Type 1 Diabetes is a lifelong disease often diagnosed in childhood. The onset of this disease is influenced by genetic predisposition as well as factors in our environment, such as what we eat or drink. One of the environmental factors that has been identified for those predisposed to Type 1 Diabetes is cow’s milk. Scholarly articles and case studies were investigated to dive into the topic of whether or not cow’s milk is a trigger for the onset Type 1 Diabetes. A wide range of studies have been conducted on cow’s milk as a whole as well as isolated components of cow’s milk. Cow’s milk as a whole, bovine insulin, and casein are of notable interest regarding their effect on the onset of the disease. When dealing with human subjects and this disease, it is more difficult to set the study parameters. More studies need to be done in this area to isolate it further. Most of the studies that have been done are on children predisposed to Type 1 Diabetes, rather than on the population as a whole. That is the focus of this paper.
Type 1 Diabetes (T1D) is an autoimmune disease where the body is no longer able to produce insulin due to the islet cells being destroyed by the body’s immune system. There is no known cure which is why preventive measures are so important. There has been an increase in the number of T1D cases. More and more children are being diagnosed and the reason why is not clear (“Rates of new diagnosed…”, 2017). Lamb et al. (2015) state that T1D is not simply a genetic disease, although if you have a first-degree relative that has T1D then you are genetically predisposed and run a higher risk of developing T1D (Weires, Tausch, Edwards, Wetter & Cannon-Alright, 2007). In addition to genetic predisposition, there are environmental factors that can act as triggers leading to islet autoimmunity (or beta cell autoimmunity) and T1D. Beta cells are a type of islet cells in the pancreas that make insulin. These are the cells that are destroyed by the immune system in the case of T1D (“What is Type 1 Diabetes”, n.d.).
We cannot change whether a child is genetically predisposed to T1D, but we do have control over some of the identified environmental factors that play a role. Given the lifelong nature of the disease, it is important to be able to identify the environmental factors in an attempt to either prevent the disease or prolong the remission period after diagnosis.
Cow’s milk has been studied as an environmental trigger for T1D. It has been shown that drinking cow’s milk creates a higher risk for either islet autoimmunity, autoantibodies, or full-blown T1D. There are several factors that have been studied, namely, straight cow’s milk, cow’s milk-based formula, bovine insulin in cow’s milk, protein in cow’s milk, and several more. Through all the methods, there is a strong correlation between cow’s milk and the ultimate result of T1D.
Several procedures were put in place during the discovery and search process. Most notably, only scholarly articles were considered for review. Additionally, only well-respected scholarly sites were included in the search process.
The sites searched were Google Scholar, PubMed, and Research Gate. Two search strings used to produce the best results. The search strings used were “cow’s AND milk AND Type AND 1 AND Diabetes” and “bovine AND insulin AND Type AND 1 AND Diabetes”. No exclusion words were necessary for the search string. The focus was PubMed and Google Scholar since Research Gate did not produce any articles that were relevant as well as accessible. All articles older than five years were excluded, except for one. Articles related to bovine insulins and Type 1 Diabetes were more difficult to find, so an older but still relevant article was allowed. Secondary sources and articles containing foundation information were allowed greater than five years since these pertain more to static information.
Cow’s milk in general
Skyler (2014) conducted a meta-analysis of studies to determine preventions for T1D. Based on studies analyzed, cow’s milk stood out as a potential trigger. A study was done with 230 babies who were predisposed to T1D. The babies either received cow’s milk whenever breast milk wasn’t available or a casein hydrolysate formula. It was conducted over the course of the first 6-8 months of life. The children were monitored for ten years. The children who did not receive cow’s milk had a reduced risk of beta cell autoimmunity with a hazard ratio for the appearance of autoantibodies of .54 when compared to the control group. The conclusion was that it is possible to prevent or delay the onset of T1D and that cow’s milk was just one of the factors involved.
Villagran-Garcia et al. (2015) conducted a study with the intent to show that consumption of cow’s milk in school age children was associated with T1D. The study involved 150 school age children, 75 were children with T1D and 75 were in the control group with no chronic diseases present. The age range of the children was 6 to 16. A face to face interview was conducted with the parents about the diet history of the child in the first 12 month of life. The study found that consumption of cow’s milk early in life was clearly associated with T1D. The risk was four-fold. The noted limitation of this study was that the sample size was small. One might also argue that a recall bias might be at play given the time frame that the parents were interviewed about.
Lamb et al. (2014) set out to study children predisposed to T1D and to see if there was an association with cow’s milk and the risk of islet autoimmunity and the later progression to T1D. Approximately 2500 (1835 actually being used) children with increased risk were enrolled. They were evaluated yearly. Another group of children were recruited at birth and are assumed to be representative of the general population. They were evaluated at 9, 15, and 24 months. Face to face diet questionnaires were administered at evaluations as well prior diet history for the predisposed children not enrolled at birth. The study showed that there was an increase in islet autoimmunity in children who consumed cow’s milk who had a low to moderate risk HLA-DR genotypes (which is a genetic determinant for T1D). This was not the case, however, for children who had high-risk HLA-DR genotypes. Additionally, cow’s milk was also shown to be associated with the progression from islet autoimmunity to the full onset of T1D.
Chia et al. (2017) propose that A1 β-casein is a primary trigger for progression to T1D. Casein makes up about 80% of the total protein in cow’s milk. Cow’s milk contains both A1 β-casein and A2 β-casein. They conducted a literature review and pieced together different studies related to A1 β-casein and T1D. There were two studies of particular interest that involved mice and rats. In the first study, either the rats were fed a “standard laboratory diet” or a semi-synthetic diet. 50% of the rats that ate the standard laboratory diet developed T1D and 15% of the rats that ate the semi-synthetic diet developed T1D. The rats on the semi-synthetic diet were then supplemented with cow’s milk and their T1D rate rose to 52%. In the next study, mice were fed a diet supplemented with A1 β-casein or A2 β-casein. None of the mice who were fed A2 β-casein developed T1D, but 47% of the mice fed A1 β-casein developed T1D.
The conclusion was that there is strong evidence for A1 β-casein being a trigger for T1D, but that causation cannot be shown. They noted that, in humans, the length of breastfeeding and whether the mother drank cow’s milk affect the outcome. A study was proposed where predisposed infants from birth would drink only cow’s milk that does not contain A1 β-casein and monitor the results.
Hummel et al. (2017) designed a study to determine if there was an association between hydrolyzed cow’s milk as an infant’s first formula and reduced islet autoimmunity. Hydrolyzed cow’s milk simply refers to the process of breaking down the proteins. They claim that most of the current studies only look at cow’s milk in general rather than protein hydrolysates and the level of hydrolysis. Data from TEDDY (The Environmental Determinants of Diabetes in the Young) was used. TEDDY identifies and follow children with an increased risk for T1D and 8506 were included in the study. A questionnaire including the age of formula introduction and type of formula was completed to get information on the infant’s diet during the first three months of life. The formulas used were then separated by type. Types included cow’s milk, no cow’s milk, extensively hydrolyzed cow’s milk, etc… Cumulative risk of developing islet autoimmunity was estimated using Kaplan-Meier analysis. The study concluded that islet autoimmunity might increase, not decrease, with the use of extensively hydrolyzed cow’s milk formula. This went against the hypothesis of the study. A follow-time limitation was noted in the study.
Bovine insulin specifically
Vaarala et al. (2012) tested whether the occurrence of T1D in predisposed children would be reduced with the use of a formula that was made from bovine-free cow’s milk. A total of 1113 predisposed babies were randomly assigned to groups. Group 1 contained 389 babies and they received regular cow’s milk formula. Group 2 contained 350 babies and they received whey-based hydrolyzed formula. Group 3 contained 365 babies and they received the whey-based formula free of bovine insulin. Their blood was tested for beta-cell autoimmunity at 3 months, 6 months, and 12 months, and then annual until the age of 3.
The results were that 6.3% of the children who received cow’s milk, 4.9% of the children who received whey-based hydrolyzed formula, and 2.9% of the children who received formula free of bovine insulin tested positive for one or more autoantibodies by the age of 3. It was noted that when autoantibodies are present before the age of 3 that there is a strong correlation with later onset of T1D. The conclusion was that bovine insulin acts as a trigger for T1D.
Paronen et al. (2000) conducted a study to determine the insulin T-cell response related to cow’s milk exposure, specifically to bovine insulin. Infants with a genetic predisposition for T1D were randomized to either receive a cow’s milk-based formula or hydrolyzed casein-based formula. This was to be introduced after 6 months of breastfeeding. The study found that the cellular response and IgG antibodies to bovine insulin in infants who consumed cow’s milk was higher than infants who consumed the hydrolyzed casein formula (P=0.01). However, there was no difference noted in T-cell response. Interestingly, T-cell response to bovine insulin and IgG antibodies to bovine insulin were shown to be lower in the case where the mother was diabetic.
Attempts to isolate the specific part of cow’s milk that is most strongly associated with the trigger for T1D is of great interest. Specifically the two greatest areas of study when narrowing it down are casein and bovine insulin. Both of these have been studied and have been shown to act as a trigger to T1D. Give that T1D is a lifelong disease and is incurable, narrowing down the specific triggers has the potential to save lives and change lives, specifically for those already predisposed for the disease.
Cow’s milk in general
Many studies show a strong correlation between the introduction of cow’s milk and either islet autoimmunity or the progression to T1D. In general, studies use the questionnaire technique to find out about dietary habits during infancy. Studies show there is a strong correlation between consumption of cow’s milk and T1D. Lamb et al. (2014), Skyler (2014), and Villagran-Garcia et al. (2015) all concluded in this is the case for humans in their studies. It would appear that early introduction is especially noteworthy. All of the studies agree that cow’s milk was a trigger. Further, the studies break down different aspects and it is shown that straight cow’s milk, cow’s milk-based formulas, A1 β-casein, and hydrolyzed cow’s milk all have associations to T1D. It is thought that hydrolyzed cow’s milk might help prevent T1D, but Hummel et al. (2017) showed it to actually increase the likelihood of islet autoimmunity.
Bovine insulin specifically
At most basic level both Vaarala et al. (2012) and Paronen et al. (2000) determine that Bovine insulin plays a role in triggering an immune response when cow’s milk containing bovine insulin is consumed. The interesting note is that bovine insulin correlates with autoantibodies and if those appear before the age of 3 then the likelihood of T1D increases.
There are many factors at play when considering T1D. Infant feedings, especially when the mother is still breastfeeding can be tricky to isolate regarding exposure. The mother could be exposing the infant to a variety of triggers in her breastmilk if she is consuming cow’s milk or other substances. Additional research is still needed to solidify the correlation. Perhaps if breastfeeding is halted early enough (by choice of the mother, never by suggestion) then studies can be conducted using questionnaires as to what type of formula or milk the child was exposed to and at what age.
There is strong evidence to suggest that the consumption of cow’s milk in infants predisposed to T1D can result in either increased islet autoimmunity, autoantibodies, or T1D. For infants who are predisposed to T1D, special dietary precautions can be taken to attempt to prevent the onset of the disease. Several environment triggers have been identified, such as gluten and cow’s milk (Hogg-Kollars, Dulaimi, Trait, & Rostami, 2014). It is not prudent to change the diet of an infant to protect them against a disease that has no cure and can affect one’s quality of life. Breastmilk is best, but in the case of formula, due-diligence should be done with a knowledgeable doctor to determine the best one, preferably one that does not contain cow’s milk. Cow’s milk is not a required part of a healthy diet. There are alternatives that, along with a healthy diet, can satisfy the dietary requirements (“In search of a milk alternative”, 2015).
While further studies are recommended, if there is a strong genetic predisposition for T1D, breastfeeding should be continued as long as possible, minimizing exposure to cow’s milk or cow’s milk-based formula. Alternatives such as organic soy-based formula can be considered after discussion with the pediatrician. The breastfeeding mother may want to consider abstaining from cow’s milk as well to decrease exposure. As already discussed, there are healthful alternative to cow’s milk if necessary.
Chia, J., McRae, J., Kukuljan, S, Woodford, K., Elliott, R., Swinburn, B. & Dwyer, K. (2017). A1 beta-casein milk protein and other environmental pre-disposing factors for type 1 diabetes. Nutrition & Diabetes 7(5). e274. doi: 10.1038/nutd.2017.16
Hogg-Kollars, S., Dulaimi, D. A., Trait, K. & Rostami, K. (2014). Type 1 Diabetes mellitus and gluten induced disorders. Gastroenterol Hepatol Bed Bench, 7(4), 189–197
Hummel, S., Beyerlein, A., Tamura, R, Uusitalo, U., Aronsson, C., Yang, J., Rookonen, A, … the Teddy Study Group. (2017). First infant formula type and risk of islet autoimmunity in the environmental determinants of diabetes in the young study. Diabetes Care, 40(3). 398-404. doi: https://doi.org/10.2337/dc16-1624
Lamb. M., Miller, M., Seifert, J., Frederiksen, B., Kroehl, M., Rewers, M. & Norris, J. (2015). The effect of childhood cow’s milk intake and HLA-DR genotype on risk of islet autoimmunity and type 1 diabetes: the Diabetes Autoimmunity Study in the Young. Pediatric Diabetes, 16(1). doi: 10.1111/pedi.12115
Paronen, J., Knip, M., Savilahti, S., Ilonen, J., Akerblom, H., & Vaarala (2000). Effect of cow’s milk exposure and maternal type 1 diabetes on cellular and humoral immunization to dietary insulin in infants at genetic risk for type 1 diabetes. Finnish trail to reduce IDDM in the genetically at risk study group. American Diabetes Association 49(10). 1657-1665. doi https://doi.org/10.2337/diabetes.49.10.1657
Rates of new diagnosed cases of type 1 and type 2 diabetes on the rise among children, teens (2017). Retrieved from https://www.nih.gov/news-events/news-releases/rates-new-diagnosed-cases-type-1-type-2-diabetes-rise-among-children-teens
Skyler, J. (2014). Primary and secondary prevention of Type 1 Diabetes. Diabetic Medicine, 30(2). 161-169. doi: 10.1111/dme.12100
Vaarala, O., Ilonen, J., Ruohtula, T., Pesola, J., Virtanen, S., Harkonen, T.,…Knip, M. (2012). Removal of bovine insulin from cow’s milk formula and early initiation of beta-cell autoimmunity in the FINDIA pilot study. JAMA Pediatrics, 166(7). 608-614. doi:10.1001/archpediatrics.2011.1559
Villagran-Garcia, E., Hurtado-Lopez, E., Vasquez-Garibay, E., Troyo-Sanroman, R., Aquirre-Salas, L., Larrosa-Haro, A. & Leon-Robles, R. (2015). Introduction of pasteurized/raw cow’s milk during the second semester of life as a risk factor of Type 1 Diabetes Mellitus in school children and adolescents. Nutricion Hospitalaria, 32(2). 634-637. doi: 10.3305/nh.2015.32.2.924
Weires, M., Tausch, B., Edwards, C., Wetter, T. & Cannon-Alright, L. (2007). Familiality of diabetes mellitus. Experimental and clinical endocrinology & diabetes, 115(10). 634-40.
What is Type 1 Diabetes? (n.d.). Retrieved from https://www.joslin.harvard.edu/info/what_is_type_1_diabetes.html