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. 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, 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).

 

It may be that if dietary proteins are removed from the diet until the gut matures, the autoimmune process will not occur. This idea is being tested in the Trial to Reduce IDDM (insulin-dependent diabetes mellitus, that is, type 1 diabetes) in the Genetically at Risk (TRIGR) study, where the introduction of foreign dietary proteins is postponed until after 6-8 months of age. In that trial, those not breastfeeding are using hydrolyzed formula instead of cow's milk formula (Vaarala 2008).

 

Normal intestinal microorganisms may be able to control intestinal inflammation, and affect intestinal permeability (Vaarala 2008). Since probiotics (e.g., the beneficial microorganisms found in yogurt) can support gut maturation in animals (Calcinaro et al. 2005), the PRODIA study plans to study 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). One type of probiotic, Lactobacillus johnsonii, has been found to delay the development of diabetes in diabetes-prone rats (Valladares et al. 2010). An analysis of gut microbiota from people who just developed type 1 related autoimmunity found that these people have an aberrant gut microbiome, as compared to controls (Brown et al. 2011).

 

Gut microbiota may be involved in the development of obesity and type 2 diabetes as well (Cani and Delzenne 2010). 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, as could overuse of antibiotics (Musso et al. 2010). In a study of rats, for example, 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). It is especially curious that gastric bypass surgery often leads to remission of type 2 diabetes, even without the associated 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.

Interestingly, Caesarean sections have been associated with an increased risk of type 1 diabetes in offspring. Why? The authors suggest that perhaps this is due to the gut microbiota. The gut microbiota differ in children born by C-section compared with those born vaginally (Cardwell et al. 2008).

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. Vitamin D may be involved in controlling gut permeability. As it stands, the fundamental reason for the inflammation and leaky gut is unknown (Vaarala 2008).

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 contaminants enter the body through the intestine, exposing the intestinal cells to significant concentrations. Some of these contaminants 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). 

In a review, Snedecker and Hay (2011) 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.

 

Only a few studies have addressed the effects of contaminants directly on the intestine. More than 90% of human exposure to POPs such as PCBs and dioxins is via food (Patandin et al. 1999). Ishida et al. (2005) studied the effects of dioxin on the intestine. They 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). 

 

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).

 

Food is also a major exposure route of bisphenol A because it can leach out of food containers into food. In rats, perinatal exposure to bisphenol A was found to promote the development of intestinal inflammation in adult female offspring, although it decreased intestinal permeability (Braniste et al. 2010). 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).

 

Cadmium, another contaminant 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). 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).

 

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 some people, an inflamed and leaky gut may contribute to the development of type 1 diabetes. The cause of this inflammation is unknown. Further studies should consider how environmental contaminants can affect gut inflammation and gut permeability. While we await the results of some intervention trials, we can support the gut immune system with probiotics and delay the introduction of 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.