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Breathing very dirty air may boost obesity risk

Beijing smog

Serious air pollution, like this smog over China’s capital city, may increase the risk of obesity.

Air pollution is bad for our lungs. It may not be great for our waistlines either, a new study in rats finds.

China’s capital city of Beijing has some of the worst air pollution in the world. On really bad days, its air can host more than 10 times as many tiny pollutant particles as the World Health Organization says is safe for human health. In a new study, rats breathed in this air. And those rodents gained more weight, and were unhealthier overall, than were rats breathing much cleaner air. The results suggest that exposure to air pollution can raise the risk of becoming extremely overweight.

And, adds Loren Wold, “It is highly likely that this is happening in humans.”

Wold works at Ohio State University in Columbus. There, he studies how air pollution affects the heart. He was not involved in the new study. But he says it agrees with many other studies that have suggested air pollution can affect metabolism, which is how the body breaks down food and uses it for fuel.

Polluted air contains particles of ash, dust and other chemicals. Sometimes these particles are so numerous that they create a thick, dense smog can cuts visibility.

Earlier experiments among 18-year olds in Southern California had linked heavier traffic with higher body mass index (a measure of overweight and obesity). Areas with heavy traffic also tend to have more of those pollutant particles. Another study found that when pregnant mice were exposed to exhaust from diesel engines, their pups grew up to be heavier. The pups also developed more inflammation in their brains.

In the new study, researchers tested how Beijing’s polluted air affects the health of pregnant rats.

Jim Zhang is an environmental scientist at Duke University in Durham, N.C. He and his co-workers put rats in two indoor chambers in Beijing. They piped polluted air from the city directly into one chamber. Air piped into the other chamber went through a filter. That filter removed almost all of the big pollution particles from the air and about two-thirds of the smaller ones. This made the air more like what people breathe in typical U.S. cities and suburbs, Zhang says.

All rats ate the same type and amount of food. But after 19 days, the pregnant rats breathing the heavily polluted air weighed more than the rats breathing the filtered air. They also had higher amounts of cholesterol — a waxy, fatlike substance — in their blood than did the rats breathing filtered air.

Those breathing the dirtier air had higher levels of inflammation. This is a sign of the body responding to tissue damage. These rats also had higher insulin resistance. This means their bodies weren’t responding as well to insulin, a hormone that helps with using sugar for energy. Insulin resistance can lead to diabetes, a dangerous health condition.

Taken together, the scientists say, these symptoms indicate the rats were developing metabolic syndrome. It’s a condition that puts the animals at risk of heart disease and diabetes.

During the experiment, the pregnant rats gave birth. Their pups stayed in the chambers with their mothers. And young rats that breathed in the polluted air were heavier than pups born to moms living in the cleaner air. Like their moms, the pups breathing very polluted air had more inflammation and insulin resistance.

The longer these pups breathed the dirty air, Zhang says, the more unhealthy they became. This suggests that breathing polluted air for a long time can lead to sickness, Zhang says.

It’s not yet clear exactly how air pollution affects rat metabolism. But it seems, Zhang says, to impair how the animals process fat and sugar. Pollution also increases signs of inflammation in the lungs, blood and fat. Zhang says this is probably what led to weight gain in the animals.

Wold says it might be possible to create medicines that reverse the negative health effects of air pollution. But these medicines will take time to develop.

Until then, Zhang and Wold say that paying attention to air pollution levels can help people manage their health risks. On days when pollution levels are high, they recommend that people stay indoors, if possible — or at least avoid tough outdoor exercise .


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Woman Becomes Obese After Fecal Transplant From Overweight Donor

While they may sound totally disgusting, fecal transplants are emerging as a promising treatment for a variety of gastrointestinal diseases, in particular infection with the bacteriaClostridium difficile. They don’t quite involve directly inserting the feces of one person into another, but rather the donor stool is rinsed and strained and then introduced into the recipient, either through an enema or endoscopy, or orally in pill form. The idea is to replace healthy bacteria in the gut after the normal balance is disturbed, for example by antibiotics.

One woman suffering recurrent C. difficile infection was recently successfully treated with this procedure, but interestingly, she also rapidly went from normal weight to becoming obese after receiving the transplant. While the weight gain could be due to a variety of factors, the donor was also overweight, and the recipient had never struggled with her weight before. Researchers are therefore speculating whether something in the transplant could have played a role in her weight gain, and have described the intriguing case in Open Forum Infectious Diseases.

The individual described in the report was a 32-year-old female who presented with recurrent C. difficile infection. This bacterium commonly affects those treated with antibiotics and can cause a variety of unpleasant symptoms, ranging from diarrhea and abdominal cramps to life-threatening complications such as severe bowel swelling.

Alongside testing positive for this particular bacterium, examination revealed that she was also infected with another species called Helicobacter pylori, a common bacterium that can also cause similar symptoms to C. difficile infection. The woman was therefore prescribed a cocktail of antibiotics, but her symptoms recurred after she completed the course. She was then put on different antibiotics, but the same thing happened again. The woman therefore decided to give fecal transplant a go, electing her daughter as the donor.

At the time, the woman was a healthy 136 pounds with a normal BMI of 26. Her daughter weighed 140 pounds at the time, with a BMI of 26.6, but became overweight shortly afterward. Following the therapy, the woman’s symptoms vanished and she no longer experienced recurrent infections.

Sixteen months later, however, the woman reported unintentional weight gain of 34 pounds and met the criteria for obesity. Two and a half years after the transplant, the woman weighed 177 pounds with a BMI of 34.5, despite a medically supervised liquid protein diet and exercise program.

“We’re questioning whether there was something in the fecal transplant, whether some of those ‘good’ bacteria we transferred may have an impact on her metabolism in a negative way,” case report author Colleen Kelly said in a statement.

This would not be the first time that an association between gut bacteria and weight has been reported. Several animal studies have shown that fecal transplant from an obese mouse into a normal-weight mouse can cause a significant increase in fat. However, there are also several other possible factors which could explain her weight gain, for example an increase in appetite following resolution of the infection. Furthermore, links between H. pylori treatment and weight gain have also previously been demonstrated. But given the fact that both the daughter and the mother gained weight, the researchers conclude that the transplant was at least partly responsible for the obesity.

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Early antibiotic exposure linked to later-life obesity, metabolic abnormalities

w study suggests that antibiotic exposure during early life may lead to permanent changes in the gut, increasing the risk of later-life obesity and metabolic abnormalities.
Girl measuring waist
Could exposure to antibiotics early in life increase the risk of obesity later in life? This latest research suggests so.

The research team, led by Laura M. Cox, PhD, of the NYU Langone Medical Center in New York, NY, recently published their findings in the journal Cell.

Past research has associated early antibiotic use with a number of subsequent medical conditions. Last year, Medical News Today reported on a study claiming that antibiotic use within the first year of life increases the risk of eczema by 40%, while a more recent study suggests infant antibiotic use may increase the risk of asthma later in life.

Both of these studies claim antibiotics interfere with beneficial gut bacteria, making infants more prone to the said conditions.

And in this latest study, Dr. Cox and colleagues report a similar theory. They found that mice given antibiotics early in life had altered gut bacteria, which reprogrammed their metabolism and made them more prone to weight gain.

Mice exposed to antibiotics in the womb had higher fat mass

To reach their findings, the researchers conducted a series of experiments on six different mouse models over 5 years.

In one experiment, the team tested low doses of penicillin on three groups of mice. The first group was exposed to antibiotics in the womb during the last week of pregnancy and continued with the antibiotics throughout their lifespan. The second group was first exposed to the penicillin at weaning and received it for life, while the third group received no antibiotics.

fat mouse
Mice that began receiving penicillin in the womb had the highest increase in fat mass, indicating that “mice are more metabolically vulnerable if they get antibiotics earlier in life.”

Dr. Cox and colleagues found that both groups that received the penicillin experienced increased fat mass. However, this gain in body fat was higher among the mice that began receiving penicillin in the womb. “This showed that mice are more metabolically vulnerable if they get antibiotics earlier in life,” says Dr. Cox.

Furthermore, when the mice were fed a high-fat diet, those that received antibiotics became fatter than those left untreated.

“When we put mice on a high-calorie diet, they got fat. When we put mice on antibiotics, they got fat. But when we put them on both antibiotics and a high-fat diet, they got very, very fat,” explains senior author Dr. Martin Blaser, professor of microbiology at the NYU Langone Medical Center.

Adult female mice usually carry around 3 g of fat. The mice fed the high-fat diet alone carried 5 g of fat. But those fed the high-fat diet in combination with antibiotics carried 10 g of fat, which accounted for a third of their body weight.

In addition to this weight gain, these mice also had high levels of fasting insulin and gene alterations linked to liver regeneration and detoxification. These effects, the researchers say, are normally found in obese patients with metabolic disorders.

The team says these findings confirm the results of a study they conducted in 2012, which found that mice given low doses of antibiotics throughout life gained 10-15% more body fat and displayed an altered metabolism in their liver, compared with mice given no antibiotics.

The next step for the researchers was to determine the mechanisms behind these effects. Are they caused by the antibiotics themselves? Or is altered gut bacteria to blame?

Weight gain ‘a result of altered gut bacteria, not antibiotics’

To find out, Dr. Cox and colleagues took gut bacteria from the mice that had been exposed to penicillin and transferred it into the guts of 3-week-old mice (the equivalent to weaning age in human infants) that had been specially bred to be germ- and antibiotic-free.

As a control, another group of specially bred mice received bacteria from mice that had not been treated with penicillin.

The researchers found that the mice that received bacteria from penicillin-treated mice became fatter than those that received bacteria from untreated mice, indicating that increased fat mass is a result of altered gut bacteria rather than the antibiotics themselves.

The team notes that contrary to previous studies investigating the link between antibiotics and gut bacteria, their research revealed that penicillin did not reduce the amount of bacteria in the gut.

However, they found that the antibiotic did abolish four bacteria they say are important for microbial colonization in early life: Lactobacillus, Allobaculum, Candidatus Arthromitus, and a member of theRikenellaceae family that is currently unnamed.

Speaking of the importance of these findings, Dr. Cox says:

“We’re excited about this because not only do we want to understand why obesity is occurring, but we also want to develop solutions.

This gives us four potential new candidates that might be promising probiotic organisms. We might be able to give back these organisms after antibiotic treatments.”

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For better weight control, fiber up!

A diet high in a fermentable type of fiber may hold the key to avoiding weight gain

The latest trick to fighting obesity isn’t a focus on eating less fat or sugar (although that would probably help): It’s eating more fiber. And not just any kind of fiber. It should be the fermentable type. Microbes in the gut chow down on this type of fiber. As they break it down, they release a chemical that moves to the brain. There it curbs appetite.

Researchers at Imperial College London, in England, say their study is the first to link eating fiber to the brain hormones that help you feel full. They published their findings April 29 in Nature Communications.

Scientists have known that obese people tend to eat foods low in dietary fiber. At some level, that made sense. Fermentable fiber — fiber that is broken down by gut microbes — makes people feel full after eating somewhat less. Such fiber is found in fruits, vegetables, oats and barley.

Hundreds of thousands of years ago, our paleolithic ancestors ate nearly 100 grams of fermentable fiber each day, says Gary Frost. He’s a dietician who led the new study. Today, people’s diets are very different. We eat only 10 to 20 grams of all types of fiber each day. Most comes from whole-grain wheat and bran. Those types do not break down in the gut, Frost notes. Modern diets also are full of convenience foods, such as snacks and frozen dinners. These tend to be high in fat and sugar. Add in our couch-potato lifestyle and it’s a recipe for obesity.

Eating more fermentable fiber reduces the risk of becoming overweight or obese. But until the new study, exactly how the fiber did that was unclear.

In the new study, researchers fed one group of mice a high-fat diet. It also was high in fermentable fiber. Another group received a high-fat diet with non-fermentable fiber. After eight weeks, the first group weighed less. Those mice also had eaten less food than the second group.

Next, the scientists looked at the effect of one particular chemical: acetate. Also known as acetic acid, it is a common by-product of the breakdown of sugars and starches by gut microbes.

To learn how the chemical affects weight, the scientists injected the mice with acetate. But first they labeled the acetate with carbon-11. This radioactive isotope of carbon has only five neutrons, rather than the usual six. The radiation it gave off allowed researchers to track its location. To do that, they put each mouse in a PET-scanner. This device creates a three-dimensional image showing the location of the radioactive “label” on each acetate molecule.

The acetate traveled through the blood and into the mice’s brains. There it collected in a region known as the hypothalamus, which controls appetite. By releasing hormones, that brain region can shut off hunger and promote satiety — a feeling of fullness. As a sign that’s indeed happened, mice injected with acetate ate less food than untreated mice.

Researchers then labeled fermentable fiber with carbon-13. This non-radioactive form of carbon contains an extra neutron. That bonus neutron causes the nucleus of this atom to spin. And that spin allowed investigators to track its movement through the body.

After feeding mice the labeled food, the researchers examined the rodents’ brains. Microbes in the gut had broken the fiber down into acetate. Again, the labeled acetate traveled to the hypothalamus. There it accumulated. This was clear evidence that chemicals released during fiber fermentation — or breakdown — act on the brain to control appetite, says Frost.

It’s a good study showing the benefits of fiber intake, says Satya Kalra. A neuroscientist at the University of Florida in Gainesville, he was not involved in the new study.

Should people start eating pure acetate to reduce food consumption? Absolutely not, says Frost. The best way to control weight is by eating food from natural sources. That means eating more foods with fermentable fiber. “The bugs in the gut will change the fiber into acetate in a way the body has always done,” he says.

So be sure to load up on those fruits and veggies.

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Children of divorced parents ‘more likely to be overweight or obese’

Obesity is a growing concern, particularly among children. In the past 30 years, rates of obesity have more than doubled in children and quadrupled in adolescents. Now, new research published in BMJ Open suggests that children whose parents divorce may be more prone to weight gain than those with a secure parental marital status.

Past research has indicated that a child’s family life may influence their weight. For example, Medical News Todayrecently reported on a study suggesting that children of strict parents are more likely to be obese. A 2012 study also indicated that parental stress may influence a child’s weight.

The researchers of this latest study – including Anna Biehl of the Norwegian Institute of Public Health in Norway – set out to determine whether a child’s family structure has any influence on their weight.

To reach their findings, the team analyzed 3,166 children (1,537 girls and 1,629 boys) from 127 schools across Norway. The children had a mean age of 8.3 years and were a part of the 2010 Norwegian Child Growth Study.

Nurses at the children’s schools measured their height, weight and waist circumference to determine whether they were generally overweight or obese, using definitions from the International Obesity Task Force. Abdominal obesity – excessive fat around the stomach or abdomen – was defined by a waist-to-height ratio of 0.5 or more.

The researchers then divided the children into groups based on the marital status of their parents, which included married, never married, cohabiting, single, separated or divorced.

Boys ‘more affected by parental divorce than girls’

Of the children, 19% were generally overweight or obese, and 8.9% were abdominally obese. More girls were generally overweight or obese than boys, but no gender differences were found for abdominal obesity.

Divorce Decree
Children whose parents have divorced may be more likely to be overweight or obese than children whose parents are still married.

Overall, the researchers found that children of parents who divorced were 54% more likely to be generally overweight or obese and 89% more likely to be abdominally obese, compared with children of parents who were still married.

The investigators say these findings remained true even after accounting for other influential factors, such as mother’s education, area of residence and ethnic origin.

The findings were more prominent in boys whose parents were divorced. These boys were 63% more likely to be generally overweight or obese and 104% more likely to be abdominally obese than boys whose parents were married.

A similar pattern was seen in girls, but the researchers claim it was not statistically significant.

Commenting on the findings, the researchers say:

“By focusing on actual societal changes, this study adds valuable background information about potentially vulnerable groups at risk of developing adiposity.”

Although the team does not know exactly why children of divorced parents appear to have a higher risk of being overweight or obese, they hypothesize that divorced parents may spend less time cooking, have a higher reliance on unhealthy convenience foods or have a lower household income.

Furthermore, they note that a divorce may disrupt parent-child relationships. It may cause continuing conflict between parents or result in a house move, meaning the child may have to strike up new relationships.

“Such emotional stress may impact on eating behavior and physical activity level and thus explain the development and maintenance of childhood overweight and obesity,” the researchers say.

When it comes to boys being more affected by parental divorce than girls, the study authors hypothesize that boys may just be more vulnerable.

Results should be ‘interpreted with caution’

However, the team notes that their findings should be “interpreted with caution,” since the number of children with divorced parents was relatively low.

They were also unable to determine how long parents had been divorced, and they could not include children’s lifestyle factors, such diet and exercise regime – information they say would have been beneficial to the study.

In addition, the study is not able to establish cause and effect, the researchers say. They could not determine “whether the development of overweight and obesity was initiated before the divorce or whether the impact on the children’s weight status was primarily attributed to marital conflict or the divorce.”

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Worldwide obesity rates see ‘startling’ increase over past 3 decades

In what is deemed the “most comprehensive global study to date,” researchers have found that over the past 3 decades, there has been a “startling” increase in rates of obesity worldwide, with no significant decline in any country.

A team of international researchers, led by Prof. Emmanuela Gakidou of the Institute for Health Metrics and Evaluation at the University of Washington, recently published their findings in The Lancet.

All over the world, obesity is becoming an increasing concern. The condition can increase the risk of numerous health problems, including high blood pressure, stroke, type 2diabetes and heart disease.

For their study, the team conducted a comprehensive review of surveys, reports and scientific literature looking at overweight and obesity prevalence among adults aged 20 years or older and children ages 2-19 years between 1980 and 2013. Data was drawn from 188 countries over all 21 regions of the world.

Overweight was defined as a body mass index (BMI) of 25 kg/m2 or higher and obese was defined as a BMI of 30 kg/m2 or higher.

Significantly high adult obesity increases in the US

The researchers found that over the past 33 years, worldwide overweight and obesity rates among adults have increased by 27.5%, while such rates among children and adolescents have increased by 47.1%. Collectively, the number of overweight and obese people worldwide has increased from 857 million in 1980 to 2.1 billion in 2013. Of these, 671 million are obese.

The biggest increases in overweight and obesity rates occurred between 1992 and 2002, primarily among adults ages 20-40.

Obese man measuring waist
The researchers found that over the past 33 years, worldwide overweight and obesity rates among adults have increased by 27.5%.

At present, more than half of the obese worldwide population reside in only 10 countries, including the US, China, Russia, Brazil, Mexico, Egypt, Germany, Pakistan and Indonesia.

The team found that 62% of the world’s obese individuals live in developed countries. The US had the highest increases in prevalence of adult obesity – a third of the population are now obese. This is followed by Australia – where 28% of men and 30% of women are obese – and the UK – where around a quarter of the adult population are obese.

Developed countries also saw very high increases in overweight and obesity rates among children. Rates increased from 17% to 24% between 1980 and 2013 among boys, and from 16% to 23% among girls in the same period.

Significantly high rates of overweight and obesity were reached in Tonga, where obesity levels among both men and women are over 50%. More than 50% of women are obese in Kuwait, Libya, Qatar, the Pacific Islands of Kiribati, Federated States of Micronesia and Samoa.

Among men, those living in the US, New Zealand, Bahrain, Kuwait and Saudi Arabia saw the highest increase in obesity levels over the past 3 decades, as did women living in Egypt, Oman, Saudi Arabia, Bahrain and Honduras.

But it is not all bad news. The researchers note that in developed countries, the rate of increase in adult obesity has slowed over the past 8 years. Furthermore, the team says that recent birth cohorts indicate a slower weight gain, compared with previous birth cohorts.

Prof. Gakidou says that unlike other major global health risks, such as smoking, obesity rates are not falling. But he says the statistics do offer some hope:

“Our findings show that increases in the prevalence of obesity have been substantial, widespread, and have arisen over a short time. However, there is some evidence of a plateau in adult obesity rates that provides some hope that the epidemic might have peaked in some developed countries and that populations in other countries might not reach the very high rates of more than 40% reported in some developing countries.”

WHO obesity campaign ‘ambitious and unlikely to be attained’

Last year, members of the World Health Organization (WHO) launched a campaign to stop increases in obesity by 2025. But the research team says that based on these latest findings, this target is “very ambitious and unlikely to be attained.”

The team says that in order to reduce rates of obesity worldwide and reach this target set by WHO, “urgent global leadership” is needed to implement strategies that discourage excessive caloric intake, physical inactivity and promotion of food consumption.

In an editorial linked to the study, Prof. Klim McPherson of Oxford University in the UK agrees. He says:

“An appropriate rebalancing of the primal needs of humans with food availability is essential, which would entail curtailing many aspects of production and marketing for food industries. To prevent unsustainable health consequences, BMI needs to return to what it was 30 years ago.”

The researchers note that there are some limitations to their study. For example, they included surveys that collected self-reported weights and heights. Although they corrected such data as best they could, this may have influenced figures.

They also point out that the statistics are based on BMI, but this measure does account for body variations across different ethnic groups.

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Scientists identify gene that ‘leads to development of bad body fat’

In a new study published in the journal Cell Metabolism, researchers from the Karolinska Institutet in Sweden have identified a gene that they believe is responsible for the development of unhealthy human body fat. The team says the gene could be a risk factor for insulin resistance and type 2 diabetes.

Adipose tissue, commonly known as body fat, is loose connective tissue mainly consisting of fat cells called adipocytes. These fat cells are important for storing and releasing energy in the body.

Humans have two types of body fat; white fat (white adipose tissue) and brown fat (brown adipose tissue). In recent years, brown fat has been deemed the “good” fat. Its main function is to generate body heat. Scientists have found that people of a healthy weight are more likely to have brown fat and, when stimulated through exercise, it can burn calories.

White fat, on the other hand, is believed to be “bad” fat. Those who are overweight or obese tend to accumulate excessive amounts of white fat.

According to the research team, an increase in the size or number of fat cells can lead to an overproduction of white adipose tissue. They note that past research has associated a low number of large fat cells – known as hypertrophy – with development of type 2 diabetes.

In this latest study, the researchers found that a gene called EBF1 may be closely linked to hypertrophy.

Low EBF1 expression ‘promotes hypertrophy and insulin resistance’

To reach their findings, the team collected adipose tissue samples from participants who had either small or large fat cells.

Obese man measuring waist
Researchers say the EBF1 gene may be responsible for the development of white adipose tissue – or “bad fat – in humans.

They found that subjects with large fat cells had much lower EBF1 expression in their adipose tissue, compared with those who had small fat cells. They also had altered lipid movement in their blood and insulin resistance.

Insulin resistance is the inability of the body’s cells to effectively respond to the hormone insulin when blood glucose levels increase, usually after a meal. The team explains that insulin resistance is an important risk factor for diabetes in people who have hypertrophy. Those with insulin resistance tend to have higher circulating glucose and lipid levels in the blood.

To investigate their findings further, the researchers analyzed mice that had been genetically modified to produce lower levels of the EBF1 gene.

The mice developed hypertrophy in their adipose tissue and showed higher lipid movement from fat cells. When the mice were fed a high-fat diet, they also developed insulin resistance.

The researchers found that the EBF1 gene acts a “transcription factor.” It binds to a protein that controls other genes and regulates fat cell formation and metabolic function.

Study co-leader Prof. Peter Arner says the team’s findings may open the doors to new treatments for type 2 diabetes:



“Our findings represent an important step forward in the understanding of how adipose tissue links to the development of metabolic disease.

This is the first time someone has identified a gene that may cause malfunctioning adipose tissue in man. In the future, it might be possible to develop drugs that improve EBF1 function in adipose tissue, which could be used to treat type 2 diabetes.”