A number of dietary factors have been studied in association with the development of type 1 diabetes, including possible risk factors like cow's milk and the gluten in wheat, as well as possible protective factors such as breastfeeding and various nutrients. See the appropriate pages for information on these foods. (Other factors that also involve diet, including vitamin D deficiency and nitrate/nitrite, are covered in other sections). Much of the focus of these studies have been diet in early life, since the autoimmune antibodies that are associated with the development of type 1 diabetes can often be detected very early in life (Hummel and Zeigler, 2011).
Razmpoosh et al. 2015). A systematic review of 6 studies and meta-analysis of 5 studies found that probiotics are associated with lower fasting blood glucose levels in people with type 2 diabetes (Samah et al. 2016).
The results of these studies have been mixed. After reading them, you might agree with the title of this editorial in the Journal of the American Medical Association (JAMA): "Infant diets and type 1 diabetes: too early, too late, or just too complicated?" (Atkinson and Gale 2003).
Knip et al. (2010) review the findings of studies on infant feeding and type 1 diabetes, and conclude that while no specific dietary factor or nutrient has been conclusively found to play a role in the development of type 1 diabetes, data do indicate that certain dietary factors may predispose to or protect against the disease.
It may be that foods like cow's milk and gluten have been associated with type 1 diabetes development for the same reason: because of a malfunctioning intestine (gut). Vaarala (2002) points out that the intestinal walls of people with type 1 diabetes have been found to be more permeable (leaky) than people without type 1, and their intestinal immune system seems to be more active as well, due to inflammation. Vaarala suggests that perhaps these irregularities in the gut immune system in people who develop type 1 diabetes underlie early dietary findings, such as the association of type 1 diabetes with the consumption of cow's milk formula in infancy.
Gut inflammation appears to increase the leakiness of the gut. This inflammation has been found in both children with type 1 diabetes and in animal models of diabetes such as non-obese diabetic (NOD) mice, and its source is unknown. A leaky gut can allow the entrance of certain proteins such as are found in wheat or cow's milk, leading to inflammation and autoimmunity. Exposure to these foods alone, however, is not likely the cause of type 1 diabetes without underlying changes in the gut immune system and a leaky gut (Vaarala 2008).
There is some discussion as to whether a leaky gut leads to diabetes, or if diabetes leads to a leaky gut. Either way, a leaky gut appears to be involved in type 1 diabetes (Li and Atkinson, 2015).
Gut inflammation and permeability are also likely accompanied by changes in gut microbiota (Vaarala 2011). The term ‘gut microbiota’ represents a complex microbial community within the body (Atkinson and Chervonsky, 2012). In fact, alterations in gut microbiota may very well explain the increased gut permeability, inflammation, and immune dysfunction in type 1 diabetes (Vaarala 2013).
The gut microbiota is intimately linked with the immune system. It is capable of affecting health by contributing to nutrition, prevention of infectious disease, and through influencing the development and maintenance of the immune system. The importance of the gut microbiota for autoimmunity has already been established, and most research now is looking into the mechanisms by which microbes specifically influence the development of autoimmune disease. An increasing body of evidence supports the idea that the gut microbiota may influence the development of type 1 diabetes, although more studies are necessary to show this for sure (Atkinson and Chervonsky, 2012).
Some research shows that the gut microbiome of people with prediabetes or diabetes is different to that of healthy people. However, these changes seem to emerge after the appearance of type 1-related autoantibodies, suggesting that the gut microbiota might be involved in the progression from beta-cell autoimmunity to clinical disease, rather than in the initiation of autoimmunity (Knip and Siljander 2016). Research does show, however, that gut microbiome development does differ in populations with differing rates of type 1 diabetes, and that the species involved are involved in immune system activation (Vatanen et al. 2016). Some authors have looked at interactions between diet, gut microbiome, and autoimmunity, and hypothesize that these together influence the development of type 1 diabetes (Endesfelder et al. 2016).
Analyses of the gut microbiota from people with type 1 related autoimmunity found that these people have an aberrant gut microbiome, as compared to controls (Brown et al. 2011; de Goffau et al. 2013). An analysis of Spanish children with type 1 diabetes found that they had different gut microbiota than children without diabetes. Some of the gut microbiota species were also correlated with blood glucose levels in the children with diabetes (Murri et al 2013). Mexican children with type 1 diabetes also have an altered gut microbiota as compared to those without diabetes (Mejía-León et al. 2014), as do Turkish children (Soyucen et al. 2014), and newly diagnosed young children from the Netherlands (de Goffau et al. 2014), and in China (Qi et al. 2016). Italian children at risk of type 1 have different gut microbiota than healthy controls, and higher gut permeability as well (Maffeis et al. 2016). Changes in gut microbiota appear to affect susceptibility to type 1 diabetes in the U.S. Alkanani et al. 2015). Also note that geography can make a difference in gut microbiota; a study of type 1 diabetes in numerous countries worldwide found that there are strong differences in microbiota types in different countries around the world (Kemppainen et al. 2014).
In animals, gut microbiota clearly has an effect on the development of diabetes. In fact, transferring the microbiota from genetically resistant mice to genetically prone mice delayed the development of type 1-like diabetes in the prone mice (Peng et al, 2014).
A German study has looked at the gut microbiota in early life, comparing children with and without islet autoimmunity, a precursor to type 1 diabetes. In both sets of children, they found that the composition of the gut microbiota changed substantially during the first year of life, and was affected by breastfeeding, food introduction, and birth delivery (e.g., vaginal vs. C-section). They did not find any differences in diversity or composition of the gut microbiota in children with and without autoimmunity. Yet they did find changes in "microbial interaction networks" in children who went on the develop type 1-related autoimmunity (Endesfelder et al. 2014). However, another study, this time from Finland, did find differences in early life gut microbiota between those who ended up developing type 1 and those who did not. They found that certain species were higher in those who developed diabetes, that that these species peaked over 8 months before the appearance of autoantibodies. The timing seems to coincide with the introduction of solid food (Davis-Richardson et al. 2014). Another study from Finland also found that the gut microbiome differed among children who went on to develop autoimmunity and then type 1 diabetes, as compared to those who did not (Cinek et al. 2016).
A group of authors that examined the gut microbiota over time in infants prone to type 1 found that an individual's microbiota remained relatively stable over time (although varied among people). And yet changes in the microbiota did appear between the development of autoimmunity and type 1 diabetes diagnosis (Kostic et al. 2015).
In animals, early life exposure to gut microbes can influence sex hormone levels and thereby the development of diabetes in non-obese diabetic (NOD) mice, an animal model of type 1 diabetes (Markle et al. 2013). Diabetes-prone NOD mice fed a gluten-free diet had a lower incidence of diabetes then those fed a gluten-containing diet, and this difference was associated with differences in their intestinal microbiota (Marietta et al. 2013). When pregnant and lactating NOD mice were fed a gluten-free diet, their offspring had a lower incidence of diabetes and different microbiota-- even when the pups ate a normal diet (Hansen et al. 2014).
Drinking water acidity was also shown to affect the development of diabetes in NOD mice, and was also associated with changes in intestinal microbiota (Sofi et al. 2014; Wolf et al. 2014). A study in Norway found that people whose drinking water was more acidic had four times as many cases of type 1 diabetes compared to people who drank less acidic water (Stene et al. 2002), and the prospective study from Germany mentioned above also found that autoantibody-positive children who drank more acidic water had a somewhat faster progression to type 1 diabetes (Winkler et al. 2008).
You might ask whether or not the use of antibiotics might be associated with the development of type 1 diabetes, since antibiotic use does affect gut microbiota composition (Korpela et al. 2016).
A number of long-term, population-wide studies from Denmark have examined this possibility. One found that taking broad-spectrum antibiotics during the first two years of life was associated with an increased risk of type 1 diabetes in the next 13 years of life, but only in children delivered by C-section (not in children delivered vaginally) (Clausen et al. 2016). Another found no association overall, except filling 5 or more broad-spectrum antibiotic prescriptions in the first two years of life did result in a higher risk of type 1 diabetes (Mikkelsen et al. 2016). An older study found no link between antibiotic use and type 1 diabetes development (Hviid and Svanström, 2009), although the latter study may not have considered all of the factors that the newer studies did.
Animal studies do show that antibiotic use does affect the intestinal microbial composition of animals, and this is associated with changes in diabetes development, in diabetes-prone BB-rats. Curiously, however, the effect was largely protective (Brugman et al. 2006). However, studies of NOD mice, another rodent strain prone to diabetes, did find that antibiotics (taken from conception through adulthood) increased the risk of diabetes (Brown et al. 2015 Candon et al. 2015; Livanos et al. 2016). Low-dose antibiotics given starting at birth transiently alters the gut microbiota leading to long-term changes metabolism, and affecting immune system genes (Cox et al. 2014). In NOD mice, the prenatal period is the most critical for antibiotic exposure, as compared to later in life. Scientists were able to prevent diabetes from appearing by targeting certain bacteria that cause infections Hu et al. 2015). Another study by the same authors shows that prenatal antibiotics affects the gut microbiota early in life and is critical for education of the immune system after that (Hu et al. 2016).
Other authors have looked at the effect of early life antibiotics on pigs, to better mimic humans than rodents do. They found that that early life antibiotic exposure affects glucose metabolism 5 weeks after antibiotic withdrawal, and was associated with changes in pancreatic development. The antibiotics had a temporary effect on postnatal gut microbiota, and the changes in pancreatic development only appeared later in life (Li et al. 2017).
Since probiotics (e.g., the beneficial microorganisms found in yogurt) can support proper gut maturation in animals (Calcinaro et al. 2005), the PRODIA study is studying whether using probiotics during the first six months of life decreases the appearance of autoantibodies in children at genetic risk of type 1 diabetes (Ljungberg et al. 2006). Another study, in Germany, is seeing whether or not prebiotics (which help the growth of microorganisms) improve blood sugar control in children with type 1 diabetes (Ho et al. 2016).
One type of probiotic, Lactobacillus johnsonii, has been found to delay the development of diabetes in diabetes-prone rats (Valladares et al. 2010). Another probiotic prevents diabetes in mice (Dolpady et al. 2016). Supplementation with probiotics in the first month of life successfully reduced the risk of type 1-related autoimmunity in children with high genetic risk of type 1 diabetes (Uusitalo et al. 2015). (This research was first presented in an abstract for the European Association for the Study of Diabetes (EASD) (Uusitalo et al. 2014).) The authors however are not yet recommending widespread supplementation-- they feel more research is needed first. Also note that the probiotics had no effect in children with lower genetic risk.
Other factors can also affect gut microbiota. For example, in infants, umbilical cord blood vitamin D levels, as well as race, breastfeeding and mode of delivery are associated with gut microbiota composition (Sordillo et al. 2016). Exercise is another factor: people with type 1 who have good blood glucose control and who exercise have similar microbiota to people without diabetes (Stewart et al. 2016). The feces of people with both type 1 and type 2 diabetes contain higher levels of Candida than people without diabetes, and no difference was found in type 1 vs. type 2 (Gosiewski et al. 2014).
Environmental factors that interfere with the gut immune system can probably influence the incidence of type 1 diabetes (Vaarala 2002). Viruses, for example, may be able to increase gut inflammation and permeability. Altered gut microbiota may also explain why children who develop type 1 diabetes are prone to stomach virus infections, or do not develop tolerance to cow's milk proteins (Vaarala 2012).
Dietary emulsifiers (found in processed foods) have been shown to affect the gut microbiota, resulting in low-grade inflammation, and promoting the metabolic syndrome in mice (Chassaing et al. 2015).
Environmental chemicals can also affect gut microbiota; see below.
As in type 1 diabetes, disturbances in the composition and function of gut microbiota may also be involved in type 2, obesity, and insulin resistance, along with a leaky gut and inflammation (Allin et al. 2014).
Amazingly, gastric bypass (bariatric) surgery often leads to remission of type 2 diabetes, even before or without weight loss (Pournaras et al. 2010). There must be something going on in the gut that can contribute to type 2 diabetes; we don't yet know what it is. You may believe that scientists are scrambling to figure this out-- it was an entirely unexpected finding-- and there are many ideas as to why it happens (e.g., gut hormones, Sala et al. 2014).
Bariatric surgery has also been used in obese people with type 1 diabetes. In this case, the diabetes is not put into remission, and patients still need to take insulin, although often much less insulin. Some have better glucose control (lower HbA1c) after the surgery than before (Brethauer et al. 2014; Chow et al. 2016; Middelbeek et al. 2014), but not necessarily, and there is also a risk of both hypoglycemia and ketoacidosis (Kirwan et al. 2016; Rottenstreich et al. 2016).
Gut microbiota may be involved in the development of obesity and type 2 diabetes (Cani and Delzenne 2010). The gut microbiota plays a significant role in the development of the metabolic syndrome as well (Mazidi et al. 2016). Gut microbial composition and functions are strongly influenced by diet, and affect metabolism via energy absorption, gut motility, appetite, glucose/lipid metabolism, as well as fat storage in the liver. An impairment of gut microbes can cause inflammation and insulin resistance (Festi et al. 2014). Animal studies show that gut microbiota can affect the development of obesity, insulin resistance, and diabetes through a variety of mechanisms. A Western diet can promote microbiota that promote obesity (Musso et al. 2010).
A study of Danish adults found that those who had a low bacterial richness in their gut were more likely to be heavier and insulin resistant. Those who were obese and had low bacterial richness also tended to gain more weight over time (Le Chatelier et al. 2013). In Korea, researchers have found changes in the composition and function of "gut microbial markers" that could be used for early diagnosis of an inflamed gut (Yassour et al. 2016).
In fact, researchers are finding that they may be able to predict type 2 diabetes -- that is, identify women who have a type 2 diabetes-like metabolism by examining the gut "metagenome" -- that is, the genetic material from the gut microbiota. They compared the genetic material from women with diabetes, impaired glucose tolerance, and with normal blood glucose levels. They found differences among these groups, and then used these differences to create a model to predict the risk of type 2 diabetes. These methods also show that the metagenome markers for type 2 diabetes differ between European and Chinese women, so these tools may have to be developed depending on the age and geographic location of the people studied (Karlsson et al. 2013).
In animals, scientists can cause (or prevent) obesity by altering the gut microbiota. They can transfer gut microbiota from a fatter mouse to a thinner mouse and the thinner mouse gains weight (Ridaura et al. 2013; Turnbaugh et al. 2006). Certain beneficial microbiota can also reduce weight gain and improve glucose tolerance in mice (Stenman et al. 2014).
There are microbiota elsewhere in the body aside from the gut. Interestingly, oral microbiota types have been associated with insulin resistance (Demmer et al. 2016).
A large analysis of data from the U.K. found that taking antibiotics was associated with an increased risk of developing type 2 diabetes, the risk increasing with the number of antibiotic courses taken (Boursi et al. 2015). A longitudinal study of U.K. children found that antibiotic use during the first six months of life was associated with higher body weight during early childhood (Trasande et al. 2013). Other studies also show that antibiotic use in the first 2 years of life is associated with childhood obesity (Bailey et al. 2014; Scott et al. 2016). In a large, long-term study, researchers found that in healthy U.S. children, antibiotic use was associated with persistent weight gain throughout childhood. Children who had used antibiotics 7 or more times weighed about 3 pounds heavier at age 15 than those who did not use antibiotics (Schwartz et al. 2015). Macrolide antibiotics are associated with weight gain in Finnish children (Korpela et al. 2016). Also in Finnish children, antibiotic use in the first six months of life, or repeated antibiotic use during infancy, was associated with excess weight gain in the first 2 years of life (Saari et al. 2015).
However, not all studies show a link-- one found that antibiotic use in the first six months of life was not associated with excess weight gain in U.S. children through age 7 (Gerber et al. 2016). And, a large U.S. study found that it was infection-- but not antibiotics-- that was associated with the risk of childhood obesity (Li et al. 2016).
Antibiotic use during pregnancy is associated with an increased the risk of obesity by 84% in U.S. children at age 7 (Mueller et al. 2014). It is also associated with lower birth weight and higher levels of the hormone leptin in umbilical cord blood (Mueller et al. 2016).
In animals, low-dose antibiotics given starting at birth transiently alters the gut microbiota leading to long-term changes in metabolism, enhancing the effect of diet-induced obesity (Cox et al. 2014). Lifelong antibiotics plus a high-fat diet led to different gut microbiota, higher weight, fat mass, and insulin resistance than in mice only exposed to a high-fat diet (Mahana et al. 2016). The effects of antibiotics on obesity also depends on genetics (Fujisaka et al. 2016).
In a study of rats the animals given probiotics had a lower body weight and more diverse intestinal biota than the controls and those who received E coli (a harmful microorganism) (Karlsson et al. 2011).
A study from China has raised another issue-- whether antibiotics given to animals (veterinary antibiotics) are a health issue for humans. This study found that although human antibiotic levels were not associated with obesity in children, veterinary antibiotic levels were (Wang et al. 2016).
A double-blind, placebo-controlled, randomized clinical trial of women with gestational diabetes found that those who took a probiotic had less weight gain and lower fasting blood glucose levels than those who received a placebo (Dolatkhah et al. 2015). Another double-blind, placebo-controlled, randomized trial of women with gestational diabetes found that those who took probiotics for 6 weeks had better glucose control, lower insulin resistance, and better triglyceride levels than those who received a placebo (Karamali et al. 2016). A third randomized controlled trial of women with gestational diabetes found that probiotics lowered inflammation and insulin levels, and improved insulin resistance (Jafarnejad et al. 2016).
One significant environmental factor that may be able to affect the gut immune system, intestinal permeability, and gut microbiota is environmental chemicals. For an article describing research on gut microbiota and autoimmune disease (including type 1 diabetes), and factors such as chemicals that may influence the gut microbiota, see The Environment Within: Exploring the Role of the Gut Microbiome in Health and Disease, published in Environmental Health Perspectives (Konkel, 2013). The relationship goes both ways-- chemicals can affect the gut microbiome structure and function, and the gut microbiome can transform chemicals (Lu et al. 2015).
When rats are given a chemical called streptozotocin (STZ) which can induce insulin-dependent diabetes, their microbiota changes drastically as diabetes develops. The diversity of the microbiota diminishes over time (Patterson et al. 2014). The microbiota also vary depending on where they are in the digestive tract (Wirth et al. 2014).
Researchers are beginning to look at the role of the intestine on the fate of contaminants in food. These contaminants can include things like pesticides, heavy metals, and persistent organic pollutants (POPs) such as organochlorine insecticides, PCBs, dioxin, and polycyclic aromatic hydrocarbons (PAHs). Many chemicals enter the body through the intestine, exposing the intestinal cells to significant concentrations. Some of these chemicals can affect the absorption of other, possibly unrelated, substances, and are likely to influence intestinal inflammation as well (some are reviewed in Sergent et al. 2008). For example, the heavy metal cadmium affects the gut microbiota and causes gut inflammation in rats (Ninkov et al. 2015). The pesticide carbendazim reduces the richness and diversity of gut microbiota in mice (Jin et al. 2015).
In a review, Snedeker and Hay (2012) look at how interactions between gut ecology and environmental chemicals may contribute to the development of diabetes and obesity. The microorganisms in the gut may affect an individual's exposure to environmental chemicals; these microorganisms can affect the absorption, distribution, metabolism, and excretion of environmental chemicals, including chemicals linked to diabetes and obesity. For an article describing this review, see Gut check: Do interactions between between environmental chemicals and intestinal microbiota affect obesity and diabetes? published in Environmental Health Perspectives (Holtcamp 2012). You can also listen to Drs. Snedeker and Hay discuss this research on the call, Gut microbiota and environmental chemicals in diabetes and obesity, sponsored by the Collaborative on Health and the Environment (CHE).
Specific studies are also enlightening. In a study of Korean women, those with higher levels of certain bacteria in their guts had higher body mass index and waist circumference. They also had higher levels of persistent organic pollutants in their bodies, suggesting that there may be an interaction among all of these factors (Lee et al. 2011). This research is also discussed on the CHE call, Gut microbiota and environmental chemicals in diabetes and obesity.
Only a few studies have addressed the effects of chemicals directly on the intestine and gut microbiota. Lu et al. (2014) found that mice who drank arsenic-laced water developed an altered gut microbiome as well as functional differences in their gut. Meanwhile, changes in the gut microbiome caused by an infection affected the absorption and metabolism of arsenic in mice (Lu et al. 2013). The gut microbiome can also turn less-harmful varieties of arsenic into more-harmful varieties (D.C. Rubin et al. 2014). For an article on this topic, see Fire in the belly? Sulfur-Reducing Gut Microbes Fuel Arsenic Thiolation, published in Environmental Health Perspectives (Potera 2014). Thus, there may be interactions between the microbiome, chemicals, and other factors such as infections that may all be important.
Ishida et al. (2005) found that dioxin damages the intestinal epithelium in one strain of mice (but not another) by increasing intestinal permeability. The dioxin-treated mice also had higher glucose levels after a glucose tolerance test. The authors suggest that dioxin initially damages the intestine, and the tissues respond by facilitating the absorption of glucose.
Another study found that some PCBs can disturb the intestinal barrier and alter gut permeability (in animals and in experiments using human intestinal cells) (Choi et al. 2010). A study of mice found that PCBs induced substantial changes to the gut microbiome, which could influence their toxicity. Interestingly, exercise reduced the severity of these changes (Choi et al. 2013). Another persistent organic pollutant (POP), TCDF, was found to alter the gut microbiota of mice in ways that may contribute to diabetes and obesity (Zhang et al. 2015). For an article explaining this study, see the article, POPs and gut microbiota: Dietary exposure alters ratio of bacterial species, published in Environmental Health Perspectives (Potera 2015). Dioxin (TCDD), also a POP, changes the gut microbiome in mice treated with a chemical to induce type 1-like diabetes, also causing liver toxicity (Lefever et al. 2016).
Pesticides can also be a food contaminant, as a result of their use in agriculture. Daily ingestion of low doses of diquat, an extensively used herbicide, induces intestinal inflammation in rats. The authors of this study suggest that repeated ingestion of small amounts of pesticides, as could be found in food, may have consequences for human health and may be involved in the development of gastrointestinal disorders (Anton et al. 2000). Chronic exposure during early life to the pesticide chlorpyrifos increases gut permeability in rats pups at the time of weaning (but not in adulthood) (Joly Condette et a. 2014). Chlorpyrifos also affects the gut microbiota, impairs the intestinal lining, and stimulates the immune system of pup rats (Joly Condette et al. 2015). Interestingly, researchers have found that giving the prebiotic inulin, which helps support gut microbiota, can actually correct the metabolic effects of early life exposure to the pesticide chlorpyrifos in lab animals (Reygner et al. 2016). Other pesticides also appear to affect the gut; the organophosphorous pesticide monocrotophos induces intestinal dysfunction in rats (Vismaya and Rajini, 2014), and the pesticide diazinon disrupts the gut microbiota of mice (Gao et al. 2016). A study from rural India shows a high prevalence of diabetes in people directly exposed to organophosphates, as well as higher long-term blood glucose (HbA1c) levels. The authors also show that these pesticides affect the gut microbiota, and confirm these findings in animal studies. They conclude that the pesticides degrade the gut microbiota and thereby cause high blood glucose levels and diabetes (Velmurugan et al. 2017).
Food is also a major exposure route of BPA because it can leach out of food containers into food. In mice, BPA has been shown to detrimentally affect gut microbiota, in the same way a high-sugar or high-fat diet does (Lai et al. 2016). In dogs, who eat canned dog food, BPA affects the gut microbiota (Koestel et al. 2017). BPA has been shown to affect gut microbiota in both exposed rodents and their offspring (Jaruvek et al. 2016). In rats, perinatal exposure to BPA was found to promote the development of intestinal inflammation in adult female offspring, although it decreased intestinal permeability (Braniste et al. 2010). BPA also makes intestinal cells absorb more cholesterol (Feng et al. 2017). Bisphenol A diglycidyl ether (BADGE), a stabilizing compound that can also leach out of food containers, may also increase apoptosis (programmed cell death) of intestinal cells (Ramilo et al. 2006). Nonylphenol, another compound found in plastics, can disrupt the permeability of intestinal cells (Isoda et al. 2006). A more recent study found that early-life exposure to BPA made rats more susceptible to intestinal infection than those unexposed, and impaired their ability to respond to food antigens (Ménard et al. 2014).
Cadmium, another chemical that can enter the body via food, induces intestinal inflammation in mice, and in high doses can disrupt permeability in intestinal cells (Zhao et al. 2006). Cadmium can also disrupt the gut microbiota (Ba et al. 2016; Zhang et al. 2015). Mercury can increase gut permeability, at levels found in food (Vázquez et al. 2014). The polycyclic aromatic hydrocarbon benzo[a]pyrene, found in barbecued food, increases intestinal inflammation caused by a high fat diet in mice (Khalil et al. 2010).
A published case study describes a man who developed type 1 diabetes while undergoing chemotherapy for cancer, accompanied by abdominal pain and nausea. This is rare but potentially fatal (Adachi et al. 2015).
More studies like these may be of interest and importance for type 1 diabetes. What might be the combined effects of all of these food contaminants? No one knows.
In late 2014, the American Diabetes Association and JDRF co-sponsored a symposium, Diabetes and the Microbiome, which included a discussion of the microbiome in relation to type 1 and type 2 diabetes as well as obesity. You can read the full text of the workshop proceedings online for free. Some highlights (Semenkovich et al. 2015):
In some people, an inflamed, leaky gut with improper microbiota may contribute to the development of type 1 diabetes. The fundamental causes of these changes are unknown. Further studies should consider how environmental chemicals can affect gut inflammation, permeability, and microbiota. While we await the results of some intervention trials, we can support the gut immune system with probiotics and appropriately introduce suspected foods such as wheat and dairy products in our children. There is no evidence yet that these actions will prevent type 1 diabetes, but they are safe and not likely to lead to any harm.
Scientists are now looking into whether gut microbiota can be used for prevention or treatment of type 1 diabetes (Gülden et al. 2015), gestational diabetes (Isolauri et al. 2015), or type 2 diabetes (He et al. 2015).
To download or see all the references on this and other diet-related pages, including breastfeeding, cow's milk, gluten, and more, see the collection Diet, nutrition, gut, microbiome and diabetes/obesity in PubMed.