Archives for posts with tag: diabetes

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.

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 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 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.

More.

From Environmental Health News:

After his first child was born, black and blue marks started showing up on Stanley Finger’s body. Jolted awake most nights by his crying infant, Finger would stumble half asleep toward her room, bumping into walls and furniture in the dark. “My wife and I would joke about it,” says Finger, a chemical engineer from Bluffton, South Carolina. But during a routine checkup, Finger learned his easy bruising was caused by a precipitous drop in blood platelets. The body relies on these cell fragments for clotting, and Finger’s platelet count had dropped to nearly a third its normal value. After ruling out cancer and other illnesses, Finger’s doctor eventually arrived at a diagnosis:  .

ITP is an autoimmune disease, a condition that occurs when the immune system attacks the body’s own cells and tissues. When Finger was diagnosed in 1974, autoimmune illnesses weren’t yet perceived as the public health menaces they’re often seen as today. But according to Fred Miller, director of the Environmental Autoimmunity Group at the National Institute of Environmental Health Sciences, autoimmune diseases are now recognized as among the leading causes of death among young and middle-aged women in the United States.

What’s more, prevalence rates for some of these illnesses are rising for what Miller says must largely be environmental reasons. “Our gene sequences aren’t changing fast enough to account for the increases,” Miller

says. “Yet our environment is—we’ve got 80,000 chemicals approved for use in commerce, but we know very little about their immune effects. Our lifestyles are also different than they were a few decades ago, and we’re eating more processed food.” Should prevalence rates for heart disease and cancer continue their decline, Miller says, autoimmune diseases could become some of the costliest and most burdensome illnesses in the United States.

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From Reuters:

Evidence strongly suggests that some chemicals, especially chemicals in cigarette smoke, might cause some cases of diabetes and obesity, U.S. government researchers said on Thursday.

A committee appointed by the National Toxicology Program went through studies looking at links between diabetes and obesity and chemicals such as arsenic, chemicals found in plastic, pesticides and cigarette smoke.

“Some of these associations are pretty strong,” said Michael Gallo of the University of Medicine & Dentistry of New Jersey, who led a two-day workshop in North Carolina that ended on Thursday.

Especially strong was the link between smoking while pregnant and a child’s later risk of becoming obese and developing type-2 diabetes. “It is consistent with our understanding of how diabetes and obesity develop,” Gallo told reporters in a telephone briefing.

When a pregnant woman smokes, the baby is often underweight at birth. This can set up a chain of mechanisms that lead to obesity later, which in turn can cause type-2 diabetes.

Gallo and others stressed that at least 70 percent of cases of obesity and diabetes are caused directly by eating poorly and exercising too little. But some cases of diabetes, especially in fit, lean people, are harder to explain.

More . . .

From IATPvideo:

Dr. John Peterson Myers, CEO of Environmental Health Sciences and co-author of Our Stolen Future, talks about environmental chemicals and public health.

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