Type 1 Diabetes Incidence is Increasing in Children, But Why?
When I began this research, I had three basic questions. Here they are, along with the answers I found.
Are more children really getting type 1 diabetes? Yes. Type 1 diabetes incidence is increasing in children, especially the youngest children, in countries around the world (Diamond Project Group 2006) (see the Incidence page for details)
If so, why? Could environmental chemical exposures contribute to this increase? No one knows why, but there are many possibilities. I think environmental chemicals could contribute to the increasing incidence of type 1 diabetes. But do they? We don't know yet.
Is there anything I can do to lower the risk of my child developing type 1 diabetes? Maybe. See the list below for some possibilities.
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 vitamin D deficiency, a leaky gut, high growth rates, viruses, stress, and 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. Yet none of the environmental factors linked to type 1 diabetes so far appear to be able to explain the increasing incidence trends (Norris et al. 2020), except, I would argue, environmental chemical exposures.
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).
So far, most intervention trials have been unsuccessful in preventing type 1 diabetes (for a free full text summary of trials and the results so far, see Beik et al. 2020). Per another review of prevention trials (Kanta et al. 2020), a number of things have been tried, including:
insulin (only successful in one subgroup)
monoclonal antibodies (one, teplizumab, was successful)
breastfeeding (might be protective)
cow's milk/gluten avoidance, bovine-insulin free infant formula (reducing intestinal inflammation may help)
probiotics (contradictory findings)
fecal microbiota transplantation (one trial was successful (de Groot et al. 2020)
vitamin D (might be most helpful in those with vitamin D deficiency)
omega 3 fatty acids (might be helpful)
nicotinamide (did not help, at low doses and late in autoimmunity process).
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).
Do Environmental Chemicals Play a Role in Type 1 Diabetes Development?
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, PFASs, 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 chemicals 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 many of the reports and consensus statements described below call for more research on the role of environmental chemicals in type 1 diabetes.
Type 1 Diabetes Incidence and Chemical Production, U.S.
Type 1 diabetes incidence has increased in conjunction with chemical production in the U.S. over the past decades. Incidence rates were low before World War 2 (the range is shown in the bars above 1920), when the widespread use of chemicals began. While correlation does not prove causation, these trends could be related.
You can click on the image to make it larger. Chemical data from Neel and Sargis 2011, type 1 incidence data from various studies, included in this PubMed collection.
Do Environmental Chemicals Play a Role in Type 2 Diabetes Development?
Consider that about 20% of adults with diabetes do not have overweight or obesity (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 some studies of people with very low levels of chemical exposures, obesity does *not* increase the risk of diabetes (Lee et al. 2006).
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.
There are a number of research efforts in the European Union that are working to address this question. The OBERON project is one effort. It aims to build an integrated testing strategy to develop and validate testing systems to understand the biological mechanisms of how endocrine disrupting chemicals influence metabolism (e.g., diabetes and obesity). OBERON will combine laboratory experiments, cell studies, screening and computational technologies, and human studies to accomplish this goal (Audouze et al. 2020). Similarly, the EDCMET project (Metabolic effects of Endocrine Disrupting Chemicals: novel testing METhods and adverse outcome pathways) aims to develop predictive methods and models to evaluate the detailed mechanisms and pathways to aid in regulatory risk assessment of endocrine disrupting chemicals (Küblbeck et al. 2020). The GOLIATH project will generate the world's first integrated approach to testing and assessment specifically tailored to metabolism-disrupting chemicals (Legler et al. 2020).
Do Environmental Chemicals Play a Role in Gestational Diabetes Development?
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.
Do Environmental Chemicals Play a Role in Diabetes Management and Complications?
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!
According to researchers, "Evidence suggests that disproportionate exposures to endocrine disrupting chemicals (EDCs) may contribute to subgroup-specific diabetes risk; however, no federal policies regulate EDCs linked to diabetes based upon diabetogenic potential. Nevertheless, analyses of European Union data indicate that such regulation could reduce diabetes-associated costs and disease burden. Federal laws only regulate EDCs indirectly. The accumulating evidence linking these chemicals with diabetes risk should encourage policymakers to adopt stricter environmental standards that consider both health and economic impacts." (Shaikh et al. 2018).
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.
Reports and Consensus Statements
NTP Report on Environmental Chemicals in Diabetes and Obesity
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 include
workshop overview (Thayer et al. 2012)
arsenic and diabetes (Maull et al. 2012)
persistent organic pollutants and diabetes (Taylor et al. 2013)
maternal smoking, childhood obesity, and metabolic disorders (Behl et al. 2013).
NIEHS Report on Environmental Factors in Autoimmune Diseases
The National Institute of Environmental Health Sciences (NIEHS) 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."
Dr. Jerry Heindel, former Scientific Program Administrator from the National Institute of Environmental Health Sciences (NIEHS), helped organize the workshop on the role of environmental chemicals in the development of diabetes and obesity, and the Parma Consensus Statement on Metabolic Disruptors.
He is interested in finding out how chemicals may affect the development of type 1, type 2, and gestational diabetes, as well as obesity and metabolic syndrome; NIEHS provides funding toward this research. He is now running HEEDS.org, Healthy Environment and Endocrine Disruptor Strategies.
CHEM Trust Report
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 Scientific Statements
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).
Parma Consensus Statement on Metabolic Disruptors
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."
Uppsala Consensus Statement on Environmental Contaminants and the Global Obesity Epidemic
This Uppsala Consensus Statement concludes, "Since there are now numerous animal and epidemiological studies indicating that environmental pollutants could contribute to the global obesity epidemic, there is an urgent need to reduce the burden of environmental contaminants so that obesity does not become the normal outlook in the future. The workshop attendees concluded that public health efforts should focus on the importance of early obesity prevention by means of reducing chemical exposures, rather than only treating the established disease. Just as a bad start can last a lifetime and beyond, a good start can last a lifetime as well." (Lind et al. 2016).
Can We Reduce Our Exposure to Environmental Chemicals?
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...). Sargis et al. (2019) provide a fabulous review of many potential interventions, and cite the science behind them. Lee and Jacobs (2019) talk about how to eliminate chemicals from the body. The Environmental Working Group and Because/Health provide 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: firstname.lastname@example.org.
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. We already know that exposure to toxic chemicals during development is harmful, it is past time to reduce population-wide exposures (Grandjean et al. 2018).
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.
Listen to Dr. Kris Thayer, formerly of the National Toxicology Program, discuss efforts to conduct research on type 1 diabetes and environmental chemicals on this call, Type 1 Diabetes and the Environment, sponsored by the Collaborative on Health and the Environment (2014).
Can We Prevent Type 1 Diabetes?
Only one successful intervention trial has found a way to prevent type 1 diabetes development, the drug Teplizumab. See the Pharmaceuticals page for details.
For a good review of what has been tried in the past, 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). The good news, however, is that researchers are calling for a "paradigm shift" to view type 1 diabetes as preventable (Schofield and Sutherland, 2019). There are reviews of efforts to prevent type 1 diabetes, either before or after antibodies develop (e.g., Primavera et al. 2020).
So, 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. Please also see the website, preventt1d.org or join the Facebook group, Prevent Autoimmune Disorders, for more details on these, and to see what others have tried. There is a trial that is open to enrollment to see if vitamin D and omega 3 supplements can help prevent the development of type 1 diabetes (Ricordi et al. 2019). For information on enrollment, see the grassroots health D*Action project. No approach is guaranteed to work, of course, an no approach will work for everyone, since there are many causes of type 1 diabetes. But these ideas are not likely to lead to any harm either (although it is possible, and always consult your doctor!). See the linked pages for more information and sources. You could try to:
Give children over age 1 who live at latitudes more than 30 degrees from the equator (that includes almost all of the U.S.) 1000-2000 IU vitamin D3 per day, especially during the winter, "to substantially reduce their risk of type 1 diabetes" (Mohr et al. 2008). Other children may benefit as well, especially if they are deficient in vitamin D. Pregnant and lactating women may require higher levels of vitamin D to avoid a deficiency. Do not assume your vitamin D levels are adequate-- get tested by your doctor.
Ensure adequate levels of omega-3 fatty acids, especially during pregnancy and in early life. Fish oil, such as cod liver oil, contains both these fatty acids and vitamin D.
Taking anti-oxidant supplements (e.g., vitamin C, nicotinamide) does not appear to reduce the risk of type 1 diabetes, but it is still possible that a diet high in anti-oxidants (e.g., vegetables) may still be protective. Eating high glycemic-index foods may accelerate the progression of type 1 diabetes (see the nutrition page).
If possible, follow the World Health Organization (WHO) infant feeding guidelines: exclusive breastfeeding for a full 6 months, the introduction of safe and complementary foods from the sixth month of life while breastfeeding continues, and then continued breastfeeding for up to 2 years of age or beyond. (Avoid eating red meat and processed meat while breastfeeding).
Do not introduce solid food in the first three months of life. Be careful introducing certain foods such as dairy, gluten, or soy. Introduce them in small amounts, while breastfeeding, and not too early in life (see the wheat and dairy page).
Support the maturation of the intestine with probiotics (see the diet and the gut page). Supplementation with probiotics in the first month of life reduced the risk of type 1-related autoimmunity in children at high genetic risk of type 1 diabetes (although had no effect in children of lower genetic risk) (Uusitalo et al. 2016).
A trial did find fecal microbiota transplantation to be successful; more research on this will be forthcoming (de Groot et al. 2020).
Moderate and vigorous exercise improves glucose tolerance in children at risk of type 1 diabetes (Johnson et al. 2022).
Try to avoid giving birth by Caesarean section if possible (although do not avoid an emergency C-section! They are not linked to diabetes) (see the gestation and birth page).
Limit beta cell stress with adequate physical exercise, by avoiding extra weight gain, and by limiting stress (Ludvigsson 2006).
Reduce exposures to environmental chemicals (see "Reducing exposures" above).
Both men and women should avoid processed meats or other foods containing nitrate or nitrite when trying to conceive a baby. Especially avoid Icelandic smoked mutton, but you'll have to read the nitrate/nitrite page for that story.
Please keep in mind that even if all these measures really do help and reduce the risk for our loved ones getting type 1 diabetes, many people still may get the disease. My younger son, who has type 1 diabetes is living proof (although I didn't try them all!). Of course, the point is not to make anyone feel guilty; I could feel guilty about being vitamin D deficient, not supplementing with omega 3s or vitamin D, and possibly even eating bacon while conceiving a baby... but that's a waste of my time.
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.
Researching Environmental Chemicals and Diabetes
Studies on Chemicals and Type 1 Diabetes
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. It has so far (2018) found that there are multiple pathways leading to the destruction of pancreatic beta-cells (Rewers et al. 2018). Yet, like most other prospective studies, it mostly 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:
Incorporating measurements of multiple environmental chemical exposures (in parents and children) into on-going, prospective studies of type 1 diabetes.
Laboratory experiments of chemical exposures in animals and cells that could shed light on possible mechanisms and help identify which chemicals are most likely to be important for type 1 diabetes.
Studies of chemical exposures across generations, especially in utero or in early life, and type 1 diabetes development.
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 chemicals, 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).
Which Environmental Chemicals Should Be Studied?
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."
Why Is It So Hard to Figure This Out?
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 epigentics and endocrine disruption pages for some examples and more information).
For more on the barriers to doing human epidemiological studies on environmental chemicals, see Lee and Jacobs 2019.
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).
Read the report, "A review of the science linking chemical exposures to the human risk of obesity and diabetes," published by CHEM Trust.
Listen to the calls/webinars:
The Obesogen Effect: Why We Eat Less and Exercise More but Still Struggle to Lose Weight, A Conversation with Scientist and Author Dr. Bruce Blumberg (March 2018)
Chemicals in House Dust: Potential Contributors to Obesity and Metabolic Disorders (Oct. 2017)
Chemical contributors to Type 2 Diabetes (Nov. 2016)
Gestational Diabetes and Environmental Chemical Exposure (June 2015)
A High Price to Pay: Obesity, Diabetes, and Associated Costs of Exposure to Endocrine Disrupting Chemicals in the European Union (Apr. 2015)
Environmental Exposures and Immune Function with Dr. Paige Lawrence (Jan. 2015)
Type 1 Diabetes and the Environment (Nov. 2014)
The Link between Arsenic Exposure and Diabetes: A Review of the Current Research (Mar. 2014)
The Role of Environmental Chemicals in the Development of Diabetes and Obesity (Dec. 2011)
Diabetes and Obesity: Evaluating the Science on Chemical Contributors (May 2011)
Calls sponsored by the Collaborative on Health and Environment.