproductive conditions from accompanying report. Expert panels evaluated the epidemiologic evidence, using adapted criteria from the WHO Grading of Recommendations Assessment, Development and Evaluation Working Group, and evaluated laboratory and animal evidence of endocrine disruption using definitions recently promulgated by the Danish Environmental Protection Agency. The Delphi method was used to make decisions on the strength of the data. Expert panels consensus was achieved for probable (>20%) endocrine disrupting chemical causation for IQ loss and associated intellectual disability; autism; attention deficit hyperactivity disorder; endometriosis; fibroids; childhood obesity; adult obesity; adult diabetes; cryptorchidism; male infertility, and mortality associated with reduced testosterone. Accounting for probability of causation, and using the midpoint of each range for probability of causation, Monte Carlo simulations produced a median annual cost of €163 billion (1.28% of EU Gross Domestic Product) across 1000 simulations. We conclude that endocrine disrupting chemical exposures in the EU are likely to contribute substantially to disease and dysfunction across the life course with costs in the hundreds of billions of Euros per year. These estimates represent only those endocrine disrupting chemicals with the highest probability of causation; a broader analysis would have produced greater estimates of burden of disease and costs.



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Childhood obesity, rapid growth linked to pregnant moms eating lots of fish

"Women who ate fish more than three times per week when they were pregnant gave birth to children with higher BMI values at 2, 4 and 6 years of age compared with women who ate fish less. High maternal fish intake during pregnancy also was associated with an increased risk of rapid growth from birth to 2 years and with an increased risk of overweight/obesity for children at ages 4 and 6 years compared with maternal fish intake while pregnant of once a week or less, the results indicate. The magnitude of the effect of fish intake was greater in girls than boys.
"Contamination by environmental pollutants in fish could provide an explanation for the observed association between high fish intake in pregnancy and increased childhood adiposity," the authors write. However, the authors note that while they collected information on the consumption of different fish types, they did not have enough data to distinguish between species, cooking procedures and the water source of the fish from rivers or the sea."



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PFOA exposure in utero linked to child adiposity and faster BMI gain

"Children whose mothers were exposed to relatively high levels of the chemical PFOA during pregnancy experienced more rapid body fat gain and higher body fat by age 8 than children whose mothers were less exposed, according to a new analysis in the journal Obesity."









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Environmental Obesogens | The Scientist Magazine®

"In 2005, Mike Skinner’s group at Washington State University published a disturbing observation: pregnant rats exposed to high levels of a commonly used fungicide had sons with low sperm counts as adults. When these male mice did succeed in impregnating a female, they bore sons who also had fewer sperm, and the gametes were less viable. The problem perpetuated through multiple generations, as Skinner’s lab observed the rats over several years.1

“We sat on [the results] for four years because it was a major observation, so we wanted to get as much on the mechanism as possible,” Skinner says. He and his colleagues found that altered DNA methylation patterns in the germ line were to blame.

To see if other environmental chemicals could have the same effect, they screened a host of potentially toxic chemicals: jet fuel, plastics ingredients, and more pesticides. Again, exposed animals had offspring with reproductive problems, which were passed down for generations. The researchers also saw another phenotype pop up again and again: obesity. Skinner first saw fat rats in his experiments after he’d injected females with a mixture of bisphenol A (BPA) and phthalates, substances used to make plastic products and, like the fungicide the researchers originally tested, known to be endocrine disruptors. The rats’ pups and their pups’ pups—animals that had direct exposure to the chemicals—showed other abnormalities, but were of normal weight. However, roughly 10 percent of third-generation (F3) rats descended from exposed females became obese.2"



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Artificial sweeteners are not the answer to childhood obesity. - PubMed - NCBI

While no single factor is responsible for the recent, dramatic increases
in overweight and obesity, a scientific consensus has emerged
suggesting that consumption of sugar-sweetened products, especially
beverages, is casually linked to increases in risk of chronic,
debilitating diseases including type 2 diabetes, cardiovascular disease,
hypertension and stroke. One approach that might be beneficial would be
to replace sugar-sweetened items with products manufactured with
artificial sweeteners that provide sweet tastes but with fewer calories.
Unfortunately, evidence now indicates that artificial sweeteners are
also associated with increased risk of the same chronic diseases linked
to sugar consumption. Several biologically plausible mechanisms may
explain these counterintuitive negative associations. For example,
artificial sweeteners can interfere with basic learning processes that
serve to anticipate the normal consequences of consuming sugars, leading
to overeating, diminished release of hormones such as GLP-1, and
impaired blood glucose regulation. In addition, artificial sweeteners
can alter gut microbiota in rodent models and humans, which can also
contribute to impaired glucose regulation. Use of artificial sweeteners
may also be particularly problematic in children since exposure to
hyper-sweetened foods and beverages at young ages may have effects on
sweet preferences that persist into adulthood. Taken as a whole, current
evidence suggests that a focus on reducing sweetener intake, whether
the sweeteners are caloric or non-caloric, remains a better strategy for
combating overweight and obesity than use of artificial sweeteners.

Taking antibiotics during pregnancy increases risk for child becoming obese -- ScienceDaily

A study just released by Columbia University's Mailman School of Public
Health found that children who were exposed to antibiotics in the second
or third trimester of pregnancy had a higher risk of childhood obesity
at age 7. The research also showed that for mothers who delivered their
babies by a cesarean section, whether elective or non-elective, there
was a higher risk for obesity in their offspring.

Research links tobacco smoke and roadway air pollution with childhood obesity

The source of virtually all roadway air pollution emissions is the exhaust (Photo credit: Wikipedia)

The study, to be posted online Wednesday, Nov. 12, 2014 in Environmental Health Perspectives, shows increased weight gain during adolescence in children exposed to secondhand tobacco smoke or near-roadway air pollution, compared to children with no exposure to either of these air
pollutants. The study is one of the first to look at the combined
effects on body mass index of exposure to both near-roadway air pollution and tobacco smoke. The
effects were substantially greater in children exposed to both air
pollutant mixtures than to either alone.

Prenatal exposure to dichlorodiphenyltrichloroethane and obesity at 9 years of age in the CHAMACOS study cohort.

In-utero exposure to endocrine-disrupting compounds, including
dichlorodiphenyltrichloroethane (DDT) and its metabolite
dichlorodiphenylethylene (DDE), has been hypothesized to increase the
risk of obesity later in life. We examined the associations of maternal
serum concentrations of DDT and DDE during pregnancy with body mass
index, obesity, waist circumference, and percentage of body fat in
9-year-old children (n = 261) in the Center for the Health Assessment of
Mothers and Children of Salinas (CHAMACOS) Study, a longitudinal birth
cohort study in the Salinas Valley, California (2000-2010). We found
associations between prenatal exposure to DDT and DDE and several
measures of obesity at 9 years of age in boys but not in girls. For
example, among boys, 10-fold increases in prenatal DDT and DDE
concentrations were associated with increased odds of becoming
overweight or obese (for o,p'-DDT, adjusted odds ratio (OR) = 2.5, 95%
confidence interval (CI): 1.0, 6.3; for p,p'-DDT, adjusted OR = 2.1, 95%
CI: 1.0, 4.5; and for p,p'-DDE, adjusted OR = 1.97, 95% CI: 0.94,
4.13). The odds ratios for girls were nonsignificant. Results were
similar for body mass index z score, waist circumference z score, and
odds of increased waist circumference but were less consistent for
percentage of body fat. The difference by sex persisted after
considering pubertal status. These results provide support for the
chemical obesogen hypothesis.

Bisphenol A exposure cost $3 billion in 2008

Leonardo Trasande, M.D., from the New York University School of Medicine in New York City, quantifies the potential disease burden and costs associated with BPA exposure in 2008 and models the potential health and economic benefits of replacing BPA in all food uses.

The author estimated that, in 2008, 12,404 cases of childhood obesity, 33,863 cases of newly incident coronary heart disease, and $2.98 billion in social costs could be attributed to BPA exposure. Removing BPA from all food uses could prevent 6,236 cases of childhood obesity and 22,350 cases of newly incident coronary heart disease annually, with potential annual economic benefits of $1.74 billion.

"Although more data are needed, these potentially large health and economic benefits could outweigh the costs of using a safer substitute for BPA," Trasande concludes

Associations Between Childhood Obesity and the Availability of Food Outlets in the Local Environment: A Retrospective Cross-Sectional Study.

 Abstract Purpose . Examine whether individual-level childhood obesity is related to residential availability of fast food and healthy food outlets. Design . Retrospective cross-sectional study. Setting . Perth, Western Australia Subjects . A total of 1850 children aged 5 to 15 years in 2005-2010 who participated in the Western Australian Health and Wellbeing Surveillance System survey. Measures . Geographical Information Systems were used to calculate a range of measures of fast food and healthy food outlet access and availability. For example, distance to nearest and access and density measures within 800 m and 3 km of each child's residence were all tested. Analysis . Multivariate logistic regression analysis, controlling for individual-level sociodemographic factors and lifestyle behaviors. Results . An increasing number of healthy food outlets within 800 m of a child's home was associated with a significantly reduced risk of being overweight/obese in all models tested. After controlling for age, physical activity, time spent sedentary, weekly takeaway consumption, area disadvantage, and count of fast food outlets, each additional healthy food outlet within 800 m was associated with a 20% decrease in the likelihood of a child being overweight or obese (odds ratio: .800, 95% confidence intervals: .686-.933). Conclusion . The local food environment around children's homes has an independent effect on child weight status. These findings highlight the importance of the built environment as a potential contributor towards child health, which should be considered when developing community health promotion programs

BPA linked to obesity risk in puberty-age girls

BPA linked to obesity risk in puberty-age girls: "Girls between 9 and 12 years of age with higher-than-average levels of bisphenol-A (BPA) in their urine had double the risk of being obese than girls with lower levels of BPA, according to a Kaiser Permanente study published today in the journal PLOS ONE."

Addiction to unhealthy foods could help explain the global obesity epidemic

 "Research presented today shows that high-fructose corn syrup can cause behavioural reactions in rats similar to those produced by drugs of abuse such as cocaine. These results, presented by addiction expert Francesco Leri, Associate Professor of Neuroscience and Applied Cognitive Science at the University of Guelph, suggest food addiction could explain, at least partly, the current global obesity epidemic. These results were presented at the 2013 Canadian Neuroscience Meeting, the annual meeting of the Canadian Association for Neuroscience - Association Canadienne des Neurosciences (CAN-ACN)."

Urinary Bisphenol A and Obesity in US Children.

Childhood obesity, a major public health problem, can lead to cardiovascular disease in adulthood. Studies have implicated exposure to bisphenol A (BPA), a commonly used chemical, in the development of obesity in adults. However, literature is limited on this association in children. We examined the association between urinary BPA and obesity in children aged 6-18 years from the National Health and Nutrition Examination Survey (2003-2008). The primary exposure was urinary BPA and the outcome was obesity, defined as the ≥95th percentile of body mass index specific for age and sex. We found a positive association between increasing levels of urinary BPA and obesity, independent of age, sex, race/ethnicity, education, physical activity, serum cotinine, and urinary creatinine. Compared with children in the lowest quartile of BPA (<1.5 ng/mL), children in the highest quartile (>5.4 ng/mL) had a multivariable odds ratio for obesity of 2.55 (95% confidence interval (CI): 1.65, 3.95) (P_trend < 0.01). The observed positive association was predominantly present in boys (odds ratio = 3.80, 95% CI: 2.25, 6.43) (P_trend < 0.001) and in non-Hispanic whites (odds ratio = 5.87, 95% CI: 2.15, 16.05) (P_trend < 0.01). In a representative sample of children, urinary BPA was associated with obesity, predominantly in non-Hispanic white boys, independent of major risk factors.

Maternal obesity and vitamin D sufficiency are associated with cord blood vitamin D insufficiency.

An inverse relationship between total serum 25-hydroxyvitamin D (25-OH D) and increased adiposity has been established in children, adolescents, and adults. However, the relationship between neonatal adiposity and vitamin D status has not been reported. Both maternal obesity and vitamin D deficiency in pregnancy are common and are associated with adverse pregnancy outcomes.

OBJECTIVE:

The aim of the study was to determine the relationship between vitamin D levels in mothers and newborns, as influenced by maternal obesity, and evaluate these associations with neonatal adiposity.

DESIGN, SETTING, AND PATIENTS:

Sixty-one maternal-neonatal pairs participated in this cross-sectional study at an academic medical center. Mothers had a prepregnancy body mass index that was normal or obese.

OUTCOME MEASURES:

Maternal and cord blood sera were assayed for 25-OH D, and neonatal body composition was measured by air displacement plethysmography.

RESULTS:

Mothers had similar and sufficient levels of 25-OH D when measured at 36-38 wk gestation, irrespective of body mass index category (normal weight, 46.05, vs. obese, 49.84 ng/ml; P = not significant). However, cord blood 25-OH D was higher in neonates of normal-weight mothers compared to neonates of obese mothers (27.45 vs. 20.81 ng/ml; P = 0.02). The variance in cord blood 25-OH D was explained by four factors: maternal 25-OH D level, the presence of maternal obesity, maternal age, and neonatal adiposity (r(2) = 0.66).

CONCLUSION:

Obese women transfer less 25-OH D to offspring than normal-weight women, despite similar serum levels. Cord blood 25-OH D levels directly correlate to neonatal percentage body fat. These novel findings underscore the evolving relationships between maternal obesity, vitamin D nutritional status, and adiposity in the neonatal period that may influence subsequent childhood and adulthood vitamin D-dependent processes.

Is there a link between childhood obesity and ADHD, learning disabilities?

A University of Illinois study has established a possible link between high-fat diets and such childhood brain-based conditions as attention deficit hyperactivity disorder (ADHD) and memory-dependent learning disabilities.

News in Brief: Chemical tied to intergenerational obesity | Environment | Science News

Exposure in the womb to a chemical used in PVC and ship paint promotes obesity in mice. And the effect is long-lasting: The mice’s grandchildren were also fat despite no exposure to the chemical.

The work shows that the effects of an obesogen — a chemical that encourages fat accumulation — can be passed on to future generations not exposed to the chemical, researchers report online January 15 inEnvironmental Health Perspectives.

Sugar fights still simmer as new brain study finds fructose might stimulate appetite

Fructose, a sugar much maligned in recent years, recently took another hit when a preliminary study by Yale University found that it might stimulate appetite more than other sugar types. The results came as no surprise to Robert Lustig, MD, a pediatric endocrinologist at the UCSF Benioff Children's Hospital who's made headlines for years with his public health crusade against excess sugar consumption.

Read more at: http://medicalxpress.com/news/2013-01-sugar-simmer-brain-fructose-appetite.html#jCp