There has long been debate (and there are innumerable studies) about cow's milk and type 1 diabetes. 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. 2014).
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. (Since this study did not include people from the general population, whether this intervention will work in people less genetically at risk of type 1 is not known). 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, a newer study that has followed the same children for a longer period of time, published in the Journal of the American Medical Association, found that the hydrolyzed formula did NOT reduce the risk of type 1 diabetes-related antibodies in these children after 7 years (Knip et al. 2014). 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).
Previous 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., 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. 2015).
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.
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; 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).
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., 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).
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).
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). It also reduces kidney disease, lowered blood glucose levels, and lowered insulin resistance in rodents with chemical-induced type 1 diabetes (Korish et al. 2015).
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).
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).
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).
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). The 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. 2015a). However, a study from Sweden (by many of the same authors) 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. 2015b). 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 systematic review of 16 earlier studies found no effect of the timing of gluten introduction or of breastfeeding on the development of celiac disease (Silano et al. 2016), and another review also suggests that early feeding practices do not influence the risk of celiac disease (Chmielewska et al. 2016).
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).
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. (2104) found the same thing, and also that this early introduction of gluten increased the risk of type 1 diabetes as well. 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).
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.
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 also 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).
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).
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).
In laboratory animals, lifetime exposure to a soy-based diet caused high blood glucose levels in adult rats (Patisaul et al. 2014).
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).
It seems that introducing food before 3 months of age is problematic, perhaps because the intestine is still immature and unable to handle these foods. Indeed, Virtanen et al. (2006 and 2011) found that introducing fruits, berries, and roots early (around 3-4 months of age) was associated with development of type 1 diabetes-related autoimmunity in genetically at-risk children.
For more information on why foods such as wheat and dairy might contribute to the development of type 1 diabetes, and the involvement of the gut immune system, see the diet and the gut page.
While all studies do not have consistent findings, we can still use them to help determine how to feed our babies. Parents could be careful introducing certain foods, 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 ensuring compliance to 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. World Health Organization (WHO) infant feeding guidelines 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. Only 5% of families of children with first degree relatives who have type 1 diabetes follow the WHO recommendations for infant feeding (Pflüger et al. 2010).
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.