Wheat and Dairy
Links Between Wheat and Dairy and Diabetes
There is a large body of research linking wheat and dairy products to an increased risk of type 1 diabetes. Not all findings are consistent, however. For more information on why foods such as wheat and dairy might contribute to the development of diabetes, and the involvement of the gut, see the Diet and the Gut page. The gut is a prime candidate for tying these dietary factors together.
Parents could be careful introducing certain foods to infants, especially wheat and cow's milk. Introduce them in small amounts, while breastfeeding, and not too early in life. Zeigler et al. (2003) suggest that using the World Health Organization WHO infant feeding guidelines, such as not introducing solid foods to infants before 3 months of age, may help reduce the incidence of type 1 diabetes. [In case you are curious, the WHO infant feeding guidelines also call for 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 (Pflüger et al. 2010). If you can't breastfeed or have financial issues with following these guidelines, please don't feel guilty! Most people don't follow them. But if you can, great.]
There has long been debate (and there are innumerable studies) about cow's milk and type 1 diabetes. As of 2019, the conclusion that one eminent type 1 researcher drew was that, "The jury is still out on possible links between cow's milk and type 1 diabetes" (Ludvigsson 2019). For the details, read on.
Recent studies that have followed children over time do find evidence that cow's milk consumption may increase the risk of type 1 diabetes and/or associated autoimmunity, although perhaps depending on genetic risk. For example:
A long-term study of U.S. children (beginning at birth) found that greater consumption of cow's milk was associated with the development of type 1-related autoantibodies-- but only in children of low to moderate risk of disease. However, cow's milk consumption was also associated with an increased risk of developing type 1 diabetes in all of the antibody-positive children (Lamb et al. 2015).
A longitudinal study from Finland found that higher cow's milk product consumption during childhood increased the risk of islet autoimmunity, and that milk processing methods did not matter (Koivusaari et al. 2020).
Published in the prestigious New England Journal of Medicine, a double-blind, randomized study assigned genetically at-risk infants to receive either regular cow's milk infant formula, or a a casein hydrolysate formula, when breastmilk was not available in the first 6-8 months of life. Over the next ten years, the children are being analyzed for type 1 diabetes as well as type 1 related autoantibodies. The first results were hopeful: the children given hydrolyzed infant formula had a 50% lower risk of developing type 1 related autoantibodies by age 10. This study was part of a larger trial, the TRIGR (Trial to Reduce IDDM in the Genetically at Risk). TRIGR began in 2002 and is currently running in 77 centers in 15 countries to answer the question of whether weaning to a hydrolyzed formula will reduce the incidence of type 1 diabetes. The authors suggest that the hydrolyzed formula reduces gut permeability, and has a beneficial effect on gut flora (Knip et al. 2010). However, after following the children for a longer period of time, it seem that hydrolyzed formula does NOT reduce the risk of type 1 diabetes-related antibodies in these children after 7 years (Knip et al. 2014), nor reduce the incidence of type 1 diabetes after 11 years (Knip et al. 2018). Nor did this intervention affect the rates of asthma, allergies, or eczema (Virtanen et al. 2021).
Dairy Products Are a Major Source of Environmental Chemical Exposure
This graph shows an estimation of per capita dietary exposure to numerous persistent organic pollutants using 2007 USDA food availability data and based on testing of food from a supermarket in Dallas, Texas. Dairy and eggs, fish, and meat, are major sources of chemicals in food.
A further study (the TEDDY study) also found that hydrolyzed infant formula did not decrease the risk of type 1-related autoimmunity at age 8-9 years. In fact, extensively hydrolyzed formula may be associated with an increased risk of autoimmunity, especially if introduced in the first week of life (Hummel et al. 2017).
A pilot study from Finland found that in comparison to regular cow's milk formula, weaning to a formula free of bovine insulin reduced the risk of type 1-related antibodies by age 3, in children at genetic risk of disease (Vaarala et al. 2012). A study found that children who later developed type 1 diabetes had higher levels of cow's milk antibodies in infancy. The authors suggest that this finding may be due to increased gut permeability or delayed maturation of the gut immune system in the children who developed diabetes. Early exposure to cow's milk may be a risk factor for type 1 diabetes only in children who have a dysfunctional gut immune system. (All the children in this study were fed cow's milk formula for at least two months; also see the breastfeeding page) (Luopajärvi et al. 2008). Weaning to an extensively hydrolyzed formula did decrease gut permeability during infancy, which could help reduce exposure to antigens in the diet (Silijander et al. 2021).
Another study from Finland found that cow's milk consumption was associated with an increased risk of type 1 diabetes-related autoimmunity, whereas breastfeeding was protective (Niinistö et al. 2017). Also in Finland, a population-wide study found that infants with cow's milk allergies had an increased risk of later developing type 1 diabetes during childhood (Lamminsalo et al. 2021).
Additional studies of cow's milk and type 1 diabetes have also been conflicting. Many studies have found that cow's milk consumption is associated with an increased risk of type 1-related autoimmunity or type 1 diabetes (e.g., El-Amir et al. 2019; Holmberg et al. 2007; Kimpimäki et al. 2001; Villagrán-García et al. 2015; Virtanen et al. 2012; Wahlberg et al. 2006), while others have not (Norris et al. 2003; Norris et al. 1996; Savilahti and Saarinen 2009; Virtanen et al. 2006; Ziegler et al. 2003). The differences may involve differences in timing, differences in the studies, genetic background in certain populations, or even the type of milk. A systematic review and meta-analysis of cow's milk studies found that cow's milk consumption in infancy to age 3 was not associated with type 1 diabetes development (Griebler et al. 2016).
Note also that eliminating cow's milk can affect growth and lead to nutritional deficiencies (Tuokkola et al. 2017).
Cow's milk contains bovine insulin, which is similar to human insulin, and can cause immune reactions in humans. Some researchers propose that an immune reaction to bovine insulin may spread to react with the body's own insulin, and eventually, in combination with other factors such as viruses, could result in an autoimmune attack against the insulin-producing beta cells, resulting in type 1 diabetes (Vaarala 2006). Mäkelä et al. (2006) have found evidence for this process in infants, finding that viral infections can enhance the immune response to insulin, induced by bovine insulin in cow's milk.
A1 vs A2 Milk
The milk protein casein has different variations (A1 or A2) depending on the breed of cow. Laugesen and Elliott (2003) found that consumption of milk containing the A1 type of casein is associated with type 1 diabetes (breeds that produce A1 milk are more common in northern Europe, where type 1 incidence is higher). Merriman (2009) argues that this association is instead due to latitude and the protective effects of vitamin D. There is quite a debate on this topic in the scientific literature, and I do not have time to properly wade through it. If you are interested in doing so, feel free. You can start here: Truswell 2005 or Clemens 2011 or Bell et al. 2006 or Chia et al. 2017; there are plenty more articles on PubMed relating to this topic. Another place to start is this article from Mother Jones, You're drinking the wrong kind of milk (March 14, 2014). Interestingly, a study on non-obese diabetic (NOD) mice found that it took a few generations for the effects of these milk proteins to show up (Chia et al. 2018).
Mycobacterium Avium Paratuberculosis (MAP)
Sardinia, Italy, is an island in the Mediterranean Sea that has a high incidence of type 1 diabetes. One study found that Sardinians with type 1 have high rates of infection with Mycobacterium avium paratuberculosis (MAP), which is transmitted from dairy herds through food to people (Masala et al. 2011). Scientists are now pursuing this topic further (e.g., Dow and Sechi, 2019; Masala et al. 2013; Masala 2014; Naser et al. 2013). People at-risk of type 1 diabetes tested positive to MAP-related markers more often than healthy controls. MAP is easily transmitted to humans with infected cow's milk and found in retail infant formulas, and possibly MAP could stimulate beta cell autoimmunity (Niegowska et al. 2016). Signs of MAP have been found in a significant number of people with type 1 diabetes in Iran, as compared to a group without diabetes (Hesam Shariati et al. 2016).
Type 2 Diabetes
While cow's milk consumption is often linked to a greater risk of type 1 diabetes, it is also often associated with a lower risk of type 2 diabetes. This association may depend on the type of milk product, however. A long-term study from the UK found that higher consumption of fermented diary products such as yogurt were associated with a lower risk of later type 2 diabetes in adults (O'Connor et al. 2014). A systematic review and meta-analysis of 16 studies that included a half million people found that a modest increase in yogurt, cheese, and low-fat dairy products was associated with a decreased risk of type 2 diabetes (Gao et al. 2013); another meta-analysis found that higher yogurt intake is associated with a reduced risk of type 2 diabetes in U.S. adults, and other dairy products are not associated (Chen et al. 2014).
Got Camel's Milk?
Get this-- of 12 people with type 1 diabetes who drank camel's milk over a 2 year period, 3 of them reduced their insulin requirement to zero! In total, the 12 showed better average blood glucose control, lower HbA1c levels, and lower insulin requirements than those who did not drink camel's milk (Agrawal et al. 2011). In people with type 2 diabetes, drinking camel's milk increases insulin levels as compared to drinking cow's milk (Ejtahed et al. 2015). In rodents with chemical-induced type 1 diabetes, camel's milk reduced kidney disease, lowered blood glucose levels, and lowered insulin resistance (Korish et al. 2015), lowered oxidative stress and helped the immune system (Badr et al. 2017), and, even better, increased insulin production and brought blood glucose levels down (other milks, including goat, cow, and buffalo, did not have this effect) (Meena et al. 2016). Other animal studies also show a benefit of camel's milk (Mansour et al. 2017). Camel's whey protein also restored glucose and insulin levels in rodents with chemical-induced type 1 diabetes (Sayed et al. 2017).
In fact, some authors propose that camel's milk consumption may be a reason the Raikas, a camel-rearing tribal group in northern India, have an extremely low incidence of type 1 diabetes-- despite their high genetic risk (Bhat et al. 2014). Raikas who do not consume camel's milk have an increased incidence of type 1, and non-Raikas who consume camel's milk have a decreased risk than those of their own ethnic group who do consume camel's milk (Agrawal et al. 2007).
A review found that most studies show a clinical benefit of camel's milk (for the treatment of many diseases, including diabetes), but that it "should not replace standard therapies" at this point (Mihic et al. 2016). Let's hope not. Additional reviews found that most studies of camel's milk show favorable effects (Mirmiran et al. 2017; Shah et al. 2019). But both camel's milk and cow's milk appear to be beneficial in rats with diabetes (Korish et al. 2019), and the probiotics in camel's milk have beneficial effects in mice susceptible to type 2 diabetes (Manaer et al. 2021).
Wheat and Gluten
Gluten may be linked to a variety of autoimmune diseases, including celiac disease and type 1 diabetes, perhaps because it can affect gut microbiota and increase intestinal permeability (Lerner et al. 2017). There is evidence that a gluten-free diet might help prevent type 1 diabetes, although as with cow's milk, I'd say the jury is still out (reviewed by Haupt-Jorgensen et al. 2018). A gluten-free diet is followed by many people with type 1 or type 2 diabetes, with or without celiac disease, and may have some benefits, as well as some disadvantages (like deficiencies in certain nutrients) (reviewed by Di Liberto et al. 2020).
Gluten During Childhood and Type 1 Diabetes
The Finnish Type 1 Diabetes Prediction and Prevention Study, a prospective birth cohort of children with genetic susceptibility to type 1 diabetes, found that those who had a high intake of oats, gluten-containing cereals, gluten, and dietary fiber during childhood (up to age 6) had an increased risk of islet autoimmunity (Hakola et al. 2019).
A large Norwegian study found that the mother's intake of gluten in pregnancy was not associated with type 1 diabetes, but a higher intake of gluten by the child at an early age was associated with a higher risk of type 1 diabetes (Lund-Blix et al. 2020).
Listen to Dr. Jill Norris, Colorado School of Public Health, discuss diet and type 1 on the call, Type 1 Diabetes and the Environment, sponsored by the Collaborative on Health and the Environment (2014).
A Gluten-Free Diet Prevents/Reverts Rype 1! Really! In Two People Anyhow...
Here's an amazing story: a 5 year old boy was diagnosed with type 1 diabetes (and not celiac disease), with high blood sugar levels (his HbA1c was 7.8%, which is not bad, but not normal either-- he must have had some residual insulin production). He was NOT given insulin, but started eating a gluten-free diet instead. His HbA1c went down to 5.8-6%, which is essentially normal, and at almost 2 years after diagnosis, he still does not need to take insulin. His diabetes is in remission, without insulin (Sildorf et al. 2012). Wow. (I would like also to point out that this does not work for everyone. My son, for example, was eating a gluten-free diet, and had been his whole life-- I even avoided gluten during his pregnancy-- and he still developed diabetes). Nonetheless, it is the first documented case I have seen in the medical literature of a person putting type 1 diabetes into remission without insulin or some other medical procedure, and it is published in BMJ, the British Medical Journal, a very reputable source.
Another boy, 15 years old, with "silent" celiac disease, had signs of glucose abnormalities, and tested positive for the autoantibodies associated with type 1 diabetes. In other words, he was well on his way to developing type 1. After 6 months on a gluten-free diet, his glucose went back to normal and the autoantibodies disappeared. Thirty six months later, he was still symptom-free. Type 1 appears to have been prevented! (Banin et al. 2002).
And, in a long-term study, children with celiac disease who had type 1 diabetes-related autoantibodies found that those antibodies gradually disappeared over two years after going on a gluten-free diet (Ventura et al. 2000). After a one-year trial of 15 children newly diagnosed with type 1 diabetes, HbA1c and insulin-dose adjusted A1c were lower in those who ate gluten-free. However, the number of people in remission (i.e., the "honeymoon" period) was not different (Svensson et al. 2016). A Swedish trial found that children diagnosed with type 1 who then ate a gluten-free diet had improvements in glucose control (Söderström et al. 2022). However, a study from Czechia found that while a gluten-free diet did affect the microbiome in children, those effects were not related to beta cell function. So some other mechanism is involved (Neuman et al. 2022).
Gluten has been thought to play a role in the development of type 1 diabetes due to the association between type 1 and the autoimmune celiac disease: around 7% of people with type 1 diabetes have celiac disease (Narendran et al. 2005). In general, for children at genetic risk of type 1 and celiac, type 1 autoantibodies tend to appear first. The occurrence of both diseases together is greater than genes or demographic factors predict, implying that shared environmental factors play a role in both diseases (Hagopian et al. 2017).
Similar to the bovine insulin in cow's milk, wheat also contains a protein that resembles another protein linked with the autoimmune attack in the pancreas (MacFarlane et al. 2003). Gluten has also been found to cause intestinal inflammation in people with type 1 diabetes (Auricchio et al. 2004).
While some reviews have found no links between the development of celiac disease and the timing of gluten introduction or of breastfeeding (Silano et al. 2016), or early feeding practices (Chmielewska et al. 2015), other studies show some associations.
While the longitudinal, international TEDDY study (The Environmental Determinants of Diabetes in the Young) found that the age of gluten introduction did not predict the development of celiac disease in children at genetic risk of this disease (Aronsson et al. 2015), it also found that higher gluten intake during the first 5 years of life was in fact associated with increased risk of celiac disease autoimmunity and celiac disease (Andrén Aronsson et al. 2019). And, it found that higher gluten in the diet in combination with more viruses in early childhood increases the risk of celiac autoimmunity (Lindfors et al. 2019). In the Swedish children in the TEDDY study, higher bread and cereal intake during the first two years of life was associated with celiac disease as well as celiac autoimmunity (Hård Af Segerstad et al. 2022).
Other studies have also found associations. A study from India found that delaying introduction to gluten, as well as breastfeeding during gluten introduction, both delayed celiac disease (Vajpayee et al. 2016). A study from Sweden found that introducing gluten before age 2 did in fact increase the risk of celiac disease in children genetically at risk for it (Aronsson et al. 2016). A longitudinal U.S. study found that toddlers (age 1-2) who ate more gluten had an increased later risk of celiac disease and associated autoimmunity (Mårild et al. 2019). A longitudinal Norwegian study found that higher gluten intake at 18 months of age was associated with an increased risk of celiac disease later in childhood. Introducing gluten after age 6 months was also associated with an increased risk (Lund-Blix et al. 2019).
A trial of hydrolyzed infant formula vs regular cow's milk formula found no difference in the development of celiac disease (Hyytinen et al. 2017). And, powdered milk in infant and young children's diet is not associated with the development of celiac either (Segerstad et al. 2018).
Some authors argue that it is other factors associated with wheat that could cause celiac disease, for example the pesticide that is used on wheat (Samsel and Seneff 2013).
Like type 1 diabetes, the prevalence of celiac disease is also rising in the U.S. (Choung et al. 2015).
Regarding other types of autoimmunity, neither the age of gluten introduction nor the amount of gluten consumed in early childhood is associated with the risk of thyroid autoimmunity (Gardner et al. 2020).
Exposure to Gluten in Infancy or In Utero and Type 1 Diabetes
Ziegler et al. (2003) found that early introduction of gluten-containing foods (before 3 months of age) to be a risk factor for the development of type 1-associated autoimmunity in children with genetic risk of type 1 diabetes. Chmiel et al. (2015) found the same thing, and also that this early introduction of gluten increased the risk of type 1 diabetes as well. Lund-Blix et al. (2019) found that introducing gluten before 4 months of age was associated with an increased risk of progressing from autoimmunity to type 1 diabetes, although that overall, eating more gluten did not increase the risk of autoimmunity or type 1. Norris et al. (2003) found that exposure to any cereals before 3 months of age (and also after 7 months), led to a higher risk of developing autoantibodies in genetically susceptible U.S. children. The authors propose that perhaps the reason that later introduction of cereals could increase risk is that older babies are likely to be fed larger amounts of food. Indeed, the study confirmed that babies given cereals at 7 months or older were more likely to be given more servings per day of cereals in the first month of exposure as compared to the others. This study also found that if cereals were introduced while the child was still breastfeeding, the risk of autoimmunity was lower. A more recently published paper from the same authors confirmed that breastfeeding at the time of wheat or barley introduction was protective against later type 1 diabetes development (Fredericksen et al. 2013).
Unlike the above studies, the TEDDY study found that early introduction of gluten (before 4 months) was associated with a decreased risk of islet autoimmunity. Like the Norris study, it also found that introducing gluten after 9 months of age was associated with an increased risk of islet autoimmunity (Uusitalo et al. 2018).
A long-term study from Denmark found that the more gluten a mother ate while pregnant, the higher the risk of type 1 diabetes in her children (Antvorskov et al. 2018).
Wahlberg et al. (2006) found that the combination of early cow's milk formula and late introduction of gluten increased the risk of autoimmunity in children.
Exposure to Gluten in Later Life
Interestingly, working as a baker, or in agriculture with grain crops, is linked to a reduced risk of type 1 diabetes. The authors suggest that exposure to gliadin via the nasal passages might be protective (Haupt-Jorgensen et al. 2017).
Animal studies support the potential role of gluten in type 1 diabetes development. A gluten-free diet dramatically inhibits diabetes development in animals, probably due to lower intestinal inflammation, lower gut permeability, and/or different gut flora (Buschard, 2011). A gluten-free diet only during pregnancy also prevents diabetes development in the offspring of non-obese diabetic (NOD) mice (a model of type 1 diabetes) (Antvorskov et al. 2016; Haupt-Jorgensen et al. 2018). Ancient forms of wheat are also linked to a lower rate of type 1 diabetes in animals, as compared to modern varieties (Gorelick et al. 2017).
An interesting study found that a gluten-free diet prevented type 1 diabetes in NOD mice as well as in their offspring, and even in the third generation as well. It appears that effects on the immune system were a critical mechanism, although gut microbiota played a role as well (Hansen et al. 2022).
Intervention Trials: Gluten-Free Diet
Based on the above research, doctors conducted a randomized intervention study to determine if delaying the introduction of gluten would prevent type 1 diabetes in children genetically at risk of the disease. They found that first introducing gluten at 6 months of age versus 12 months of age was safe, but did not change the risk of developing type 1 related autoantibodies, or type 1 diabetes by age 3 (Hummel et al. 2011). Following these children for a longer period, up to age 13, the study still did not find any effect of the timing of gluten introduction on the development of type 1 diabetes or its related autoantibodies. Nor did breastfeeding during gluten introduction make a difference (Beyerlein et al. 2014).
Another intervention trial aimed to see if a gluten-free diet would influence the development of type 1 diabetes in people who were already autoantibody positive. The subjects ate gluten-free for 6 months, then gluten for 6 months. Neither gluten removal nor reintroduction affect antibody levels. However, insulin response and insulin resistance both improved on a gluten-free diet, and worsened after the reintroduction of gluten. Thus a gluten-free diet may help preserve beta cell function and insulin secretion in people at risk of type 1 diabetes (Pastore et al. 2003). A similar study used a 12 month gluten-free diet and 12 month reintroduction. They also found that antibody levels were not affected by the gluten-free diet or gluten reintroduction (Hummel et al. 2002).
In the Czech Republic, an intervention trial of a gluten-free diet maintained over the first year after type 1 diabetes diagnosis was associated with better HbA1c and a prolonged partial remission period, with a possible slower decline in beta cell function (Neuman et al. 2020).
A trial that replaced wheat with either organic modern whole wheat or organic whole Kamut wheat found that those who ate Kamut wheat lost more fat and had lower levels of insulin than those who ate modern wheat, showing that wheat consumption may have implications for type 2 diabetes and obesity as well (Trozzi et al. 2017).
Gluten and Type 2 Diabetes
Higher gluten intake (up to a certain point) is associated with a lower risk of type 2 diabetes in healthy U.S. men and women (Zong et al. 2018). This could be related to higher whole grain intake being associated with a lower risk of type 2 diabetes (Kyrø et al. 2018).
In animals, however, a gluten-free diet increases the volume of beta cells and improves glucose tolerance in mice that are a model of type 2 diabetes (Haupt-Jorgensen et al. 2016).
Soy proteins have been shown to cause diabetes in animals. One human study from China found that infants given soy-based infant formula had double the risk of type 1 diabetes. It also found that more children with type 1 had been introduced to solid food before 3 months of age than children without diabetes (Strotmeyer et al. 2004).
Low soy intake in pregnant women, however, was found to increase the risk of gestational diabetes in Chinese women (Wang et al. 2021).
In laboratory animals, lifetime exposure to a soy-based diet caused high blood glucose levels in adult rats (Patisaul et al. 2014).
Food Allergy and Intolerance
Is the potential link between type 1 diabetes and wheat/dairy etc. caused by an allergy or intolerance to these foods? One long-term study of U.S. children measured antibody levels (IgG4) that are associated with food intolerances in children during the period before type 1 development. They found that while higher antibody levels to dairy products were associated with less breastfeeding and an earlier introduction of cow's milk, these antibody levels were not associated with the later development of autoimmunity or type 1 diabetes. They also found that while higher antibody levels to gluten were associated with a later introduction of wheat/gluten, these antibodies were also not associated with autoimmunity or type 1 diabetes development. Nor were total antibody levels. However, there was a small association between antibodies to egg proteins in antibody-positive children and later development of type 1 diabetes (Lamb et al. 2013).
To download or see all the references on this and other diet-related pages, including breastfeeding, nutrition, and more, see the collection Diet, nutrition, gut, microbiome and diabetes/obesity in PubMed. This collection also includes numerous additional studies on cow's milk and gluten, not mentioned above.