When I began this research, I had three basic questions. Here they are, along with the answers I found.
A number of environmental factors have been associated with the development of type 1 diabetes. It is not yet known which of these factors are responsible for the increasing rates of disease in children, but since many of these factors influence and interact with each other, multiple factors are probably involved. The why is diabetes increasing? page describes a number of possible factors and how they may interact. Different factors may be operating in different populations and in different parts of the world, making generalizations difficult. It is also not clear whether type 1 diabetes incidence is also increasing in adults, or whether people are simply being diagnosed at younger and younger ages.
Nevertheless, there is evidence that a number of different environmental factors can contribute to the development of type 1 diabetes, such as inadequate vitamin D levels, a leaky gut, high growth rates, viruses, perhaps stress, and, probably, exposure to some environmental chemicals. Many of these factors have changed over time, and could conceivably contribute to the increasing incidence of type 1 diabetes in children.
How could we find out what factors are contributing to the increasing incidence of type 1 diabetes in children? We would need to know what factors can contribute to the development of the disease, by following people over time before they develop the disease and keeping track of their environmental exposures. We could identify biological mechanisms whereby factors contribute to diabetes in animals, although animals are not quite the same as humans. And, if possible, intervention trials to prevent type 1 might also be feasible (e.g., by giving people vitamin D supplements, for example, to see if people with higher vitamin D levels have a lower risk of developing type 1 diabetes over time).
The article, Environmental Trigger(s) of Type 1 Diabetes: Why So Difficult to Identify? describes a number of the ongoing studies of type 1 diabetes, and some of their major findings. The author proposes that the various existing cohort studies work together to provide data that is available to analyze across all of the different studies (Rønningen 2015). This article was published in a special issue of the journal BioMed Research International on environmental triggers of type 1 diabetes (Rønningen et al. 2015), which includes the comprehensive article, Can exposure to environmental chemicals increase the risk of diabetes type 1 development? (Bodin et al. 2015).
The U.S. National Toxicology Program (NTP) held a workshop to evaluate the scientific evidence on chemicals in diabetes and obesity, and published a review of the evidence Role of environmental chemicals in the development of diabetes and obesity: A National Toxicology Program workshop report.
The NTP found that, “Overall, the existing literature was judged to provide plausibility, varying from suggestive to strong, that exposure to environmental chemicals may contribute to the epidemic of diabetes and/or obesity....Research on environmental chemical exposures and type 1 diabetes was very limited. This lack of research was considered a critical data gap.” (Thayer et al. 2012).
Reports from this workshop that have been published so far include
Additional papers on BPA, phthalates, and pesticides have not yet been published, but drafts and other information are available on the workshops's website: Role of environmental chemicals in the development of diabetes and obesity.
The National Institute of Environmental Health Sciences (NIEHS) also held a workshop to evaluate scientific evidence of environmental factors in autoimmune disease. Their report is available online: Miller et al. 2012.
The NIEHS found that: "There has been virtually no epidemiologic research on risks associated with relatively widespread synthetic chemical exposures, such as plasticizers (e.g., phthalates and bisphenol A). Some of these chemicals can act as endocrine or immune disruptors, and increased risks of some immune-mediated diseases, including asthma and eczema, in relation to exposure levels, have been reported in children. More research is needed to determine the role of plasticizers and other industrial chemicals in consumer products in the development of autoimmune disease."
CHEM Trust has published a report in 2012, "A Review of the Science Linking Chemical Exposures to the Human Risk of Obesity and Diabetes" which is an excellent review of the evidence.
The Endocrine Society's Second Scientific Statement on Endocrine-Disrupting Chemicals devotes a section to diabetes and obesity. They conclude, "...there is sufficient evidence to conclude that some EDCs act as obesogens and others act as diabetogens." Also, "...animal studies indicate that some EDCs directly target beta and alpha cells in the pancreas, adipocytes, and liver cells and provoke insulin resistance together with hyperinsulinemia." They also call for more research on EDCs and type 1 diabetes: "Studies relating EDCs and other contaminants to T1D are beginning to emerge, although they are still very preliminary... this is an important area that deserves further research and more studies in humans" (Gore et al. 2015).
In 2014, a group of experts met in Parma, Italy and developed a consensus statement on chemicals that disrupt metabolism (Heindel et al. 2015). They are confident that, "There is more to the environmental component of obesity, diabetes and metabolic syndrome than overeating and poor nutrition, lack of exercise and changes in lifestyle. The environmental component is multifactorial and includes prescription drugs, stress, nutrition, microbiome, infections, sleep patterns, nocturnal illumination and environmental chemicals," and that, "susceptibility to metabolic disorders is, at least in part, ‘programmed’ in utero and early postnatal life by exposure to environmental factors including stress, drugs, nutrition and environmental chemicals."
They predict that, "we are underestimating the importance of metabolic disruptors in obesity, diabetes, and metabolic syndrome because current research designs focus on studying one or a small subset of chemicals at a time, during limited windows of sensitivity, in single tissues (including only one adipose tissue) and often only endpoints related to a single disease outcome per study," and that, "reducing exposures to environmental chemicals and improving nutrition during development offers the possibility of preventing obesity and metabolic diseases."
They conclude the statement with, "History shows that prevention is always the best strategy. Increased understanding of the importance of the metabolic disruptor hypothesis to the epidemics of obesity and metabolic syndrome offers the potential for these diseases to be mitigated by modifying exposures, thereby creating a healthier environment for future generations."Lind et al. 2016).
What is the evidence that environmental chemicals might have something to do with the increasing incidence of type 1 diabetes? A growing number environmental chemical exposures have been associated with type 1 diabetes in studies of people (PCBs, air pollutants, arsenic metabolism, PFOS, some heavy metals, and nitrate/nitrite), however, most studies of type 1 have not included measures of environmental chemical exposures. A number of chemicals have been associated with diabetes (type 2, gestational, or unspecified) in humans. A number of chemcials have been associated with risk factors of type 1 diabetes, such as weight gain, in humans and animals. A number of chemicals have been found to affect beta cells, and to induce or exacerbate autoimmunity, inflammation, insulin resistance, or oxidative stress in animals and sometimes humans, all processes that may play a role in the development of type 1 diabetes.
While exposure to environmental chemicals is not traditionally thought to be a risk factor for type 1 diabetes, the weight of all this evidence suggests that there is certainly potential for chemicals to contribute to the development of type 1 diabetes. The historical patterns of contamination are consistent with historical patterns of type 1 diabetes incidence. Whether some or many environmental chemicals are contributing to the rising rates of disease in children remains unknown, but it is plausible and possible.
Note that the Parma Statement above calls for more research on the role of these chemicals in type 1 diabetes, as does the NIEHS workshop above.
When I started reading these studies, I did not expect to find that type 2 diabetes may be linked to chemical exposures. Like most people, I thought that weight gain, a poor diet, and lack of exercise could explain the increasing rates of type 2. I now think, like many scientists, that chemicals probably play a role in the development of type 2 diabetes as well. The effects of chemicals may be exacerbated by obesity and other lifestyle factors, but lifestyle and genes alone do not account for all cases of type 2 or all of its increasing incidence. In fact, there is growing scientific evidence that chemical exposures can contribute to the development of type 2 diabetes.
Consider that about 20% of adults with diabetes are not overweight or obese (Nguyen et al. 2011); gastric bypass surgery often leads to remission of type 2 diabetes even before any weight loss occurs (Pournaras et al. 2010); and in people with very low levels of chemical exposures, obesity does *not* increase the risk of diabetes (Lee et al. 2006).
There is preliminary evidence linking gestational diabetes to environmental chemicals (e.g., see the pesticides, arsenic, air pollution, and bisphenol A pages). But since gestational diabetes is so common, and can increase the risk of type 1 or type 2 in the mother, more research should be devoted to the possibility that chemicals may affect the risk of gestational diabetes development.
Researchers suggest that both avoiding the intake of toxic chemicals, and increasing their elimination from the body, may help prevent or treat diabetes and other "diseases of civilization" (Lee et al. 2008, Hennig et al. 2007). Hennig et al. (2007) discuss a number of possible ways to use nutrition and diet to both reduce exposure and increase elimination. The authors describe one case study where a person with insulin-dependent type 2 diabetes (possibly as a result of PCB poisoning) was treated and the diabetes resolved (over 2 years). Watkins et al. (2007) also provide suggestions, including increasing consumption of omega-3 fatty acids and flavonoids (like chocolate...). The Environmental Working Group provides information on how to avoid toxic chemicals in consumer products. Buying organic food, limiting animal fats, avoiding plastic food containers (especially heating food in plastic), limiting fish high in mercury; these are just some of the things you can do to reduce chemical exposures. Let me know if you try any of these strategies, and whether or not they appear to have any effect (better yet; document it with medical records if possible).
Did you develop type 1 diabetes following a chemical exposure? A number of people have emailed me who are in this situation; we may be able to work together to figure out what chemicals may be of concern. My email: email@example.com.
Most chemical exposures, however, are widespread, ongoing, and unavoidable. Societal action to reduce exposures are necessary as well as individual actions, in order to really prevent disease on a population level.
This website focuses on the development of diabetes-- but what about managing diabetes and avoiding complications? Lee et al. (2008) found that people with higher levels of various persistent organic pollutants (POPs), specifically organochloride pesticides, had higher hemoglobin A1c levels (a measure of long term glucose control) and more neurological complications. This finding could be really important for people with diabetes, and deserves more study. Additional studies have also found associations between a higher HbA1c (or other complications) and environmental chemical levels. More study is welcome!
We do know that some people have a harder time managing diabetes, but we don't know why. There is no evidence (yet!) that reducing exposures/increasing elimination of chemicals could help in diabetes management, but the possibility exists. It might be worth a try.
There have not yet been any successful intervention trials shown to prevent type 1 diabetes or its associated autoimmunity. For a good review of what has been tried, see Skyler 2013. He concludes, "Based on our current concepts of the immunopathogenesis of Type 1 diabetes, it should be possible to delay or prevent the disease. Unfortunately, to date, for both primary and secondary prevention studies there has not been unambiguous evidence of clinical benefit from any intervention tested." However, some of the interventions may have helped certain subgroups (Skyler 2013). (Skyler 2015 discusses suggestions for future trials and what may have gone wrong in past trials).
But, if you have type 1 diabetes in your family, and/or are interested in reducing the risk of your children developing the disease, studies do suggest a number of possible steps to try. None is guaranteed to work, of course, but these recommendations are not likely to lead to any harm either. See the linked pages for more information and sources. You could try to:
Timing may be critical, in that these factors may be most important during gestation, in infancy, or early childhood, or even puberty. If you are interested in reducing the risk of type 1 diabetes in an older child, like I am, then it may already be too late. Also bear in mind that diabetes has been around since ancient times, and will probably never be prevented entirely. That said, it used to be a rare disease.
There are a number of on-going, prospective studies of type 1 diabetes taking place now that follow people over time, and keep track of various environmental exposures before diagnosis. These studies are important in that they can help determine what factors can contribute to the development of disease. The Environmental Determinants of Diabetes in the Young (TEDDY) is one such study (TEDDY Study Group 2008). TEDDY includes measurements of many of the other environmental factors discussed in these pages, such as dietary factors, viruses, vaccines, and stress. Yet, like most other prospective studies, it does not include measurements of many of the environmental chemical exposures discussed on this webpage (with some exceptions). Since the search for the cause of the rising rates of type 1 diabetes has thus far largely been fruitless, research into the possible involvement of multiple environmental chemicals in the development of the disease is in order. This research should entail:
According to type 1 diabetes expert Dr. Mark Atkinson, "...the list of potential environmental triggers and regulators of disease in type 1 diabetes remains considerable. It stands likely that only through continued efforts within large, prospective, multicenter screening programs will specific environmental factors (and the influence of genetic and immunologic factors on them) truly associated with the development of the disease be identified. In addition, the complexity of these efforts must go beyond the simplicity of previous efforts and delve into areas not subject to much in the way of previous investigation (e.g., antibiotic use, fever, exposure to environmental toxins, etc.), throughout pregnancy and into early infancy" (Atkinson 2012).
Dr. Atkinson also argues that researchers face pressures (for grant money, publications, etc.) that lead them to publish "safe" research that does not question the dominant paradigm. Yet type 1 diabetes is complex, heterogeneous, and many of the things we "know" about the disease may be wrong. New, "bold" research is what we need in order to identify the cause(s) of type 1, as well as the cure(s) (Battaglia and Atkinson 2015).
We should focus research on those chemicals that humans are exposed to, especially in utero, via breastmilk, in food, or in consumer goods, and those that show effects in the laboratory that might be important in the development of type 1 diabetes. Many of the these chemicals have already been identified, but that does not rule out the possibility of additional substances as yet unstudied. Chemicals in combination with each other, or with other environmental factors may also be critical. Those that can disrupt the endocrine system and the development and function of the immune system deserve special focus.
The National Institute of Environmental Health Sciences (NIEHS) has used data from 1860 chemicals to attempt to determine which ones show biological effects that may play a role in the development of diabetes or obesity (including those that affect beta cells). Their results are available online for free (see Auerbach et al. 2016). The tests (assays) they used relate to various aspects of diabetes/obesity, including insulin resistance, pancreatic islet and beta cell function, fat cell differentiation, and feeding behavior/appetite. Those relating to beta cell function would be especially applicable to type 1 diabetes. The article concludes, "The results of this screening-level analysis suggest 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."
Elucidating the role of chemicals may be complex. Effects are likely to depend on the dose, timing, gender, and other factors. Chemicals may act via a variety of mechanisms; the evidence of exposure may be long gone by the time the disease develops; chemicals may act in combination with other factors such as diet or lifestyle (or other chemicals) to influence the progression of disease; the effects of exposure may in part depend on an individual's genetic susceptibility; and cumulative exposures over the duration of life, beginning in utero (or even earlier?), may be important.
Another complication, which should give anyone the shivers, is the possibility that chemicals can have effects that can be passed down from one generation to the next. Children today may be showing health outcomes from exposures their parents or grandparents had. The implications of this possibility are frightening, but cannot be ruled out (see the gene expression and endocrine disruption pages for some examples and more information).
As it now stands, safety data for chemicals has relied on exposures to adults to predict the effects of individual chemicals on the immune system. Yet for many substances, these adult exposures are not the same as an exposure in utero, in infancy, or in early childhood, particularly because the immune system is developing during these times. Considering how many environmental chemicals can affect the developing immune system, it is likely that they could be involved in the development of autoimmune disease later in life. Safety evaluations should consider exposures during the developmental period, not only during adulthood (Dietert and Piepenbrink 2006) (see the autoimmunity page).
It's not just type 1 diabetes that is a concern. Up to 25% of children in some developed countries suffer from an immune-based disease. And yet, only a few existing chemicals have been tested for how they may affect the developing immune system (Dietert 2011).
Here is what some researchers say about the need to protect health by reducing chemical exposures: "All of this evidence should encourage regulatory agencies to apply the precautionary principle and thus ban and/or substitute those chemicals that are likely to be harmful to the normal development of humans and wildlife" (Vandenberg et al. 2009).... "We are likely to witness dramatic improvements in human health, and reductions in medical costs, if environmental pollution is decreased" (Edwards and Myers 2007).
According to my U.S. Senator, Kirsten Gillibrand, the Environmental Protection Agency (EPA) has the authority to regulate more than 80,000 existing chemicals, yet has only had the resources to restrict the production of 5 chemicals over the past 30+ years. Efforts to reform the U.S. Toxic Substances Control Act are now underway and sorely needed.
Indeed, preventing pollution may be the most important action we can take. Like drugs, chemicals should be "presumed guilty until proven innocent," or shown to be safe before they are used. Scientists are not allowed to experiment on children in the lab; why should children be exposed to chemicals such that they are effectively experimental subjects in the real world?
If exposure to environmental chemicals is ultimately found to contribute to the development of type 1 diabetes, then this disease may in part be preventable.
A number of researchers have been kind enough to look at and comment on this website. Here are some of their comments.
Type 1 diabetes researchers have said:
Type 2 diabetes researchers have said:
Toxicologists have said:
The RSS Feed of new articles on diabetes and chemicals below is provided courtesy of Health & Environment. Many more articles are categorized by topic on the References page.