Air Pollution and Weight Gain, Insulin Resistance and Metabolic Syndrome: Recent Findings

written by Sarah Howard
Coordinator of the Diabetes-Obesity Spectrum Working Group

Two studies published this month provided strong support for the idea that air pollution may cause weight gain, insulin resistance, and metabolic syndrome.

In the first study, pregnant rats exposed to Beijing’s air gained significantly more weight during pregnancy than those breathing filtered air. Their offspring (exposed pre- and postnatally) were also significantly heavier at 8 weeks of age.

In the second study, Mexican Americans living in Southern California exposed to ambient air pollutants had lower glucose tolerance, higher insulin resistance, and adverse blood lipid concentrations.  According to the authors, “the magnitudes of effect from a 1-[standard deviation] difference of [fine particulate matter] on metabolic outcomes were similar compared with the impact of a 1-unit change in percent body fat or [body mass index] BMI on the same metabolic outcomes.”

New Insights into Chronic Stress, Obesity, and Metabolic Syndrome: Further Support for an Ecological Model of Health and an Integrated Approach to Care

Ted Schettler MD, MPH
CHE Science Director

Summary

In laboratory animal studies a combination of chronic stress and a high-fat, high-sugar diet causes more abdominal fat to accumulate than that diet alone. This effect seems to be mediated, at least in part, by a substance called Neuropeptide Y (NPY) released from sympathetic nerves supplying adipose tissue in response to certain kinds of stress. A new study reports the same phenomenon in chronically stressed women.[1]

Scientists at UC San Francisco studied a group of 61 disease-free women, about half of whom were chronically stressed caring for a spouse or parent with dementia, while the others were relatively stress-free. They found that the stressed women who ate larger amounts of high-fat, high-sugar food were more prone to abdominal obesity and insulin resistance than the low-stress women who ate the same amount of unhealthy food. As in the animal studies, these effects were also associated with NPY levels, which were significantly higher in the group of stressed women. According to lead author Kirstin Aschbacher, “This study suggests that two women who eat the same thing could have different metabolic responses based on their level of stress. There appears to be a stress pathway that works through diet.”

Is the Environment Making Us Fat and Sick?

‘Obesogens’, other environmental factors contribute to metabolic syndrome

Based upon the May 7 CHE Partnership Call

Conventional wisdom says that the meteoric rise in obesity and related health conditions – the early stages of which are now called metabolic syndrome – is due to the West having a bad case of “couch potato syndrome.” That is, over the past few decades, we have been eating too much and not exercising enough.

While poor diet and inactivity play an undeniable role in fostering metabolic syndrome, that’s not the whole story. Clinical and epidemiological evidence increasingly implicates another culprit: the environment.

An insufficient explanation

Some scientists suspect that a combination of environmental factors, including a group of chemicals called obesogens, share the blame for the explosion of metabolic syndrome and its later stages: diabetes, obesity, cardiovascular disease, and even Alzheimer’s.    

“Despite what we’ve heard,” said Dr. Bruce Blumberg, Professor of Developmental and Cell Biology and Pharmaceutical Sciences at the Univeristy of California, Irvine, “diet and exercise alone are insufficient to explain the obesity epidemic.”   

A May 7 teleconference presented by the nonprofit Collaborative on Health and the Environment explored this urgent and compelling topic. This article is based upon that teleconference.
   
Metabolic syndrome is estimated to affect more than one-third of U.S. adults, 60% of them under 65 years old.

When environment collides with human biology

Speaker Dr. David Jacobs, Professor of Public Health at the University of Minnesota, a chronic-disease epidemiologist, defined metabolic syndrome as “a constellation of related metabolic abnormalities (body fatness, blood fat handling, insulin, glucose).”
   
Environmental factors suspected to contribute to metabolic syndrome include the food system, the transportation system, the built environment, air pollution, obesogens, other environmental contaminants, and socioeconomic stress.
   
These stressors alter pathways in the body, causing inflammation, oxidative stress, and disrupted insulin signaling. Altered pathways can, in turn, lead to diabetes, obesity, cardiovascular disease, and abnormal lipids (tied to dementia and Alzheimer’s).
   
You can think of metabolic syndrome as a crossroads, said speaker Dr. Jill Stein, co-founder of the Massachusetts Coalition for Healthy Communities, board member of Greater Boston Physicians for Social Responsibility, and co-author of the recent report Environmental Threats to Healthy Aging.
   
“This is where the environment meets human biology in the early stages of the disease process. You can think of environmental factors as kind of colliding with human biology here.” 
    

Chemical culprits

The obesity epidemic, as Dr. Bruce Blumberg pointed out, roughly correlates with the rise in the use of industrial chemicals (plastics, pesticides, etc.) in the years since World War Two.

Though, he reminded listeners, “correlation is not causation.”
   
Also, many environmental contaminants affect the endocrine system, which plays a big part in determining weight by controlling the appetite and metabolism, fat cell development, and lipid balance. These basic facts, plus suggestive laboratory research, has led scientists to propose an additional label for certain chemicals: obesogen.
   
Some time ago, Dr. Blumberg and his colleagues proposed “the obesogen hypothesis,” which defined obesogens as “chemicals that inappropriately stimulate adipogenesis and fat storage, exist and contribute to the obesity epidemic.”
   
Varioius studies have found that pre- and post-natal exposure to obesogens reprograms the metabolism of exposed animals, predisposing them to obesity later in life.   
   
Dr. Pete Myers, founder, CEO, and chief scientist of Environmental Health Sciences, began the teleconference by describing one such study, by Soo Lim et al., published in the journal PLoS One in April 2009. You can access the study at www.plosone.org/article/info:doi/10.1371/journal.pone.0005186
   
The study involved chronic exposure of rats to low levels of the common herbicide atrazine. After five months of exposure, the rats showed descreased basal metabolic rate, increased body weight, increased intra-abdominal fat, and increased insulin resistance. The effects were even stronger when the rats were fed a high-fat diet.
   
The scientists concluded that long-term atrazine exposure could contribute to the development of insulin resistance and diabetes in people, especially where high-fat diets are prevalent.
   
“The exposures they used were well within the range that people are often exposed to, “ said Dr. Myers, “especially within corn-growing areas. I think we’ll be hearing more about this line of research in the future.”    

POPS, diabetes, and metabolic syndrome

When the CDC tested the blood of 2,016 adults for the presence of six POPS (Persistent Organic Pollutants) as part of the National Health and Nutrition Examination Surveys (NHANES, 1999-2002), they found that each of the POPS was related to increasing occurrence of diabetes. People with POPS levels in the top quarter had a risk of developing diabetes 38 times greater than those with bottom-quarter levels.
   
Among non-diabetics in NHANES, people with organochlorine pesticide levels in the top quarter had five times the risk of metabolic syndrome compared to those in the bottom quarter.
   
These pollutants, though mostly banned in the 1970s, still linger in our foods. They are also found in computers, refrigerators, flame retardants, and waste dumps.        

What you can do

As far as prevention goes, Dr. Stein said, there are three major things you can do as an individual to reduce your risk of metabolic syndrome.

“The route that you take depends on the particulars of your life and your community. There are many dietary interventions – I’ll just throw out the Mediterranean diet because there is very compelling data about its effect in reducing not only metabolic syndrome but all the other conditions we’ve been talking about, and others beyond that. Taking general steps to reduce chemical exposures. Exercise.”
   
The Mediterranean diet is one composed of mostly fruits and vegetables, with lots of whole grains, fish, and olive oil, and very little processed food or red meat.    

What we can do

When asked for his thoughts on prevention, Dr. Jacobs underscored the need to think on a macro level.
   
“We really need the political will to examine our society,” he said, “and make some changes in it. They’re not going to come overnight. If you’re talking about reengineering where sidewalks are to encourage more physical activity, that’s difficult. If we’re talking about having an entirely different way of delivering food to the people other than the food industry, that’s a massive change.
   
“If we’re talking about the chemicals – they’re in computers. I like computers. They’re in refrigerators… The cleverness is to figure out how to have the things we want to have in our lives from industry without disrupting health.”
   
A final point to consider reminds us that we are only beginning to understand the complex relationship between our health and our environment.
   
Dr. Blumberg brought up the emerging paradigm of developmental origins of adult disease.
   
“Many of the afflictions we have as adults arise during development and early childhood,” he explained, “as a result of the foods we eat, the chemicals we’re exposed to, a variety of factors. We need a lot more research in this area to help us prevent chronic disease in later life.”