Is Supersize More than Just Too Much Food?

Linda S. Birnbaum, Director, NIEHS and NTP, National Institutes of Health, Department of Health and Human Services, Research Triangle Park, North Carolina, E-mail:

Citation: Birnbaum LS 2012. Is Supersize More than Just Too Much Food? Environ Health Perspect 120:a223-a224.

Online: 01 June 2012

Linda S. Birnbaum, director of the NIEHS and the NTP, oversees a budget that funds multidisciplinary biomedical research programs and prevention and intervention efforts that encompass training, education, technology transfer, and community outreach. She recently received an honorary Doctor of Science degree from the University of Rochester, the distinguished alumna award from the University of Illinois, and was elected to the Institute of Medicine. She is the author of > 700 peer-reviewed publications, book chapters, abstracts, and reports. Birnbaum received her M.S. and Ph.D. in microbiology from the University of Illinois, Urbana. A board-certified toxicologist, she has served as a federal scientist for more than 32 years, 19 with the U.S. EPA Office of Research and Development, preceded by 10 years at the NIEHS as a senior staff fellow, a principal investigator, a research microbiologist, and a group leader for the institute’s Chemical Disposition Group.

The author declares she has no actual or potential competing financial interests.

Diabetes and obesity are two of the most significant public health issues of our day, and both are major epidemics in the United States and abroad. These conditions are interrelated; obesity has been long recognized as a common precursor to adult-onset (type 2) diabetes, although “adult-onset” is becoming an outdated term. In the United States, the prevalence of obesity among children and adolescents has almost tripled since 1980, and an estimated 12.5 million children and adolescents (16.9%) are considered obese (Ogden and Carroll 2010). This trend is also apparent in preschool children 2–5 years of age, a group in which obesity increased from 5% in 1976–1980 to 10.4% in 2007–2008 (Ogden and Carroll 2010). One report based on well-child visits at a health maintenance organization in Massachusetts was particularly disturbing: The prevalence of overweight in infants 0–6 months of age almost doubled between 1980 and 2001, from 3.4% to 5.9% (Kim et al. 2006). This finding suggests that factors other than changes in physical activity or diet are contributing to these trends, pointing to possible changes in fetal programming.

The most recent estimates of diabetes prevalence in the United States are equally staggering. Based on data from 2005 through 2008, 25.6 million (11.3%) of all people in the United States ≥ 20 years of age have diagnosed or undiagnosed diabetes (Centers for Disease Control and Prevention 2011). Another 35% have prediabetes, a condition in which blood glucose is higher than normal but not high enough to be classified as diabetes. People with prediabetes have an increased risk of developing type 2 diabetes, heart disease, and stroke.

Being overweight or obese has been estimated to account for approximately 70% of the cases of type 2 diabetes (Eyre et al. 2004). However, the etiology of the remaining 30% is unknown. Given the sheer numbers of people with the disease—now estimated globally at 220 million and expected to grow to 366 million by 2030 (World Health Organization 2011)—it is easy to understand the growing consideration of “nontraditional” risk factors (e.g., environmental chemicals, stress, microbiome) as contributors to these diseases. A growing scientific literature implicating a role for environmental chemical exposures has been developed largely through the funding of the National Institute of Environmental Health Sciences (NIEHS) as part of the institute’s broader interest in understanding endocrine-related disorders and the developmental origins of adult disease. Endocrine-disrupting chemicals alter control of adipose tissue development and function, control of food intake, insulin sensitivity, glucose homeostasis, and lipid metabolism (Janesick and Blumberg 2011; Nadal et al. 2009; Thayer et al. 2012). If the exposure occurs during development, the result could possibly be an altered “set point” or sensitivity for developing obesity or diabetes later in life.

Research addressing the role of environmental chemicals in diabetes and obesity has rapidly expanded in the past several years. Both the May 2010 White House Task Force on Childhood Obesity (2010) and the 31 March 2011 Strategic Plan for NIH Obesity Research [NIH (National Institutes of Health) Obesity Research Task Force 2011] acknowledge the growing science base in this area and cite the need to understand more about the role of environmental exposures as part of future research and prevention strategies.

To help develop such a research strategy, the National Toxicology Program (NTP), with collaboration from the NIEHS intramural and extramural program scientists, organized a state-of-the-science workshop in January 2011 titled “Role of Environmental Chemicals in the Development of Diabetes and Obesity.” The technical background documents assembled for this workshop were extensive, totaling > 500 pages and spanning the range from epidemiological data to high throughput screening results. As an additional scientific resource, approximately 800 main findings from the epidemiological studies of diabetes and childhood obesity have been compiled into a searchable graphing software program. A diverse group of > 150 scientists, including toxicologists, epidemiologists, and bioinformaticists, as well as experts in the pathobiology of diabetes and obesity, attended the meeting to review the existing literature and shape a research strategy.

The review of the collected literature supported the plausibility of certain environmental chemicals acting as “obesogens” or diabetogenic agents. In some cases, the conclusions were based on surprisingly consistent epidemiological associations. With other chemicals or chemical classes, consistency was found in mechanisms of action. We have little appreciation for the extent to which environmental chemical exposures may be influencing obesity and diabetes rates, but it is becoming increasingly clear that overnutrition and a lack of exercise are not the entire story.

The first of a series of articles stemming from the January 2011 workshop appears in this issue of Environmental Health Perspectives (Thayer et al. 2012). Kristina Thayer, director of the NTP Office of Health Assessment and Translation, other NIEHS staff, and the workshop chair, Michael Gallo (University of Medicine and Dentistry of New Jersey–Robert Wood Johnson Medical School) provide an introduction to the topic and an orientation to the workshop and key outcomes. Upcoming reports will examine the influence of smoking during pregnancy, as well as nicotine and arsenic exposures, on diabetes and obesity outcomes and mechanisms.

References Top

  1. Centers for Disease Control and Prevention 2011. Diabetes Data & Trends. Available:​.aspx [accessed 12 December 2011].
  2. Eyre H, Kahn R, Robertson RM. 2004. Preventing cancer, cardiovascular disease, and diabetes: a common agenda for the American Cancer Society, the American Diabetes Association, and the American Heart Association. CA Cancer J Clin 54(4):190–207. Find this article online
  3. Janesick A, Blumberg B.. 2011. Minireview: PPAR© as the target of obesogens. J Steroid Biochem Mol Biol 127(1–2):4–8. Find this article online
  4. Kim J, Peterson KE, Scanlon KS, Fitzmaurice GM, Must A, Oken E, et al. 2006. Trends in overweight from 1980 through 2001 among preschool-aged children enrolled in a health maintenance organization. Obesity (Silver Spring) 14(7):1107–1112. Find this article online
  5. Nadal A, Alonso-Magdalena P, Soriano S, Quesada I, Ropero AB. 2009. The pancreatic ®-cell as a target of estrogens and xenoestrogens: Implications for blood glucose homeostasis and diabetes. Mol Cell Endocrinol 304(1–2):63–68. Find this article online
  6. NIH Obesity Research Task Force 2011. Strategic Plan for NIH Obesity Research. NIH publication no. 11-5493. Available:​/strategic-plan.aspx [accessed 12 December 2011].
  7. Ogden C, Carroll M 2010. Prevalence of Obesity among Children and Adolescents: United States, Trends 1963-1965 through 2007-2008. Available:​ity_child_07_08/obesity_child_07_08.htm [accessed 12 December 2011].
  8. Thayer KA, Heindel JJ, Bucher JR, Gallo MA. 2012. Role of environmental chemicals in diabetes and obesity: a National Toxicology Program workshop review. Environ Health Perspect 120:779–789. Find this article online
  9. White House Task Force on Childhood Obesity 2010. Solving the Problem of Childhood Obesity Within a Generation: White House Task Force on Childhood Obesity Report to the President. Available:​ov/files/TaskForce_on_Childhood_Obesity_​May2010_FullReport.pdf [accessed 12 December 2011].
  10. World Health Organization 2011. Diabetes Programme: Facts and Figures about Diabetes. Available: [accessed 12 December 2011].


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One Response to Is Supersize More than Just Too Much Food?

  1. Diane Kress, RD CDE says:

    “ Endocrine-disrupting chemicals alter control of adipose tissue development and function, control of food intake, insulin sensitivity, glucose homeostasis, and lipid metabolism (Janesick and Blumberg 2011; Nadal et al. 2009; Thayer et al. 2012). If the exposure occurs during development, the result could possibly be an altered “set point” or sensitivity for developing obesity or diabetes later in life”.
    Am I the only person who sees that the “endocrine disrupting chemical” causing excess adipose development, increased appetite/food intake, increased insulin resistance, lack of glucose homeostasis, and flawed lipid metabolism is the nutrient CARBOHYDRATE? Yes, Carbohydrate.
    A low fat, low cholesterol, low calorie platform left us to consume a higher carbohydrate diet as fat free foods are higher in carb grams. A food plate emphasizing fruit, veggies, whole grain starches, fat free milk (all healthy carbs…but still carbs) and decreasing protein and fat intake is hazardous to the health of over 60% of the US population.
    If 11.3% of the population has diabetes, 35% has pre diabetes, and most likely over 15% have the genes for metabolic syndrome and have not yet progressed to prediabetes or type 2 diabetes….then 61% of US population (or more) have a metabolism that finds a higher carbohydrate diet toxic.
    A high carb diet, even if the carb grams are from fruit, whole grains, legumes, sweet potatoes, low fat milk, yogurt, whole grain pasta, brown rice, multi grain cereal, will trigger hyperinsulinism that begets increased adipose cell size that leads to insulin resistance, leading to blood sugar fluctuations, leading to pancreas fatigue and eventually type 2 diabetes. A high carb diet is leading the majority of down the road to becoming fatter and sicker.
    Does stress play a role? YES. Do blood sugar provoking medications (some antihypertensives, prednisone, cortisone, antidepressants, etc) add to the problem? YES Does physical inactivity speed obesity and diabetes? YES.
    But…the underlying problem is insulin imbalance and the nutrient that causes insulin release = carbohydrate.
    So…when Supersizing took place…it wasn’t necessarily the increase in calories and fat that caused the epic landslide to obesity…it was the supersizing of the CARBOHYDRATE in foods:
    Supersized fries, sugary drinks, shakes, Slurpees, Italian Ice, pizza slices, bagels, muffins, pasta portions, breaded foods, sub rolls, soft pretzels, beans/rice in burritos, take out Chinese food….Carb, Carb, and did I mention..Carb.
    I will continue to ask medical associations like the AMA, ADA, Academy of Nutrition and Dietetics, NIH, CDC and major colleges and universities to PLEASE study the core program that is the basis for The Metabolism Miracle/The Diabetes Miracle. Compare the weight, body fat composition, glucose, lipids, Vitamin D, C reactive protein, hemoglobin A1C of 3 groups:
    1. Diet with no restrictions…these people would eat as always
    2. Diet low in calories, fat, cholesterol
    3. Diet following the core program of The Metabolism Miracle
    Why spend more time, money, energy looking for some dark hidden secret as to what is causing the epidemics of obesity and diabetes? The answer has been right in front of us since the early 1970’s. Let’s do some quality research and based on solid research really begin to save some lives. Thank you.

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