Which Chemicals Are Linked to Diabetes and Obesity? Perhaps More Than We Think.

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

Sarah HowardResearchers from the National Institute of Environmental Health Sciences (NIEHS), EPA, research centers and universities have just published an article, Prioritizing environmental chemicals for obesity and diabetes outcomes research: a screening approach using toxcast high throughput data (Auerbach et al. 2016).

The intent of this project was to use new rapid screening methods to identify chemicals that may be able to affect biological processes linked to the development of diabetes and/or obesity. The researchers screened 1860 chemicals and found that, “the spectrum of environmental chemicals to consider in research related to diabetes and obesity is much broader than indicated from research papers and reviews published in the peer-reviewed literature.”

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Review of the Evidence on Developmental Exposure to Certain Endocrine Disrupting Chemicals and Obesity

written by Sarah Howard
CHE Diabetes-Obesity Spectrum Working Group Coordinator

Sarah HowardA review article on prenatal exposure to endocrine disrupters and obesity was just published. Overall, it found that, “For certain EDCs, early life exposure may be associated with weight homeostasis later in life, however not necessarily in an obesogenic direction.” The review includes both human and laboratory evidence (19 studies) published since 1995. (The review did not include studies on BPA.) Here are their findings for the chemical classes included:

Organotins

Organotins are well-documented obesogens in laboratory studies. Human studies, however, are not available. Prenatal exposure to tributyltin causes adioposity in exposed mice, and these effects may be transmitted to future generations as well.

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Multiple and Interacting Contributors to Obesity

Written by Elise Miller, MEd
CHE Director

Elise MillerThe obesity rate for children aged 2-5 years dropped a stunning 43% over the past decade, according to a report published last week by the Centers for Disease Control and Prevention (CDC). This is of course extremely good news. Researchers, however, are not sure what combination of factors may have contributed to this significant decrease. Some theories are that a number of programs, such as the federally-funded Women, Infants and Children (WIC) initiative, which now subsidizes proportionately more vegetables and whole grains, and First Lady Michelle Obama’s “Let’s Move” campaign, which focuses on improving exercise and eating habits in child care settings, are making a difference. Others suggest that former New York Mayor Bloomberg’s declaration that restaurants should no longer use transfats has played a role or that programs started in the 1980s when people became aware that there was a growing obesity problem are finally having a positive effect on this new generation.

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Top 10 Selections: April 2013

For our third quarterly Top 10 list, we again selected from several dozen candidate news articles, journal articles, policy decisions and reports that have had a significant impact or are likely to have a significant impact on thinking and action in the field of environmental health. We consider these selections to be the biggest contributors toward new insights, toward changing the conversation or expanding the scope of the conversation on a topic to a new audience or awareness, or toward defining a new trend. Comments are welcome.

The selections, in no particular order:

  1. Report: Late Lessons from Early Warnings: Science, Precaution, Innovation from the European Environment Agency.
    As stated in the promotional text for this report: “The case studies across both volumes of Late Lessons from Early Warnings cover a diverse range of chemical and technological innovations, and highlight a number of systemic problems. The ‘Late Lessons Project’ illustrates how damaging and costly the misuse or neglect of the precautionary principle can be, using case studies and a synthesis of the lessons to be learned and applied to maximizing innovations whilst minimizing harms.” This report explores weaknesses in regulatory science and expands on histories of past environmental and public health mistakes. It includes new substances with potential for harm and several false positives. All is drawn together to provide a framework in which precaution guides policy.
    See more information about the partnership call CHE hosted on this report: Late Lessons from Early Warnings: A Retrospective Look at Learning about Precaution.
  2. The need to look at mixtures in assessing safety.
    Two items this quarter address the need to look at interactions among exposures when determining risk of exposures. First is Research Brief 217: Majority of Women Exposed to Multiple Pollutants, from the National Institute of Environmental Health Sciences (NIEHS). According to a new analysis of thousands of US women of child-bearing age, almost 83% of women aged 16 to 49 meet or exceed median blood levels of one or more of three environmental pollutants—lead, mercury, and polychlorinated biphenyls (PCBs)—that are known to harm brain development of fetuses and babies. Most women exceeded the median blood level for two or more of these pollutants, even though “scientists do not yet know whether co-exposure to all three chemicals is more harmful than each chemical alone.” With exposures this pervasive, it is imperative that risks be assessed and policies adopted to protect fetuses and children. The second item is a statement from NIEHS on this topic:  Unraveling the health effects of environmental mixtures: an NIEHS priority. NIEHS recognizes that it “is imperative to develop methods to assess the health effects associated with complex exposures in order to minimize their impact on the development of disease.” NIEHS draws from its background in both supporting and conducting combined exposure research to state that this topic will continue to be a priority at the Institute.
  3. America’s real criminal element: lead  and Correlation between exposure to lead and violence is being taken seriously across scientific world.
    “New research finds that lead is the hidden villain behind violent crime, lower IQs, and even the ADHD epidemic. And fixing the problem is a lot cheaper than doing nothing.” This line of investigation has deep repercussions socially. With substantial costs not only to individuals and their families, but to our entire society, from crime, lowered educational attainment and attendant problems. There is new impetus to prevent or to find and remediate lead in housing, in soil, and in consumer goods. Beyond the social significance, though, this story is a great case study in epidemiology and criminology.
  4. New report: U.S. Health in International Perspective: Shorter Lives, Poorer Health.
    This report from the National Research Council and the Institute of Medicine investigates potential reasons for the US health disadvantage and assesses its larger implications. No single factor can fully explain the US disadvantage:  It likely has multiple causes and involves some combination of inadequate health care, unhealthy behaviors, adverse economic and social conditions, and environmental factors, as well as public policies and social values that shape those conditions. This report packages the ecological model of health which CHE encourages our partners to consider when investigating environmental effects on health.
  5. Further impacts from smoking tobacco.
    Three studies provide new thinking around an old problem, in case anyone still needed a reason to reduce tobacco use.

    1. Passive smoking can dramatically increase the risk of developing severe dementia Breathing in someone else’s cigarette fumes increases your risk of severe dementia, according to researchers. The study is the first to find a significant link between passive smoking and the neurological disease.
      See the study: Association between environmental tobacco smoke exposure and dementia syndromes
      Between the widespread exposure to environmental tobacco smoke and the substantial costs to society of dementia, this is a huge public health issue. If reducing exposures to tobacco smoke can decrease the incidence or severity of dementia, the benefits to society could be enormous, in addition to the improvement in quality of life for individuals and their families.
    2. Cigarette smoke may increase microbial virulence
      A new study expands the potential health effects to a new front, showing that acute in vitro exposure of Staphylococcus aureus to cigarette smoke promoted biofilm formation and adhesion to human cells.
      See the study: Cigarette smoke increases staphylococcus aureus biofilm formation via oxidative stress.
    3. Cutting smoking saves more in health bills than lost tax: EU
      The cost and health benefits of getting people not to smoke—and better still, not to start—more than outweigh the taxes the tobacco industry pays to governments, the European Commission said Monday.
  6. Pollution crisis in China.
    A long series of news reports on air and water pollution, the resulting unrest in the population, and the government’s response describes a society’s struggle with chemical contamination in China.

    1. Chinese struggle through ‘airpocalypse’ smog
    2. Beijing air pollution soars to hazard level
    3. Beijing orders official cars off roads to curb pollution
    4. Chinese take fight against water pollution to social media
    5. Chinese Internet users scream for clean air act
    6. Eye-stinging Beijing air risks lifelong harm to babies
    7. Water pollution: a Bay of Pigs moment in China
    8. China’s toxic harvest: a “cancer village” rises in protest
    9. China steps up toxics controls
    10. Waiting to exhale in China
    11. A new environment for fight against pollution
    12. In China, breathing becomes a childhood risk
  7. Global data and meta-analayses of prenatal exposures and birth outcomes.
    Two large studies showcase the effects of environmental exposures on pregnancy outcomes.

    1. Environmental risk factors of pregnancy outcomes: a summary of recent meta-analyses of epidemiological studies
      The meta-analyses found statistically significant negative associations between environmental tobacco smoke and stillbirth, birth weight, and any congenital anomalies; PM2.5 and preterm birth; outdoor air pollution and some congenital anomalies; indoor air pollution from solid fuel use and stillbirth and birth weight; polychlorinated biphenyls (PCB) exposure and birth weight; disinfection by-products in water and stillbirth, small for gestational age, and some congenital anomalies; occupational exposure to pesticides and solvents and some congenital anomalies; and agent orange and some congenital anomalies.
    2. Maternal exposure to particulate air pollution and term birth weight: A multi-country evaluation of effect and heterogeneity
      A growing body of evidence has associated maternal exposure to air pollution with adverse effects on fetal growth; however, the existing literature is inconsistent. The objectives of this study were to quantify the association between maternal exposure to particulate air pollution and term birth weight and low birth weight (LBW) across fourteen centers from nine countries and to explore the influence of site characteristics and exposure assessment methods on between-center heterogeneity in this association. Maternal exposure to particulate pollution was associated with low birth weight at term across study populations. This study helps clarify previous disparate findings on air pollution and birth weight. Taking into account differences in location and methodology, these findings support the association between maternal particulate matter exposure and low birth weight.
  8. US report urges deeper look into breast cancer’s environmental links.
    A new federal advisory panel report makes a forceful case for more research into environmental causes of breast cancer, which was diagnosed in 227,000 women, killed 40,000 and cost more than $17 billion to treat in the United States last year. For years, the focus in breast cancer has been on early detection and treatment, and this move toward prevention shifts the focus upstream.
    See the report: Breast Cancer and the Environment: Prioritizing Prevention and information about CHE’s partnership call on the report.
  9. UN, WHO panel calls hormone-disrupting chemicals a ‘global threat.’
    An international team of experts reported today that evidence linking hormone-mimicking chemicals to human health problems has grown stronger over the past decade, becoming a “global threat” that should be addressed. There’s still much research needed, but this moves the conversation about health effects of endocrine disrupting chemicals onto a bigger stage.
    See the report: State of the Science of Endocrine Disrupting Chemicals and other coverage: European Parliament vote on EDCs conveys urgency of protecting health.
  10. Transgenerational effects of prenatal exposure to environmental obesogens in rodents.
    Three studies were published this quarter:

    1. Transgenerational inheritance of increased fat depot size, stem cell reprogramming, and hepatic steatosis elicited by prenatal obesogen tributyltin in mice
    2. plastics derived endocrine disruptors (bpa, dehp and dbp) induce epigenetic transgenerational inheritance of obesity, reproductive disease and sperm epimutations
    3. Hydrocarbons (jet fuel JP-8) induce epigenetic transgenerational inheritance of obesity, reproductive disease and sperm epimutations

    This is a new finding in both obesity research and in transgenerational research. These studies all show the ability of environmental chemicals (not only endocrine disruptors, but also jet fuel) to promote obesity in three generations of rodents.
    See information about CHE’s working group call on these studies: Transgenerational Effects of Prenatal Exposure to Environmental Obesogens in Rodents.

Letter to Michelle Obama

March 25, 2010 

First Lady Michelle Obama
The White House
1600 Pennsylvania Avenue NW
Washington, DC 20500

Dear Mrs. Obama:
 
We, the undersigned, are partners in the Collaborative on Health and the Environment, an international network of scientists, health professionals and advocates committed to using the best available science to improve the health of our families and our communities. We are deeply grateful for your leadership in facing the challenge of the obesity epidemic, which has concerned many of us for years. We also strongly support the initiatives that you are undertaking to address this major public health issue, which is having such a devastating effect on the health of American families.

We would like to underscore in this letter that the obesity epidemic is the result of many interacting factors and not just a lifestyle challenge—something that you acknowledge, but is rarely highlighted in the media or understood by the general public. The Institute of Medicine (IOM), for example, has publicly stated the importance of access to healthy food to help curb the increasing prevalence of obesity.[1] Along these lines, it is clear the federal government, given its ability to influence food production through subsidies, needs to incorporate strategies to promote more healthful and less calorie-dense, nutrient-poor food.

Other factors contributing to obesity include socioeconomic status and genetic predisposition, as well as poorly designed communities that discourage walking and biking.

In addition to these issues, the prestigious international Endocrine Society published a seminal report last year stating that, “scientific research implies the impact of environmental substances in the generative roots of obesity.”[2] The rapidly growing body of scientific evidence suggests that chemicals known as endocrine disruptors may be associated with a range of health concerns, including various cancers, developmental disabilities and infertility. In addition, some of these chemicals may also act as “obesogens” – that is, substances that trigger the propensity to develop obesity. Of critical importance, these obesogens appear to reprogram metabolism starting before birth, thereby increasing a child’s predisposition for obesity before he/she is even born. In addition, research shows that these chemicals may also promote the development and maturation of fat cells throughout life. In other words, we cannot ignore the evidence that these chemicals, found in everyday products and in our food and water, may also contribute to this epidemic.

The science on obesogens is very clear in animal studies (please see the attached article in press for the San Francisco Medical Society Journal [available on CHE’s website]). Although we have little information yet about how obesogens impact humans, there is some initial research in humans suggesting the urgent need for further study.[3]

The truth is that we as a society need to recognize all the interacting factors that can contribute to obesity—including the risk that exposures to obesogens can pose. Any campaign that does not take into account the role of these chemicals in the obesity epidemic will run counter to President Obama’s promise that this administration will be guided by the best available science. Given this, the emerging science clearly indicates that national chemical policy reform is an essential ingredient of your campaign against childhood obesity.

We congratulate you on your foresightedness in choosing obesity as one of your signature issues as First Lady. Please know we would also be happy to discuss ways to address the full range of concerns associated with obesity and to work with you and your colleagues to champion prevention as essential to real health care reform for all Americans.

Thank you again for your leadership and consideration.

With best wishes,

Bruce Blumberg, PhD, Professor, Departments of Developmental and Cell Biology and Pharmaceutical Sciences, University of California, Irvine

Susan Braun, Executive Director, Commonweal

Linda C. Guidice, MD, PhD, MSc, Professor and Chair, Department of Obstetrics, Gynecology and Reproductive Science, The Robert B. Jaffe, MD Endowed Professor in the Reproductive Sciences, Director, Center for Research on Origins and Biological Consequences of Human Infertility, Director UCSF Women’s Reproductive Health Research Career Development Center, University of California, San Francisco

Andrea Gore, PhD, Gustavus and Louise Pfeiffer Professor, Division of Pharmacology and Toxicology, The University of Texas, Austin

Richard J. Jackson, MD, MPH, Chair and Professor, Environmental Health Sciences, School of Public Health, University of California, Los Angeles

Phil Landrigan, MD, MSc, Ethel H. Wise Professor and Chairman, Department of Preventive Medicine, Professor of Pediatrics and Director of the Center for Children’s Health and the Environment, Mount Sinai School of Medicine

Philip R. Lee, MD, Former United States Assistant Secretary of Health, Chancellor of the University of California at San Francisco, Professor at Stanford University

Michael Lerner, PhD, President, Commonweal

Elise Miller, MEd, Director, Collaborative on Health and the Environment

John Peterson Myers, PhD, Founder, CEO and Chief Scientist of Environmental Health Sciences

Ted Schettler, MD, MPH, Science Director, Science and Environmental Health Network

Carlos Sonnenschein, MD, Professor, Department of Anatomy and Cellular Biology, Tufts University School of Medicine

Ana Soto, MD, Professor, Department of Anatomy and Cellular Biology, Tufts University School of Medicine

R. Thomas Zoeller, PhD, Chair and Professor, Biology Department, Morrill Science Center


[1] Institute of Medicine reports: The Public Health Effects of Food Deserts. Workshop Summary, Local Government Actions to Prevent Childhood Obesity and Progress in Preventing Childhood Obesity: Focus on Industry—Brief Summary: Institute of Medicine Regional Symposium. Available on the IOM website, http://www.iom.edu/Reports.aspx?search=obesity, viewed March 11, 2010.

[2] Diamanti-Kandarakis E et al. Endocrine-disrupting chemicals: An Endocrine Society Scientific Statement. Endocr Rev. 2009 Jun;30(4):293-342. Available online at http://www.endo-society.org/journals/scientificstatements/, viewed March 11, 2010.

[3] Grün F, Blumberg B. Endocrine disrupters as obesogens. Mol Cell Endocrinol. 2009 May 25;304(1-2):19-29. Heindel JJ, vom Saal FS. Role of nutrition and environmental endocrine disrupting chemicals during the perinatal period on the aetiology of obesity. Mol Cell Endocrinol. 2009 May 25;304(1-2):90-6.

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.”