International Journal of Obesity

Obese stomachs tell us diets are doomed to fail

Public release date: 16-Sep-2013 [

Contact: Amanda Page amanda.page@adelaide.edu.au 61-882-225-644 University of Adelaide

The way the stomach detects and tells our brains how full we are becomes damaged in obese people but does not return to normal once they lose weight, according to new research from the University of Adelaide.

Researchers believe this could be a key reason why most people who lose weight on a diet eventually put that weight back on.

In laboratory studies, University of Adelaide PhD student Stephen Kentish investigated the impact of a high-fat diet on the gut’s ability to signal fullness, and whether those changes revert back to normal by losing weight.

The results, published in the International Journal of Obesity, show that the nerves in the stomach that signal fullness to the brain appear to be desensitized after long-term consumption of a high-fat diet.

“The stomach’s nerve response does not return to normal upon return to a normal diet. This means you would need to eat more food before you felt the same degree of fullness as a healthy individual,” says study leader Associate Professor Amanda Page from the University’s Nerve-Gut Research Laboratory.

“A hormone in the body, leptin, known to regulate food intake, can also change the sensitivity of the nerves in the stomach that signal fullness. In normal conditions, leptin acts to stop food intake. However, in the stomach in high-fat diet induced obesity, leptin further desensitizes the nerves that detect fullness.

“These two mechanisms combined mean that obese people need to eat more to feel full, which in turn continues their cycle of obesity.”

Associate Professor Page says the results have “very strong implications for obese people, those trying to lose weight, and those who are trying to maintain their weight loss”.

“Unfortunately, our results show that the nerves in the stomach remain desensitized to fullness after weight loss has been achieved,” she says.

Associate Professor Page says they’re not yet sure whether this effect is permanent or just long-lasting.

“We know that only about 5% of people on diets are able to maintain their weight loss, and that most people who’ve been on a diet put all of that weight back on within two years,” she says.

“More research is needed to determine how long the effect lasts, and whether there is any way – chemical or otherwise – to trick the stomach into resetting itself to normal.”

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This study has been funded by the National Health and Medical Research Council (NHMRC).

Media Contact:

Associate Professor Amanda Page Nerve-Gut Research Laboratory School of Medicine The University of Adelaide Phone: +61 8 8222 5644 amanda.page@adelaide.edu.au

The epigenetics of increasing weight through the generations ” resulting in amplification of obesity across generations “

Re-Post from 2008

Contact: Dipali Pathak
pathak@bcm.edu
713-798-4710
Baylor College of Medicine

Overweight mothers give birth to offspring who become even heavier, resulting in amplification of obesity across generations, said Baylor College of Medicine researchers in Houston who found that chemical changes in the ways genes are expressed – a phenomenon called epigenetics — could affect successive generations of mice.

“There is an obesity epidemic in the United States and it’s increasingly recognized as a worldwide phenomenon,” said Dr. Robert A. Waterland, assistant professor of pediatrics – nutrition at BCM and lead author of the study that appears in the International Journal of Obesity. “Why is everyone getting heavier and heavier? One hypothesis is that maternal obesity before and during pregnancy affects the establishment of body weight regulatory mechanisms in her baby. Maternal obesity could promote obesity in the next generation.”

Waterland and his colleagues studied the effect of maternal obesity in three generations of genetically identical mice, all with the same genetic tendency to overeat. One group of mice received a standard diet; the other a diet supplemented with the nutrients folic acid, vitamin B12, betaine and choline. The special ‘methyl supplemented’ diet enhances DNA methylation, a chemical reaction that silences genes.

“We wanted to know if, even among genetically identical mice, maternal obesity would promote obesity in her offspring, and if the methyl supplemented diet would affect this process,” said Waterland. “Indeed, those on the regular diet got fatter and fatter with each generation. Those in the supplemented group, however, did not.”

“We think DNA methylation may play an important role in the development of the hypothalamus (the region of the brain that regulates appetite),” said Waterland.

“Twenty years ago, it was proposed that just as genetic mutations can cause cancer, so too might aberrant epigenetic marks – so called ‘epimutations.’ That idea is now largely accepted and the field of cancer epigenetics is very active. I would make the same statement for obesity. We are on the cusp of understanding that,” he said.

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Waterland is also a researcher at the USDA/ARS Children’s Nutrition Research Center at BCM and Texas Children’s Hospital. Others who contributed to this research include Kajal Tahiliani, Marie-Therese Rached and Sherin Mirza of Baylor College of Medicine and the USDA/ARS Children’s Nutrition Research Center in Houston and Michael Travisano of the University of Minnesota in St. Paul.

Funding for this work came from the National Institutes of Health, the March of Dimes Birth Defects Foundation and the U.S. Department of Agriculture.

When the embargo lifts, this report is available at the website of the http://www.nature.com/ijo/index.html.

For more information on basic science research at Baylor College of Medicine, please go to http://www.bcm.edu/fromthelab/.

Antibiotic use in infants before 6 months associated with being overweight in childhood

Contact: lorinda klein lorindaann.klein@nyumc.org 212-404-3533 NYU Langone Medical Center / New York University School of Medicine

New York City (August 21, 2012) – Treating very young infants with antibiotics may predispose them to being overweight in childhood, according to a study of more than 10,000 children by researchers at the NYU School of Medicine and the NYU Wagner School of Public Service and published in the online August 21, 2012, issue of the International Journal of Obesity.

The study found that on average, children exposed to antibiotics from birth to 5 months of age weighed more for their height than children who weren’t exposed. Between the ages of 10 to 20 months, this translated into small increases in body mass percentile, based on models that incorporated the potential impacts of diet, physical activity, and parental obesity. By 38 months of age, exposed children had a 22% greater likelihood of being overweight. However, the timing of exposure mattered: children exposed from 6 months to 14 months did not have significantly higher body mass than children who did not receive antibiotics in that same time period.

The NYU School of Medicine researchers, led by Leonardo Trasande, MD, MPP, associate professor of pediatrics and environmental medicine, and Jan Blustein, MD, PhD, professor of population health and medicine, caution that the study does not prove that antibiotics in early life causes young children to be overweight. It only shows that a correlation exists. Further studies will need to be conducted to explore the issue of a direct causal link.

“We typically consider obesity an epidemic grounded in unhealthy diet and exercise, yet increasingly studies suggest it’s more complicated,” said Dr. Trasande. “Microbes in our intestines may play critical roles in how we absorb calories, and exposure to antibiotics, especially early in life, may kill off healthy bacteria that influence how we absorb nutrients into our bodies, and would otherwise keep us lean.”

In recent years there has been a growing concern about the overuse of antibiotics, especially in children. Preliminary studies of the microbiome, the trillions of microbial cells inhabiting our bodies and outnumber our own cells 10 to 1, implicate obesity, inflammatory bowel disease, asthma, and other conditions with changes in the microbiome. It is still a field in its infancy, however, and no one has yet proved that altering the composition of bacteria in the body leads to disease.

This is the first time that a study has analyzed the association between the use of antibiotics and body mass starting in infancy. One previous study had identified a link between antibiotic use in early infancy and obesity at seven years of age, but was unable to examine potential impacts of antibiotic use later in infancy on body weight in childhood.

The NYU School of Medicine researchers evaluated the use of antibiotics among 11,532 children born in Avon, United Kingdom, during 1991 and 1992. The children are part of the Avon Longitudinal Study of Parents and Children (ALSPAC), a long-term study that provides detailed data on the health and development of these children.

The NYU School of Medicine researchers analyzed health information on these children during three periods: from birth to 5 months of age; 6 months to 14 months; and, finally from 15 to 23 months. They also examined body mass or weight at five different points of time—6 weeks, 10 months, 20 months, 38 months, and 7 years of age.

Antibiotic use only appeared to have an effect in very young infants (those given antibiotics from birth to 5 months of age.) Although children exposed to antibiotics at 15 to 23 months had somewhat greater BMI (Body Mass Indices) for their age and gender by the age of 7, there was no significant increase in their being overweight or obese.

“For many years now, farmers have known that antibiotics are great at producing heavier cows for market,” said Dr. Blustein. “While we need more research to confirm our findings, this carefully conducted study suggests that antibiotics influence weight gain in humans, and especially children too.”

In addition to Dr. Trasande, who is also associate professor of health policy, NYU Wagner School of Public Service, and Dr. Blustein, who is also a professor of health policy at the NYU Wagner School of Public Service, the authors of the study are: Mengling Liu, PhD, associate professor of environmental medicine, NYU School of Medicine; Elise Corwin, BA, NYU Wagner School of Public Service; Laura M. Cox, BA, Department of Microbiology, NYU School of Medicine; Martin J. Blaser, MD, the Frederick H. King Professor of Internal Medicine and chair Department of Medicine, and professor of microbiology, NYU School of Medicine.

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Support for this preliminary work with the ALPSAC database was provided through a pilot grant from the NYU Global Public Health Research Challenge Fund, and by NIH grants 1GM090989 and 1UL1RR029893.

Disclosures:

All authors have no financial relationships or conflicts of interests to declare.

About NYU School of Medicine:

NYU School of Medicine is one of the nation’s preeminent academic institutions dedicated to achieving world class medical educational excellence. For 170 years, NYU School of Medicine has trained thousands of physicians and scientists who have helped to shape the course of medical history and enrich the lives of countless people. An integral part of NYU Langone Medical Center, the School of Medicine at its core is committed to improving the human condition through medical education, scientific research and direct patient care. The School also maintains academic affiliations with area hospitals, including Bellevue Hospital Center, one of the nation’s finest municipal hospitals where its students, residents and faculty provide the clinical and emergency care to New York City’s diverse population, which enhances the scope and quality of their medical education and training. Additional information about the NYU School of Medicine is available at http://school.med.nyu.edu/