Archives for posts with tag: obesity

From New York Times:

Obesity and the form of diabetes linked to it are taking an even worse toll on America’s youths than medical experts had realized. As obesity rates in children have climbed, so has the incidence of Type 2 diabetes, and a new study adds another worry: the disease progresses more rapidly in children than in adults and is harder to treat.

“It’s frightening how severe this metabolic disease is in children,” said Dr. David M. Nathan, an author of the study and director of the diabetes center at Massachusetts General Hospital. “It’s really got a hold on them, and it’s hard to turn around.”

Before the 1990s, this form of diabetes was hardly ever seen in children. It is still uncommon, but experts say any increase in such a serious disease is troubling. There were about 3,600 new cases a year from 2002 to 2005, the latest years for which data is available.

The research is the first large study of Type 2 diabetes in children, “because this didn’t used to exist,” said Dr. Robin Goland, a member of the research team and co-director of the Naomi Berrie Diabetes Center at Columbia University Medical Center in New York. She added, “These are people who are struggling with something that shouldn’t happen in kids who are this young.”

Why the disease is so hard to control in children and teenagers is not known. The researchers said that rapid growth and the intense hormonal changes at puberty might play a part.

The study followed 699 children ages 10 to 17 at medical centers around the country for about four years. It found that the usual oral medicine for Type 2 diabetes stopped working in about half of the patients within a few years, and they had to add daily shots of insulin to control their blood sugar. Researchers said they were shocked by how poorly the oral drugs performed because they work much better in adults.

The results of the study and an editorial were published online on Sunday by The New England Journal of Medicine.

The findings could signal trouble ahead because poorly controlled diabetes significantly increases the risk of heart disease, eye problems, nerve damage, amputations and kidney failure. The longer a person has the disease, the greater the risk. So in theory, people who develop diabetes as children may suffer its complications much earlier in life than previous generations who became diabetic as adults.

“I fear that these children are going to become sick earlier in their lives than we’ve ever seen before,” Dr. Nathan said.

But aggressive treatment can lower the risks.

“You really have to be on top of these kids and individualize therapy for each person,” said Dr. Barbara Linder, a senior adviser for childhood diabetes research at the National Institute of Diabetes and Digestive and Kidney Diseases, which sponsored the new study.

Sara Chernov, 21, a college senior from Great Neck, N.Y., learned that she had Type 2 diabetes when she was 16. Her grandfather had had both legs amputated as a result of the disease, and one of the first questions she asked was when she would lose her legs and her eyesight.

A doctor scolded her for being fat and told her she had to lose weight and could never eat sugar again. She left the office in tears and did not go back; soon after, she joined the study at Columbia. Like many of the children in the program, she did not even know how to swallow a pill.

Ms. Chernov believes that the disease “is not a death sentence,” she said, if she is careful about controlling her blood sugar. But it has been a struggle. Her family tends to be overweight, she sometimes craves sweets and she has orthopedic problems that have required surgery and have made it hard for her to exercise. She is also being treated for high blood pressure.

A few weeks ago, because her blood sugar shot up despite the diabetes pills she was taking, Ms. Chernov began using insulin.

Most of the participants in the study came from low-income families: 42 percent had yearly incomes under $25,000, and 34 percent below $50,000. About 40 percent were Hispanic, 33 percent black, 20 percent white, 6 percent American Indian and less than 2 percent Asian. Poor people and minority groups have some of the highest rates of obesity and diabetes in both adults and children.

Dr. Phil Zeitler, an author of the study and a professor of pediatrics at the University of Colorado, Denver, said many participants lived with a single parent or guardian and, like Ms. Chernov, came from families with a history of diabetes and had relatives with kidney failure or amputations.

“They’re wrapped up in a lot of family chaos,” Dr. Zeitler said, calling them a “challenging population” with a lot of stress in their lives, on top of the normal chaos of the teenage years.

Type 2 diabetes used to be so rare in children that it was called adult-onset diabetes. Type 1, a much less common form, was most likely to strike children and teenagers, and was called juvenile diabetes. Both forms of the disease cause high blood sugar, but their underlying causes are different.

Type 1 occurs because the patient’s own immune system mistakenly destroys the cells in the pancreas that make insulin, a hormone needed to control blood sugar levels. Patients have to take insulin.

Type 2 is thought to be brought on by obesity and inactivity in people who have a genetic predisposition to develop the disease when they gain weight. And they may also have an inborn tendency to put on weight. The pancreas still makes insulin, though not enough, and the body does not use insulin properly — a condition called insulin resistance. High blood pressure and cholesterol often come with the disease. Initial treatments include dietary changes, exercise and oral medicines, but many people eventually need insulin.

Doctors began noticing an alarming increase in Type 2 cases in children in the 1990s, especially among blacks and Hispanics from poorer families. The problem had started even earlier in American Indians, who have had sharp increases in obesity in recent years.

More.

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From CHE Blog (post by Sarah Howard):

The UK nonprofit organization CHEM Trust (Chemicals, Health and Environment Monitoring Trust) just released a report on the links between chemicals and diabetes/obesity. Studies published in recent years provide compelling evidence that human chemical contamination can play a part in both conditions. The report concludes that the chemicals that we accumulate throughout life, via our everyday lifestyles, is likely to contribute to these modern epidemics. This is the same conclusion reached by the National Toxicology Program’s review of the scientific evidence on chemicals and diabetes/obesity, published last month.

The CHEM Trust report, entitled Review of the Science Linking Chemical Exposures to the Human Risk of Obesity and Diabetes, is written by two of the world’s leading experts: Professor Miquel Porta, MD, MPH, PhD, of Spain and Professor Duk-Hee Lee, MD, PhD, of South Korea.

The report focuses on endocrine disrupting chemicals in both obesity and diabetes. Exposures to these chemicals in the womb, at other critical periods of life, and in adulthood may be linked to obesity and disruption of the normal functioning of insulin in later life. Evidence of the role of hormone disrupting chemicals comes from both laboratory studies and studies on human populations.

In one example, the report describes a study from the general US population that found that persistent organic pollutants (POPs) in fatty tissue, even more than the fat itself, plays a critical role in the development of diabetes. People who were obese did not have an increased risk of diabetes if their levels of POPs were low. People who were thin did have a higher risk of diabetes if their POP levels were higher. And those with higher POP levels who were also obese had the highest diabetes risk of all.

The chemicals suspected of increasing weight gain or diabetes in humans include a variety of chemicals, including numerous POPs, arsenic, BPA, phthalates, pesticides (including atrazine, organophosphorous and organochlorine pesticides), brominated flame retardants, metals (including cadmium, mercury, organotins), and more. Many of these are endocrine disrupting chemicals (EDCs), and have the ability to disrupt our natural hormones which control both fat storage and blood sugar regulation, and hence can play a role in obesity and diabetes.

Professor Miquel Porta stated, “The epidemics in obesity and diabetes are extremely worrying. The role of hormone disrupting chemicals in this must be addressed. The number of such chemicals that contaminate humans is considerable. We must encourage new policies that help minimize human exposure to all relevant hormone disruptors, especially women planning pregnancy, as it appears to be the fetus developing in utero that is at greatest risk.

Elizabeth Salter Green, CHEM Trust Director stated, “If exposure to hormone disrupting chemicals is programming us to be fat, it is high time that public health policy takes into account cutting edge science. Obesity and diabetes are examples of the adverse health trends linked with endocrine disruption which need to be urgently addressed. We are talking about prevention, and in this time of financial squeeze, anything that can help with prevention is a good idea. CHEM Trust is calling for the UK Government and the EU to urgently identify hormone disruptors to ensure that chemicals suspected of playing a role in diabetes and obesity are substituted with safer alternatives.”

Summary of the report’s conclusions

  • Studies suggest that exposure to certain chemicals in the environment can play an important role in obesity and diabetes. The chemicals implicated include some to which the general population are exposed on a daily basis.
  • Substantial evidence exists to consider exposure to EDCs with estrogenic activity as a risk factor for the etiology of obesity and obesity-related metabolic dysfunction.
  • Evidence suggesting a relationship between human contamination with environmental chemicals and the risk of diabetes has existed for more than 15 years, with the volume and strength of evidence becoming particularly persuasive since 2006.
  • Obesity is a known risk factor for diabetes, and chemicals that accumulate in body fat (e.g., POPs) may play a role in the causal relationship between obesity and diabetes.
  • Many of the chemicals that can cause weight gain and related metabolic effects have endocrine disrupting properties.
  • Embryonic, fetal, and infantile stages may be especially vulnerable to obesity from relatively low doses of EDCs. Nonetheless, the risk of obesity due to obesogenic pollutants can also increase during adolescence and adulthood.

Summary of the report’s recommendations

  • Action to reduce exposures to such chemicals is warranted on a precautionary basis, and is likely to be cost-effective.
  • National governments and the EU need to urgently put forward mechanisms to identify EDCs to ensure that currently used chemicals suspected of playing a role in obesity and diabetes are substituted with safer alternatives.
  • Health professionals, citizens’ organisations, companies, authorities and society at large need to be better informed of the role that chemical exposures may play in causing diabetes and obesity.
  • Individuals, industry, the agricultural sector, dieticians and the medical professions all have roles to play in reducing exposures both in the home and in occupational settings.
  • Personal changes in lifestyle are certainly important for the prevention of obesity and diabetes, but this should not obscure the need for government policies within and outside the health sector to decrease human exposure to obesogenic and diabetogenic environmental compounds.
  • As many of the chemicals implicated widely contaminate the animal and human food chains and some are also released from some food containers, dietary interventions ignoring the presence of contaminants in food may hamper the expected beneficial effects of dietary recommendations.
  • In order to protect fetuses and newborn babies, specific advice is needed for pregnant women and midwives regarding EDCs in the diet and in consumer products used by pregnant women and/or babies.
  • Public health policies, including those seeking to reduce exposure to suspect chemicals, need to be implemented swiftly. To preserve quality of life, prevention in both cases is vastly preferable to treatment.
  • Evidence for the association between exposure to EDCs and obesity should lead to a paradigm shift in how to tackle obesity. The focus should be broadened from one based on individual lifestyle, diagnosis and treatment to one that includes population prevention measures.
  • Population-based biomonitoring must be strengthened to provide a better understanding of the extent of human contamination by environmental obesogens and diabetogens in the general population.
  • Progress is also needed in identifying the sources of exposure (e.g., which food products, which consumer products). Further research is particularly warranted on the role that food additives, contaminants in animal feed and human food, and packaging may play in obesity and diabetes.
  • Screens and tests to identify chemicals that can impact on obesity and diabetes should be developed, and certain chemicals should be required to undergo such testing.
  • More attention should be given to protecting populations in the developing world from exposure to environmental pollutants, including that arising from electronic waste, food contamination, air pollution and the erroneous use of certain pesticides.

CHEM Trust’s goal is to protect humans and wildlife from harmful chemicals. They have published previous reports on chemicals and the developing brain, breast cancer, reproductive health, and more.

This report as well as others are available at the CHEM Trust website.

Visit the CHE Blog.

From The Independent:

Man-made chemicals present in homes, schools, offices, cars and food are probably contributing to the sharp rise in obesity and diabetes in western societies, according to a review of scientific literature published today.

Until now lifestyle factors such as lack of exercise and poor diet were believed to be the primary causes of the increased incidence of both conditions, whose proliferation has strained global health budgets.

While these remain undisputed factors, the review of 240 scientific papers by two leading experts, Professor Miquel Porta of Spain and Professor Duk-Hee Lee of South Korea, suggests chemicals in plastics and other surfaces play an important and avoidable role.

Their study assessed the impact of chemicals including the now banned PCBs, the plastic-softeners phthalates, and the plastic-hardener Bisphenol A, or BPA, a common substance in food packaging and plastic bottles which The Independent has written widely about. All 240 studies they reviewed – whether in test-tubes, on animals or on humans – had been peer-reviewed and published in scientific journals.

The paper, the Review of the Science Linking Chemical Exposures to the Human Risk of Obesity and Diabetes, found some of the chemicals appeared to have a causal effect on obesity, some on diabetes and some on both.

Many are endocrine disruptors, which can change human hormones, including the stimulation of appetite and fat storage and regulation of sugar.

* * *

One of the study authors, Professor Miquel Porta, of the Hospital del Mar Research Institute, Barcelona, said: “The epidemics in obesity and diabetes are extremely worrying.

“The role of hormone disrupting chemicals in this must be addressed. The number of such chemicals that contaminate humans is considerable.

“We must encourage new policies that help minimise human exposure to all relevant hormone disruptors, especially women planning pregnancy, as it appears to be the foetus developing in utero that is at greatest risk”.

* * *

BPA is commonly found in the plastic lining inside tinned foods, on thermal till receipts and in consumer electronics such as mobile phones and televisions, while phthalates are present in vinyl flooring, shower curtains and children’s toys.

CHEM Trust (Chemicals Health & Environment Monitoring Trust), the British pressure group which commissioned the research, urged the UK Government and the EU to press industry to find safer alternatives.

Elizabeth Salter Green, director of CHEM Trust, said: “If exposure to hormone disrupting chemicals is programming us to be fat, it is high time that public health policy takes into account cutting edge science. Obesity and diabetes are examples of the adverse health trends linked with endocrine disruption which need to be urgently addressed.

“We are talking about prevention, not cure here, and in this time of financial squeeze, anything that can help with prevention, reducing NHS spending, is a good idea.”

More.

AIRS THIS THURSDAY, JAN 12

We’re fat. Really fat. Almost 60% of Canadians are now either overweight or obese, and that figure is expected to climb even higher. But what if we have an excuse?

In Programmed to be Fat?, we explore controversial new science that suggests being overweight is not just the result of too much food, too little exercise, and genetics.  Exposure to environmental chemicals such as Bisphenol A, pesticides and herbicides during fetal development may be changing our physiology forever. That, say some scientists, could explain the alarming statistics on obesity – like the fact that the number of overweight infants rose 74% in just twenty years.  Scientists are now moving beyond their mice and rat studies, to test the theory in people.  In Programmed to Be Fat?, we will get the skinny on the science of fat.

Premiering January 12, 2012 on CBC TV’s “The Nature of Things” with David Suzuki.

Directed by Bruce Mohun, written by Bruce Mohun and Helen Slinger, produced by Sue Ridout, Helen Slinger and Sara Darling.

Preview below:

From

Mount Sinai’s Dr. Landrigan discusses how obesity has become an epidemic within the United States. The rates of obesity have tripled since the 1970s, and this has led to a significant increase in type 1 and type 2 diabetes as obese children are at a much higher risk of developing diabetes.

Dr. Landrigan also provides tips on how to prevent obesity and the diabetes that commonly follows obesity. Studies are being conducted at the Children’s Environmental Health Center to determine whether there is a link between common chemicals and obesity.

To view Mount Sinai’s Children’s Health Campaign containing tips, facts, videos, articles and more on important children’s health issues such as diabetes, autism, asthma, allergies and nutrition, click here.

To view the Children’s Environmental Health Center, click here.

From The Collaborative on Health and the Environment:

DATE: Wednesday, December 14, 2011, 9:00 am Alaska Time/ 10:00 am Pacific/ 1:00 pm Eastern

RSVP: To join this free call and receive the dial-up instructions, please RSVP to Alaska Community Action on Toxics at diana@akaction.org or (907) 222-7714.

Emerging scientific studies suggest environmental chemicals may be contributing factors to the epidemics of diabetes and obesity. Can a fetus’ exposure to toxic chemicals in the womb cause obesity or diabetes at age 5, 15, or 25? Is part of the obesity epidemic in the U.S. linked to chemical exposures that occur in childhood? A growing number of researchers are exploring how chemicals used in plastics, food packaging, pesticides and cosmetics can corrupt normal function of metabolic hormones and trigger dramatic increases in body fat. Guest speakers Bruce Blumberg, PhD and David O. Carpenter, M.D. will discuss the cutting-edge science linking chemical exposures to the growing epidemics of diabetes and obesity.

Featured speakers include:

Bruce Blumberg, Ph.D., Professor in the Departments of Developmental and Cell Biology, Pharmaceutical Sciences, and Biomedical Engineering at University of California, Irvine. Bruce Blumberg received his Ph.D. from the University of California, Los Angeles in 1987. His postdoctoral training was in the molecular embryology of vertebrate development at the Department of Biological Chemistry in the UCLA Medical School. Dr. Blumberg’s current research at the Blumberg Laboratory at UC Irvine focuses on the role of nuclear hormone receptors in development, physiology and disease. Particular interests include patterning of the vertebrate nervous system, the differential effects of xenobiotic exposure on laboratory model organisms compared with humans, interactions between xenobiotic metabolism, inflammation, and cancer, and the role of environmental chemicals on the development of obesity and diabetes.

David O. Carpenter, M.D., director of the Institute for Health and the Environment at the University at Albany and Professor of Environmental Health Sciences at UAlbany’s School of Public Health. Dr. Carpenter previously served as director of the Wadsworth Laboratory of the New York State Department of Health.  He received his doctorate from Harvard Medical School and has hundreds of publications to his credit. Dr. Carpenter’s area of expertise is human health effects of environmental contaminants, including metals and organic compounds.

From Harvard Gazette:

Every day, the government’s food stamp program buys Americans 20 million servings of soda, paying billions for a program that fosters the obesity that the government then has to pay again for in increased health care expenditures.

“That is arguably the single largest contributor to obesity,” said David Ludwig, a pediatrics professor at Harvard Medical School (HMS) and Harvard-affiliated Children’s Hospital Boston and professor of nutrition at the Harvard School of Public Health (HSPH). “It makes no sense … especially when we might wind up paying for that as a society in obesity and diabetes.”

The food stamp program was front and center on campus and on the Internet Thursday during a session of The Forum at Harvard School of Public Health, which regularly brings experts together to discuss important issues in the field. The session examined reforms needed in the federal government’s farm bill to improve public health. The farm bill, expected to come up for discussion in Congress in 2012, is the federal government’s major agriculture subsidy program.

Participants included Ludwig; Walter Willett, Fredrick John Stare Professor of Epidemiology and Nutrition and chair of the HSPH Department of Nutrition; Barry Popkin, a professor of nutrition and of economics at the University of North Carolina; and Gary Williams, a professor of agricultural economics at Texas A&M University. The event was moderated by former Washington Post health editor Abigail Trafford.

Several panelists blamed U.S. agricultural policy over the past four decades for creating a food system where healthier fruits and vegetables are relatively expensive while high-starch, processed foods and red meats are cheap and widely available. The first farm bill was passed in the 1930s as a way to help the nation’s struggling agricultural sector, which at the time not only fed the country but, in a more rural America, also provided many jobs.

With ensuing technological changes in the years after World War II, the United States ramped up its subsidies, steering production toward what at the time was thought to be a healthy diet of starches and meat. Popkin said the program worked well, as illustrated by statistics showing the prices of those staples came down in the ensuing decades, while those left alone by government policy — fruits and vegetables — became more expensive.

“What is cheap today is what we made cheap. What we ignored, we made more expensive,” Popkin said.

The problem, Willett said, is that we now know that a healthy diet is not dominated by processed starches and red meat, but is just the opposite. A healthy diet is composed of whole grains, nuts, beans, fruits, and vegetables, with red meat in moderation and very little refined starches and added sugar. The result is that today two-thirds of Americans are overweight or even obese, diabetes is rising across the country, and in some parts of the country, life expectancy is actually dropping.

“If we judge by its impact on human health, the American food supply is a disaster,” Willett said. “We’re not using the levers we potentially have to make an impact.”

Williams, however, said it is wrong to blame the farmers for doing what was asked of them by the government. In addition, he said, there is a lot that is right with the American food supply, which made food plentiful and inexpensive.

Williams pointed out that subsidies to farmers make up just 15 percent of the farm bill’s expenditures and, given the nation’s budget problems, farmers are bracing to see those subsidies cut. The lion’s share of expenditures in the bill go toward providing food for America’s poor through what was formerly the food stamp program, and is now the Supplemental Nutrition Assistance Program (SNAP).

Panelists decried the lack of limits on the kinds of food that SNAP can fund, citing the U.S. Department of Agriculture’s rejection of New York City Mayor Michael Bloomberg’s request that purchase of sugar sweetened beverages be banned from the city’s SNAP program.

Panelists said there is an opportunity to change the incentives in the system to emphasize healthy eating, and they suggested separating the food assistance from the farm assistance portions of the bill in order to treat the two issues separately. They cited the federal government’s Women, Infants, and Children (WIC) program as a successful example of federal food aid. Poor mothers can get food assistance through WIC, but the program includes healthy foods, such as fruits and vegetables, along with nutritional education.

Other issues discussed by the panel include the school lunch program, whose menu was described by one panelist as largely junk food, and food marketing to children, a major focus of food manufacturers — and something Ludwig recommended banning. Ludwig told of seeing a 200-pound, 8-year-old girl in his clinical practice who was pre-diabetic and who insisted her mother buy food branded after iCarly, a popular children’s show.

“Busy working parents are undermined by this massive marketing campaign,” Ludwig said. “The industry knows that parents are going to cave.”

More.

From Reuters:

Adding to the mixed bag of research on bisphenol A and diabetes, a new study suggests that people with higher urinary levels of the controversial chemical do have a higher risk of diabetes.

Bisphenol A — better known as BPA — is a so-called endocrine disruptor, which means it may affect normal hormone activity in the body.

It’s also all around us. BPA has been used for decades to make hard plastic containers, as well as linings for metal food and drink cans. Research suggests that most people have some amount of BPA in their blood, including about 95 percent of Americans.

Recent animal studies have hinted that the chemical could play a role in certain cancers, heart disease and abnormal brain development in children. But BPA’s true effects in humans remain unknown.

Two large studies have found a link between higher BPA levels and higher heart disease risk. And a 2008 study found that of Americans in a government health survey, those with higher BPA levels showed a higher diabetes risk.

None of that, however, proves cause-and-effect. And a recent study of Chinese adults found no link between BPA levels and diabetes risk.

This latest study is based on data from a federal health study done between 2003 and 2008. Researchers found that of nearly 4,000 U.S. adults involved, those with the highest urinary BPA levels were more likely to have diabetes.

Just under 12 percent of all study participants had diabetes, based on blood sugar tests. And the odds of having the disease rose as urinary BPA increased.

Of people with the highest levels (more than 4.2 nanograms per milliliter, ng/mL), almost 13 percent had diabetes, versus 8 percent of adults with the lowest BPA levels (less than 1.1 ng/mL)

For comparison, the typical urinary BPA level among Americans has stood at about 2 ng/mL in recent years.

The findings, reported in the Journal of Clinical Endocrinology & Metabolism, do not prove that BPA is responsible for the higher diabetes risk.

“Since BPA measurements as well as diabetes diagnosis were conducted at the same time, we cannot say for sure that BPA exposure preceded diabetes development,” lead researcher Dr. Anoop Shankar, of the West Virginia University School of Medicine, said in an email.

The researchers did account for a number of other factors in diabetes risk — like body weight, age and race. And the BPA-diabetes link still held; people with the highest levels had a 68 percent greater risk of diabetes than those with the lowest levels.

But what’s needed, according to Shankar, are long-term studies that start with diabetes-free adults, measure their BPA levels, then see who develops diabetes over time.

Shankar said he and his colleagues are planning such a study.

More.

Image from Flickr.

From Forbes:

The debate over air pollution and, more specifically, the regulation of air pollution, raged on this week as the Environmental Protection Agency (EPA) watered down its cross-state pollution rule and House Republicans moved to delay new rules on toxic air pollution from cement plants, solid waste incinerators, and industrial boilers.  These latest debates come on the heels of President Obama’s move last monthto reneg on promises to tighten up smog standards, a decision that angered environmentalists and led to speculation that EPA Administrator Lisa Jackson might be ready to walk. In all cases, the argument against regulation goes something like this: The last thing a down economy needs is new regulation, and the EPA is overstepping its boundaries.

These arguments center largely around the idea that current air pollution regulation is good enough as-is, and that any further restrictions are aimed at tackling environmental issues and climate change, both typically seen as luxuries in a down economy. But research is continuing to pile up in support of the claim that not only are current air pollution regulations inadequate, but that air pollution is very much a public health issue.

When viewed through the public health lens, the economic arguments against regulation of air pollution begin to unravel, particularly in the face of rising healthcare costs. Consider, for example, a spate of new studies that have found a rather convincing correlation between the presence of small particulate matter (PM2.5, the ultrafine particles blown into the air by road traffic, coal-fired power plants, industrial manufacturing, and residential wood fuel combustion) and both obesity and diabetes.

Medical research has long supported the fact that exposure to ultrafine particulate matter increases the risk of various respiratory, cardiovascular, and pulmonary illnesses. Incidences of asthma, heart attacks, and chronic bronchitis are all higher in areas where the concentration of ultrafine particulate matter is higher. The correlation between particulate matter and these health issues is particularly pronounced in children, as well as low-income communities, which are often located closer to the sources of particulate matter (highways, factories, power plants) than their higher income neighbors.

Over the past decade, new studies have emerged that link air pollution to two of this country’s most pressing (and expensive) health epidemics: obesity and type II diabetes. Both are not only on the rise in terms of diagnoses, but also in terms of the costs associated with treatment. According to a January 2011 study by the Society of Actuaries, the current cost of the obesity epidemic in the United States is $270 billion a year.  The American Diabetes Association puts the current cost of dealing with diabetes (over 90 percent of U.S. diabetes cases are type II) at $174 billion. According to the Center for Disease Control, asthma is a leading cause of school absenteeism in the United States, and the cost of treating asthma in children 18 and under alone is $3.2 billion per year. Meanwhile, financial analysts estimate the cost of tightened air pollution regulations at $130 billion. Granted, these are not budget line items that are easily swapped in for each other, but a tie-in to obesity and diabetes may just make tackling air pollution more economically viable.

Of course, no one is saying, “hey, forget about diet and exercise, just take care of air pollution!” Nonetheless, even after controlling for factors such as genetics, income levels, weight, diet and exercise, Harvard researchers found a “consistent and significant” relationship between Type II diabetes prevalence and exposure to ultrafine particulate matter in a recent study.

More.

From Leadership:

Why are some people predisposed to being anxious, overweight or asthmatic? Why are some of us prone to heart attacks, diabetes or high blood pressure? You may say it’s our genes. Or our childhood experiences: How we were treated especially during those crucial first three years. Or maybe our well-being stem from lifestyle choices we make as adults, like our diet and how much exercise we get.

But what about your life in the womb? The nutrition you received; the pollutants, medicines and infections you were exposed to; your mother’s health, stress and state of mind while she was pregnant with you – pioneers in the controversial field of fetal origins say these factors shaped you as a baby – and for the rest of your life.

They assert the nine months in the womb permanently influence the wiring of the brain, the functioning of organs such as the heart, liver and pancreas, how prone we are to disease, our appetite and metabolism, our intelligence and temperament.

Much of what a pregnant woman encounters in her daily life – the air she breathes, the food and drink she consumes, the chemicals she’s exposed to, even the emotions she feels – are shared with her fetus. It incorporates these into its own body, making them part of its flesh and blood.

Research on fetal origins, also called the developmental origins of health and disease, is prompting revolutionary shifts in thinking about where human qualities come from and when they develop.

* * *

Two decades ago, a British doctor named David Barker noticed an odd . pattern on a map: The poorest regions  of England and Wales had the highest rates of heart disease. But heart disease was supposed to be due to a sedentary lifestyle and rich food?
After comparing the health of 15,000 adults with their birth weights, he discovered an unexpected link between small birth size, often an indication of poor prenatal nutrition, and heart disease in middle age.

Dr Barker theorized that when a fetus does not get enough nutrition, it diverts nutrients to the brain, while skimping on other parts of its body. This shows up in later life as a weaker heart.

When he presented his findings to colleagues, he was mocked. “Heart disease was supposed to be all about
genetics or adult lifestyle,” says Dr Barker, now 72, and a professor at the University of Southampton in  England and at Oregon Health and Science University. “People scoffed at the idea that it could have anything to do with intrauterine experience.”
For years, the idea was just known as the Barker hypothesis. But in time, it began to win converts. Dr Janet Rich-Edwards, an epidemiologist at Brigham and Women’s Hospital in Boston analysed findings from the Nurses’ Health Study, a long-running investigation of more than 120,000 nurses in the US.

* * *

The good news is that fetal researchers are also finding out that life in the womb can make things go better for your child in later life.

* * *

Take your weight. Two studies by researchers at Harvard Medical School suggest your mother’s weight affects  yours. One study found that the more weight a woman gains during pregnancy, the more likely her child is to be overweight by age three.

* * *

“The bodies of the children conceived after their mothers had weight-loss surgery process fats and carbohydrates in a healthier way than the bodies of their brothers and sisters  who were conceived at a time when their mothers were still overweight,” says John Kral, a professor of surgery and medicine and a co-author of both papers.

“It may be the intrauterine or womb environment is more important than genes or shared eating habits in passing on a tendency to be obese,” says Professor Kral. If that’s so, helping women maintain a healthy weight during pregnancy may be the best hope for stopping obesity before it starts.

* * *

How does air pollution affect a baby in the womb? More than 30 years ago, [Upstream Contributor] Dr. Frederica Perera, the director of the Center for Children’s Environmental Health at Columbia University, was researching air pollution and cancer in adults. “I was looking for control subjects to compare to adults. I wanted individuals completely untouched by pollution,” she says.

She decided to use babies just out of the womb as her controls. So she sent samples of umbilical-cord blood and placental tissue to a laboratory to be analysed. When she got the results back, “I was shocked. These samples already had evidence of contamination.”

More.

From Los Angeles Times:

We’ve all heard that the overuse of antibiotics is making them less effective and fueling the rise of dangerous drug-resistant bacteria. But did you know it may also be fueling the rise of obesity, diabetes, allergies and asthma?

So says Dr. Martin Blaser, microbiologist and infectious disease specialist at New York University Langone Medical Center who studies the myriad bacteria that live on and in our bodies. He explains his theory in a commentary published in Thursday’s edition of the journal Nature.

In recent years, scientists have developed a growing appreciation for the “microbiome,” the collection of mostly useful bacteria that help us digest food, metabolize key nutrients and ward off invading pathogens. Investigators have cataloged thousands of these organisms through the National Institutes of Health’s Human Microbiome Project, begun in 2008.

Blaser is interested in why so many bacteria have colonized the human body for so long – the simple fact that they have strongly suggests that they serve some useful purpose. But these bacteria have come under attack in the last 80 or so years thanks to the development of antibiotics. The drugs certainly deserve some of the credit for extending the U.S. lifespan, Blaser notes – a baby born today can expect to live 78 years, 15 years longer than a baby born in 1940. But in many respects, an antibiotic targets a particular disease the way a nuclear bomb targets a criminal, causing much collateral damage to things you’d rather not destroy.

“Antibiotics kill the bacteria we do want, as well as those we don’t,” Blaser writes. “Sometimes, our friendly flora never fully recover.”

And that can leave us more susceptible to various kinds of diseases, especially considering that the typical American is exposed to 10 to 20 antibiotics during childhood alone. Blaser points out that the rise (let along overuse) of antibiotics coincides with dramatic increases in the prevalence of allergies, asthma, Type 1 diabetes, obesity and inflammatory bowel disease. That isn’t proof that the two are related, but it’s a question worth exploring, he says.

Take the case of Helicobacter pylori. As Blaser explains, this bacterium was “the dominant microbe in the stomachs of almost all people” in the early 1900s. But 100 years later, it is found in less than 6% of American, Swedish and German kids. One likely reason is that a single course of amoxicillin or another antibiotic to treat an ear or respiratory infection can wipe out H. pylori 20% to 50% of the time.

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From Montreal Gazette:

People with relatively high levels of certain pesticides in their blood may have an increased risk of Type 2 diabetes — particularly if they are overweight, a new study suggests.

The study, reported in the journal Diabetes Care, is not the first to link chemical pollutants to diabetes.

A number of studies have found a connection between diabetes risk and exposure to older pesticides known as organochlorines, PCBs and other chemicals that fall into the category of “persistent organic pollutants.”

Organochlorines are now banned or restricted in the U.S. and other developed countries, after research linked them to cancer and other potential health risks. PCBs, which were once used in everything from appliances to fluorescent lighting to insecticides, were banned in the 1970s.

However, as the name suggests, persistent organic pollutants remain in the environment for years and build up in animal and human body fat.

In the U.S., diet is the main potential source of exposure, according to the Centers for Disease Control and Prevention (CDC) — with fatty foods, like dairy products and oily fish, topping the list.

Lab research has suggested that some persistent organic pollutants impair the body’s ability to regulate blood sugar, which could help explain the link to Type 2 diabetes.

Some of the compounds also have been shown to promote obesity, which is itself a major risk factor for diabetes, noted Riikka Airaksinen of Finland’s National Institute for Health and Welfare, who led the new study.

For the study, Airaksinen’s team measured blood levels of several persistent organic pollutants in about 2,000 older adults.

Just over 15 per cent had Type 2 diabetes. The risk was higher, the researchers found, among people with the highest levels of organochlorine pesticides.

Those with levels in the top 10 per cent were about twice as likely to have diabetes as their counterparts in the bottom 10 per cent.

But the link appeared to be limited to people who were overweight or obese.

That, the researchers write, suggests that the pollutants and body fat “may have a synergistic effect on the risk of Type 2 diabetes.”

The results alone do not prove that organochlorine pesticides were the reason for the higher diabetes risk, Airaksinen told Reuters Health in an email.

The researchers accounted for participants’ age, sex, waist size and blood pressure levels. But they had no information on things like diet and exercise habits — which might help explain the pesticide-diabetes link.

But the overall body of research, according to Airaksinen, is pointing toward a cause-and-effect relationship.

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From UCTelevision:

Robert H. Lustig, MD, UCSF Professor of Pediatrics in the Division of Endocrinology, explores the damage caused by sugary foods. He argues that fructose (too much) and fiber (not enough) appear to be cornerstones of the obesity epidemic through their effects on insulin.

From The Globe and Mail:

In the 1980s, back when obesity and diabetes were considered problems, not plagues, a British researcher dished up a wild idea to explain the diet-related ills of the world.

While studying the causes of death for England and Wales, David Barker, an epidemiologist with the University of Southampton, stumbled upon the fact that, in the 1970s, deaths due to heart disease were highest in poor regions that 60 years earlier also had the highest rates of infant mortality.

Prof. Barker considered that curious, since coronary disease was thought to be the result of rich living. He went on to trace the fate of 15,000 people born before 1930 in the English county of Hertfordshire and discovered that those with the lowest birth weights, presumably because their mothers were malnourished, again had the greatest risk of heart disease.

Prof. Barker, who published his initial findings in The Lancet in 1986, eventually came to the conclusion that a mother’s nutrition can shape the metabolic future of her baby – affecting the child’s lifelong risks for heart disease and all the health problems related to it.

At the time, the idea seemed almost absurd. The prevailing view held that susceptibility to disease was something chiselled into your genes from prehistoric times, not dictated by a pregnant woman’s diet. The theory of the thrifty gene ruled the day, with the idea that former hunter-gatherer populations faced steady pressures of feast and famine that gave them fat-storing genes to survive the lean times – thrifty genes that made their descendants, aboriginal people in particular, obese and diabetic in the modern world.

But 25 years on, science, and society, have evolved.

With failed efforts to find a thrifty gene, or any genetic explanation for the rapid global rise in obesity and diabetes, Prof. Barker’s hypothesis, better known today as the developmental origins theory, has emerged as a leading explanation. It’s also a more attractive one: If correct, it suggests that something can be done to turn the tide.

Rewriting nature’s script

Support for the developmental origins idea has grown alongside epigenetics, a budding branch of biology that is forcing a radical rethinking of genetic science as it reveals how the environment can alter DNA.

Dramatic experiments have shown that even small environmental changes can have a powerful, and permanent, impact on the way genes work: Tweaking the diets of pregnant rats, pigs, guinea pigs, rabbits and sheep can induce obesity and a range of other metabolic ills among the offspring. In one case, it changed the colour of a mouse.

The implication is that DNA may be the script that nature provides, but nurturing determines how that script will be performed – and, according to the origins theory, rehearsals begin in the womb.

“It’s almost a sensing system of what’s going on in the environment, so that a fetus can adapt,” says Rosanna Weksberg, an epigenetics researcher at Toronto’s Hospital for Sick Children. Problems can arise when the world outside the womb is dramatically different – “there’s an epigenetic memory of nutrition.”

Growing in a woman who is malnourished – either from eating too little or receiving too few nutrients – primes the fetal DNA to hoard every calorie available, only to be vulnerable to obesity and diabetes in a postnatal world of caloric overload. At the end of the Second World War, for instance, children born to women pregnant during the Dutch “hunger winter” proved susceptible to diabetes, obesity, heart disease and other health problems.

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From The Boston Channel:

With two-thirds of Americans now overweight or obese, new research suggests there may be more to it than poor diet and not enough exercise. Hidden chemicals, called obesogens, are the building blocks of everyday household items.

Researchers say they’re wreaking havoc on our bodies by disrupting our hormonal systems, which affect fat cells and gene function.

“Certain cells that would normally differentiate into cells that would develop into, say, muscle tissue, or connective tissue, would change and develop into fat tissue or fat cells,” said Dr. Theresa Piotrowski, medical director of Lahey Clinic’s Medical and Surgical Weight Loss Center.Obesogens include now infamous bisphenol-A, or BPA, phthalates, which are synthetic chemicals found in plastics, and Perfluorooctanoic acid, or PFOA, which is found in non-stick and stain resistant products. Obesogens are also found in plastic shower curtains, canned goods and cosmetics.

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