Diabetes Research and Resources

"Since 1980, age-standardised diabetes prevalence in adults has increased, or at best remained unchanged, in every country. Together with population growth and aging, this rise has led to a near quadrupling of the number of adults with diabetes worldwide."1

Diabetes is a large and growing public-health concern worldwide. On this page we sumarize trends in prevalence and the evidence surrounding environmental contributors to the cluster of diseases known as diabetes.

data from the International Diabetes Foundation IDF Diabetes Atlas 7th Edition. ©CHE

data from the International Diabetes Foundation IDF Diabetes Atlas 7th Edition

Diabetes Overview

Diabetes mellitus is a class of diseases characterized by high glucose levels in the blood. The pancreas, an organ involved in digestion, releases the insulin hormone that affects the blood’s glucose content by allowing glucose to enter the body’s cells. In diabetes, the glucose in the blood cannot get into the body’s cells to provide the energy needed to function. There are three major types of diabetes, plus a condition called prediabetes.2

Type and Etiology Time of Onset Prevalence/Risk Factors

Type 1 diabetes is an autoimmune disease that occurs when the body does not make enough insulin. The body’s immune system malfunctions, attacking and killing the insulin-producing beta cells in the pancreas.

Type 1 diabetes can develop at any age, often in childhood, and there is no known way to prevent the disease.3 Over 18,000 youth are diagnosed with type 1 diabetes each year in the US, accounting for about five percent of all diagnosed diabetes cases.4 Exposure to certain environmental factors, such as viruses, can potentially trigger the autoimmunity involved with type 1 diabetes.5

In type 2 diabetes the body develops insulin resistance and cannot use insulin properly. Insulin resistance occurs when the body’s cells do not allow insulin to enter the cells, despite the presence of insulin in the blood. Insulin resistance can eventually lead to the pancreas's failure to keep up with insulin demands.6

Most cases occur in middle-aged and older individuals, but type 2 diabetes is now also appearing in children.7 Risk factors for type 2 diabetes:8
  • Overweight or low physical activity; however, 20 percent of cases occur among lean individuals, and the mechanism is not well understood9
  • A family history of diabetes
  • Developing gestational diabetes

Gestational Diabetes 

 During pregnancy Overweight and obese women are at the highest risk for developing gestational diabetes. While gestational diabetes normally resolves after birth, both the mother and baby are at increased risk of developing type 2 diabetes later in life.10

Prediabetes refers to high blood glucose levels, but not high enough to be classified as diabetes.11

  86 million people in the US have prediabetes, and nine out of ten people with prediabetes do not know they have it. Without weight loss and moderate physical activity, 15 to 30 percent of individuals with prediabetes will develop type 2 diabetes within five years.12

Chronic Inflammation and Insulin Resistance

Inflammation is involved in the development of both type 1 and type 2 diabetes. The autoimmune reaction involved in type 1 diabetes leads to higher levels of inflammatory markers, such as cytokines, that control the strength of the immune response.13

The major risk factors for type 2 diabetes—overnutrition, low dietary fiber, sedentary lifestyle, sleep deprivation, and depression—have been found to induce low-grade inflammation.14 Excess fat cells promote the formation of visceral adipose tissue, increasing the risk of insulin resistance and resulting in activation of pro-inflammatory antibodies, leading to a cycle of chronic inflammation.15

Insulin resistance can also be caused by endocrine disrupting chemicals (EDCs). Widespread EDCs, such as dioxins, pesticides and bisphenol A (BPA), cause insulin resistance and alter beta cell function in animal models. These EDCs are present in human blood and can accumulate in and be released from fat cells. After binding to cellular receptors and other targets, EDCs either imitate or block hormonal responses.16 See the tables below for more information.

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Related Concerns

Those living with diabetes are at increased risk for other health problems:17

  • Blindness/retinopathy
  • Kidney failure/nephropathy
  • Heart disease/cardiovascular disease
  • Stroke
  • Nerve damage/neuropathy
  • Amputation of toes, feet, or legs
  • If type 1, then other autoimmune diseases (thyroid disease, celiac disease, autoimmune gastritis, and Addison's disease)18
  • Metabolic syndrome—a set of risk factors for heart disease, including high blood glucose, abdominal obesity, high blood pressure and high cholesterol/triglyceride levels19

Diabetes Prevalence

According to a 2015 report from the International Diabetes Foundation, 415 million adults are living with diabetes globally. Of those living with diabetes, 80% live in low- or middle-income countries.20

According to the most recent report from the US Centers for Disease Control and Prevention (CDC), in 2014 there were 29.1 million people living with diabetes in the US.21 Among the 29.1 million, an estimated 8.1 million people are undiagnosed and living with diabetes.

Of those aged 65 years or older in the United States, 25.9 percent have diabetes, followed by 16.2 percent of individuals aged 45 to 64 and 4.1 percent of those aged 20 to 44.22

diabetes rates by age and gender

Diabetes affects men and women somewhat equally in the United States, with men experiencing a rate of about 13.6 percent and women about 11.2 percent.23 Overall, both genders tend to be at comparable risks for diabetes.

A 2013 report from the CDC found that those in the United States with the lowest levels of education and income experienced the highest rates of diagnosed diabetes.24 Among adults aged 20 years or older, the Native American population experiences a disproportionately high rate of type 2 diabetes, while non-Hispanic whites have the lowest rates of type 2 diabetes.25

diabetes rates by education and income level

Among children, non-Hispanic whites are at highest risk for type 1 diabetes, and Native Americans are at the lowest risk. However, the reverse is true for type 2 diabetes, with Native Americans being most at risk and non-Hispanic whites being at the lowest risk.26


The burden of diabetes, both in terms of prevalence and number of adults affected, has increased faster in low-income and middle-income countries than in high-income countries.27

In the United States, a 2014 study published in the Journal of the American Medical Association (JAMA) found the prevalence of type 1 and type 2 diabetes doubled among US adults between 1990 and 2008. The same study also identified a plateau, or leveling off, of diabetes cases from 2008 to 2012. Researchers suggest this could be from the slowing rate of obesity cases (a major risk factor for type 2 diabetes) and better diagnostic testing. However, the rates of diabetes continued to grow in Hispanic individuals, non-Hispanic black individuals, and populations that achieved a high school education or less.28

A different study published the same year concluded that among US children, type 2 diabetes prevalence increased by 30.5 percent, and type 1 diabetes increased by 21.1 percent between 2001 and 2009.29 With 13,000 cases each year, the US leads all other countries in new cases of type 1 diabetes among children.30

Environmental Contributors

 The Lancet infographic on environmental risk factors for type 1 diabetes


Infographic from The Lancet; click to open the infographic on The Lancet website or read the full series: The Lancet: Risk factors for type 1 diabetes.

Chemical Exposures

Studies examining the effect chemicals have on diabetes risk have reported significant findings. 

A summary of evidence regarding chemical exposures and the various types of diabetes follows. Information in the tables is from Bodin et al.31 unless otherwise indicated. The “strong”, “good”, and “limited” categories refer to the CHE Toxic and Disease Database definitions.

Type 1 Diabetes




Strong Evidence

Pyrinuron (Vacor)

Rodenticide, banned in the US

Destroys pancreatic beta cells; causes type 1 diabetes in humans

Good Evidence

Air pollution

Traffic-related air pollution from cars, trucks, and diesel exhaust

Some studies find associations between various air pollutants and type 1 diabetes.

Limited Evidence


Contaminates drinking water

Impairs the immune system, alters the gut microbiome diversity, lowers insulin secretion, and destroys beta cells32


Plastics, epoxy resins lining metal cans, thermal cash register receipts, dental sealants

Animal studies show that BPA can affect beta cells, promote autoimmunity, and exacerbate diabetes development in a mouse model of type 1 diabetes.33 BPA has not been studied in relation to human type 1 diabetes

Nitrate/nitrite/N-nitroso compounds

Nitrite can be found in processed meats; nitrate can be found in groundwater Associated with type 1 diabetes in numerous, but not all, human and animal studies34

Persistent organic pollutants

Widespread environmental contaminants including PCBs, dioxins/furans, and organochlorine pesticides such as DDT  Some studies find associations with type 1 diabetes or autoimmunity35


Used for pest and weed control One human study found associations with type 1 diabetes36


  One human study found an association with type 1 diabetes37


Type 2 Diabetes




Strong Evidence

Air pollution38

Traffic-related air pollution

Enhanced insulin resistance and inflammation around major organs, promoting diabetes


contaminates drinking water


Impairs the immune system, alters the gut microbiome diversity, impairs insulin secretion, destroys beta cells



Found in the herbicide Agent Orange used during the Vietnam War, also a persistent organic pollutant

Linked to type 2 diabetes in exposed veterans

Persistent organic pollutants41

Widespread environmental contaminants including PCBs, dioxins/furans, and organochlorine pesticides such asDDT.

DDE, heptachlor, HCB, DDT, trans-nonachlor, and chlordane most strongly linked to type 2 diabetes

Good Evidence

Bisphenol A (BPA)

Plastics, epoxy resins lining metal cans, thermal cash register receipts, dental sealants

BPA causes insulin resistance in animal studies and is associated with type 2 diabetes in humans.


Used in batteries, pigments, coatings and platings, stabilizers for plastics; found in cigarette smoke


Impairs insulin release and disrupts glucose homeostasis


Used for pest and weed control

Odds of diabetes incidence increased with both ever use and cumulative days of use.


Soil; in some dietary supplements

Interferes with insulin signaling, which is critical to the regulation of glucose levels

Limited Evidence

Mercury and other metals

  Conflicting evidence

Perfluorinated compounds (PFCs), also known as perfluoroalkyl substances (PFAS)

Used in fire-fighting foam, textiles, kitchenware, and food packaging materials; Human exposure to PFAS is mainly through diet via marine food and game Some studies find associations with type 2 diabetes


Used as plasticizers in a variety of consumer products, like paint and cosmetics Promotes insulin resistance through sustained oxidative stress and inflammation


  High doses of radiation (nuclear accidents) have shown some indication of being linked to diabetes.

Gestational Diabetes

Very preliminary (limited) evidence links the development of gestational diabetes to environmental chemical exposures. Most of these associations have not been studied in additional cohorts or in the laboratory:

Lifestyle Factors


Type 1 Diabetes  Type 2 Diabetes
Consumption of cow's milk, infant formula, gluten, processed foods, and numerous other dietary factors in early life have been studied in relation to type 1 diabetes development, but none have been shown to unequivocally affect the risk of type 1 diabetes.51 Probiotics, omega-3 fatty acids, and breastfeeding are being studied as possible protective factors for type 1 diabetes.52 Sugar-sweetened beverage consumption has a strong association with increased risk of type 2 diabetes.53 Consumption of omega-3s (primarily found in fish) have shown protective effects against type 2 diabetes.54 Human guts low in bacterial richness have been associated with higher risks of obesity and insulin resistance, both risk factors for type 2 diabetes.55


Type 1 Diabetes  Type 2 Diabetes
Numerous studies indicate an association with weight gain, and numerous studies do not. One study found a middle ground, reporting a slight increased risk for type 1 diabetes in those with a higher BMI.56 The associations between weight gain and type 2 diabetes are well established. The Diabetes Prevention Program has found that weight reduction and intensive lifestyle interventions reduce the incidence of diabetes by 58 percent.57

Physical Activity

Greater physical activity has shown to lower all-cause mortality in patients with diabetes.58


Type 1 Diabetes  Type 2 Diabetes
Studies show that stress is associated with type 1 diabetes development for both children and adults.59 Post-traumatic stress disorder (PTSD)60 and high-stress jobs61 have been associated with increased risk of type 2 diabetes.

 See the Psychosocial Environment webpage for further information about stress and health.

Other Contributors

Vitamin D Deficiency

Studies have found that areas with lower levels of ultraviolet B radiation (the main source of vitamin D in humans) had a higher incidence of type 1 diabetes.62 Vitamin D intake in early life is associated with a lower risk of type 1 diabetes, and maternal vitamin D intake during pregnancy may decrease the risk of type 1 diabetes in the offspring, although the evidence is not yet conclusive.63

Healthy Gut/Microbiome

A healthy gut is full of good bacteria that promote a healthy immune system to fight off bad bacteria and other pathogens. Broad exposure to a wealth of non-pathogenic microorganisms early in life is associated with protection against allergies, type 1 diabetes, and inflammatory bowel disease.64 Studies have found differences in gut microbacteria from individuals that have diabetes and those that do not, and these differences may affect type 1 diabetes susceptibility.65 Several lines of evidence suggest that the microbiome may influence the development of type 1 diabetes, and increasing evidence suggests that microbiome-host interactions may be one environmental factor that influences type 2 diabetes risk as well as its progression. Environmental circumstances including method of birth, breastfeeding, antibiotics, diet, exposure to toxics, and hygiene can modify the microbiome.66

Genetic Factors


Epigenetics is a set of mechanisms that can turn particular genes or sections of chromosomes on or off.67 Environmental cues for a developing fetus or child can program persistent epigenetic modifications.68 See our Gene-Environment Interaction webpage for further information.

Nutrition and exposure to certain chemicals in utero have been hypothesized to increase later risk of the offspring developing type 2 diabetes.69 Maternal malnourishment, obesity or diabetes each may predispose the fetus to develop metabolic disease later in life.70

Endocrine disrupting chemicals are thought to interfere with fetal programming by affecting gene regulation and gene expression (epigenetics). Environmental exposures that the fetus encounters can become persistent alterations in the fetal epigenome, leading to increased risk of diabetes across multiple generations.71 The link between epigenetics and diabetes remains an active area of research.

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Genome studies have found numerous genes associated with higher or lower risks of type 1 and type 2 diabetes.72 However, genes alone cannot explain the rising rates of diabetes seen throughout the world.  Some studies even suggest that genetic predisposition to type 1 diabetes is decreasing and becoming less prevalent in children.73 Diabetes is a complex, multifactorial disease; see our Gene-Environment Interaction webpage for further information on this topic.

Interaction of Factors

These mechanisms—chemical exposures, lifestyle factors, vitamin D, our microbiome and genetics—are all interconnected and act together in promoting or suppressing the incidence of diabetes. The contributions of these various mechanisms may vary by location.74

Costs Associated with Diabetes

According to a 2012 CDC study, the direct and indirect costs of diabetes totaled $245 billion in the US. The medical costs associated with diabetes patients are 2.3 times the cost of those without diabetes, totaling $196 million in 2012. Indirect costs of diabetes—disability, work loss and premature death—were calculated at $69 billion.75 According to the American Diabetes Association, one of every five health care dollars in the United States is spent caring for those with diabetes.76

costs of diabetes care

One study estimated the lifetime medical costs of diabetes to be $124,600 if diagnosed at age 40, $91,200 if diagnosed at age 50, $53,800 if diagnosed at age 60, and $35,900 if diagnosed at age 65.77 The cost of treating diabetes is high for all patients and makes low-income groups even more vulnerable to the worst effects of diabetes.

Ethical Considerations

A diabetes diagnosis oftentimes comes with diabetes-related stigma. Due to landmark studies that have shown type 2 diabetes can be prevented by maintaining a healthy lifestyle, individual behavior is often called into question regarding why an individual may have diabetes. For example, people with diabetes often perceive the public as blaming them for inflicting themselves with the disease. This may impact many aspects of psychological well-being and may also result in sub-optimal clinical outcomes for people with diabetes.78 Another source of stigma is the required needle use for insulin treatment and worry of being mistaken as an illicit drug user. These sources of stigma and others can have real impacts on both psychological health and physical health.

See more about environmental contributors to obesity in the list of CHE publications and Dig Deeper resources in the right sidebar.

This page was last revised by student intern Jessica Hale and Sarah Howard, with editing by Nancy Hepp in August 2016. 

CHE invites our partners to submit corrections and clarifications to this page. Please include links to research to support your submissions through the comment form on our Contact page.

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