Cow's milk is a staple in many Americans' foods. Milk is in our grocery stores, schools, and commercials, gaining immense popularity in our diet. The benefits of milk are well advertised: Who hasn't ever seen a 'Got Milk' ad nor knows by now that milk provides calcium, a mineral essential for bone growth. Milk is cheap, versatile, and undeniably a classic, whether baked in cake and bread, enjoyed warm in a glass before bed, or complementing a favorite cereal. We are loathe to imagine a world without milk chocolate and ice cream, but with the increase of milk consumption follows an increase of milk intolerance and milk allergy. Of course, this is to be expected, because without the consumption of milk, we cannot find out that there are people with inabilities to absorb it, but the problem lies deeper than just the incapability to process milk. Milk has long been established in Europeans' diet for thousands of years and has only relatively recently spread to accompany other cultures' diets as complements and a vital ingredient in our food. For a drink that has so much history, it is odd so many individuals have contracted intolerance to the food. Intolerance does not only exist in cultures without a rich background with milk, like many East Asian countries, but also exists in individuals of heavy European descent. Human bodies were never originally made to process the proteins in milk. Only through evolution did some obtain the enzymes to break a few of milk's components down. Its consumption may bear more damage than benefits to the body in the long term. Certain diseases, such as type-1 diabetes, can be developed faster with the consumption of milk. Scientific research suggests its consumption contributes to the pathogenesis of type-1 diabetes. The human body's inability to digest certain protein molecules can lead to rejection of both the protein and molecules in the body resembling the protein. The rejection leads to autoimmune diseases, like type-1 diabetes. This does not mean individuals cannot enjoy the beverage, but eating and drinking it should be consumed in moderation. Some geographical, economic, and genetic influences affect the availability of milk and the way each individual's body processes the drink, meaning everyone's response to milk varies. In the case of people at jeopardy of developing type-1 diabetes, whether by genetic or lifestyle influences, milk can stand to be cut out of the grocery list and is best left to be consumed by cows. 

The most common argument for the detriment of milk and its harmful relationship on individuals at risk of diabetes is that the proteins in milk and meat in general triggers an autoimmune response in the body to indiscriminately attack both the protein and pancreas beta cells. A video on YouTube by Vegsource, "Milk, Type-1 Diabetes & Autoimmune Disease.", explains that with the continuous consumption of milk products, your body cannot keep the amount of milk proteins entering the body from the gut. Dr. John A. McDougall, the spokesperson for this video, shows that with the inability to keep these proteins out, the body will tag and identify these proteins as harmful antigens and produce antibodies to these proteins. Milk proteins contain beef proteins has a chain of identical amino acid construction as the pancreas beta cells, the structure that produce insulin. The body will attack both of these molecules on the protein and cell, leading to the inability to produce insulin. The inability to produce insulin means the body cannot store sugar. Inability to store sugar leads to high levels of blood sugar and eventually to type-1 diabetes if left untreated. While milk and meat proteins, as seen by many studies, do affect individuals already at risk, it is incorrect to assume only persons with susceptible genes can develop the disease. As explained by John A. McDougall in the Vegsource video, constant consumption of dairy and meat based products wear down the body's natural line of defense at keeping out meat proteins. Another source, "Confirmed Anew: Cow's Milk May Trigger Type One Diabetes" by Sayer Ji, goes on to identify the antibody-inducing protein as the beta-casein A1 molecule. He pulls up a Finnish study that tested 1113 type-1 diabetes susceptible infants by giving them both cow's milk and whey-based formula. The group with cow's milk formula (CMF) produced the most beta-cell autoantibodies. Ji states that the protein molecule is difficult to digest for humans because milk was never intended to be consumed by people. It is a food designed for another species: the cow's young. A video uploaded by upcycle, titled "Dairy and Diabetes", also finds the beta-casein molecule to be the harmful molecule in triggering type-1 diabetes. The spokesperson in the video goes into detailed explaining that the molecule casein has some digestible parts, but some non-digestible parts become "translocated" from the gut to the bloodstream. There, the body recognizes casein as a foreign agent and produces the matching antibodies.  Virtanen and Knip released an article titled "Nutritional Risk Predictors of Beta-Cell Autoimmunity and Type-1 Diabetes at a Young Age". The articles states that "increased numbers of antibodies toward a series of cow milk proteins have been detected repeated in children with newly diagnosed type 1 diabetes. Increased concentration of IgA-class beta-lactoglobulin and IgA cow milk formula antibodies were related to an increased risk of type-1 diabetes. Both infant feeding patterns and current milk consumption affect cow milk antibody titers." Doheny's article, "New Clue to Milk and Diabetes Link" raised some points about consumption of cow's milk formula for infants. While Ji recognized the molecule causing the autoimmune reaction to be a casein protein, Doheny speculates that it is the beta-lactoglobulin molecule in milk. The beta-lactoglobulin molecule is similar in structure to glycodelin, which controls T-cell production. T-cells protect the body by attack foreign antigens, but if nothing regulates T-cell production, they could attack the body's cells as well.  The author takes a study conducted on five adults without type-1 diabetes and five children with type-1. Their blood was taken and in all five children, antibodies to beta-lactoglobulin were found, but only two adults had antibodies. This may suggest some correlation between Doheny's speculation about beta-lactoglobin and type-1 diabetes.  Unfortunately, reviews by M.D.s on Doheny's page find her article left with too many gaps to fill. Her proposal for beta-lactoglobulin's role in type-1 diabetes does not have much research to be backed up even though it is possible. Antibodies made again beta-lactoglobulin have not been proven to affect or produce antibodies against glycodelin. Her article's reviewers' opinions are mixed, some glad that Doheny supports breastfeeding while others are doubtful because lack of evidence. 

Disregarding the technical details of milk's effects on the body, there are still economic, social and genetic causes contributing to milk's relationship with type-1 diabetes. Muntoni's article, "Nutritional factors and Worldwide Incidence of Childhood Type 1", points out geographical and economic factors that are associated with high population densities of afflicted people with type-1 diabetes. Muntoni presents census-type data gathered from registries converting the incidences of type 1 diabetes and dietary patterns in different countries. Countries with higher GDPs had more incidences of type-1 diabetes while lower GDP countries had lower incidences. This is reasonable since countries with higher GDP like the United States and many European countries have more access to milk and meat products. There were higher rates of type-1 diabetes in areas that consumed relatively larger amounts of meat and dairy products. On the other hand, areas that consumed more plant material and less animal proteins had lower cases of type-1 diabetes. The increase of type-1 diabetes is possibly related to the dairy-rich diet formed in wealthy European and non-European countries after World War II. Muntoni explains this could be the reason why people with vegetarian diets experience less chronic diseases such as diabetes. Another article brings up genetic factors as causative agent in type-1 diabetes. Virtanen et al.'s article presents the Finnish case-control study that first hinted at a relationship between drinking cow's milk and increased risk of type-1 diabetes. A study was conducted using siblings of affected children with type-1 diabetes and studies their milk consumption behavior. The study conducted in the article looks at two factors: the age at which the child was introduced to cow's milk supplement (milk formula) and the occurrence of genes that increase the risk of type-1 diabetes. Certain genes, such as the HLA-DQB1 gene can stimulate the antibodies created by consumption of cow's milk. Smith's article, "Type 1 Diabetes Causes", explains that HLA is an acronym for human leukocyte antigen. Several HLA genes are associated with type 1 diabetes, and all of them are on chromosome six. This further pushes the argument for genes being a causative factor in type-1 diabetes. The article states "both increased humoral and cell-mediated immune responses to cow 's milk proteins have been observed in newly diagnosed children with type 1 diabetes compared with those in control children (10). Cow's milk protein antibody levels were also found to be higher in affected children than in control siblings when matched for HLA-DQB1 risk alleles (11)" (Virtanen et al. 912). Specific alleles on the HLA-DQB1 gene, when expressed, possibly creates a higher inclination of developing diabetes. The alleles DQB1*02 and DQB1*0302 expressed together indicates high risk and expression of only the DQB1*0302 indicates moderate risk. The article takes children with and without the allele and compares their milk antibody productions. The article pulls some studies conducted that show early introduction of milk supplements may contribute to milk protein antibody production and records the ages of milk supplement introduction for each child, but the research concluded that "both high consumption of cow's milk during childhood and moderate- and high-risk genotypes were related to development of type 1 diabetes, whereas the age at introduction of supplementary milk feeding was not yet significantly associated with the development of diabetes" (Virtanen et al. 916).  The article could vouch for the higher risk in siblings of children in general, and strongly suggests the HLA-DQB1's alleles plays a part in risk factors and states "[its] results provide support for the hypothesis that high consumption of cow's milk during childhood can be diabetogenic in siblings of children with type 1 diabetes. However, further studies are needed to assess the possible interaction between genetic disease susceptibility and dietary exposures in the development of this disease" (Virtanen et al. 912). 

Not everyone is keen on believing milk to be the root of all diabetic evils. Many refuting articles claim that insufficient and biased data from studies conducted on milk and type-1 diabetes influence the results and makes the studies inconclusive and weak. Dr. Jeanne Goldberg, a learned author with a PhD from Tufts University counters radical anti-milk campaigns for their blatant exaggeration of milk's damage and confronts the Finnish case-control study with type-1 diabetically susceptible children. She finds that the study concludes that a short breastfeeding term or early introduction to formula causes a rise in beta-cell autoimmunity, but finds that the autoimmunity is not specific to cow's milk and could just be a reaction to anything that was not formula or breastmilk. Goldberg states, "Given evidence available at the present time, it would seem that type-1 diabetes develops in only 5% of individuals at risk based on familial disease ... " She does not believe this is a high enough percentage to imply direct causation of milk's effect on type-1 diabetes. Another article by Carolyn D. Berdanier, "Diet, Autoimmunity and Insulin Dependent Diabetes Mellitus: A Controversy", harps on similar points. In her article, she analyzes that IDDM (insulin dependent diabetes Mellitus) patients do produce more antibodies again milk and its own beta pancreas cells. Patients with IDDM had elevated levels of IgG antibodies created again casein and beta-lactalbumin, another protein found in both sheep and cow's milk in a study taken by Karjalainen et al. The study experiment on 142 children with diagnosed IDDM and tests their exposure to dairy foods at different points in their development. Another experiment also finds that children who were exposed to dairy products within two months of their lives had a higher risk of developing IDDM whether or not their gene codes for risk of the disease. Unfortunately, whether or not the antibodies made are actually milk-specific is questionable. Correlation does not imply causation, even though "population studies have suggested a link between diet, particularly dairy products, and autoimmune IDDM, proof of this has not been provided." (Berdanier 228) Another study by Knipp et al. points out the faulty logic in associating cow's milk with the increased production of antibodies by stating "in a multiple logistic regression analysis, the authors observed that IgA antibodies to beta-lactoglobulin were significantly associated with an increased risk of diabetes at young age, independent of islet cell antibody status and of early weaning to cow's milk-based formula. These observations could be interpreted as supporting the idea that enhanced consumption of cow's milk before the presentation of clinical type 1 diabetes is a risk factor." The antibodies do attack the beta-pancreas cell that produce insulin, but it is not certain that the antibodies were created due to the presence of dairy products. Bias was found concerning the geographical and demographical factors of the experiment; Finnish people have the highest incidences of IDDM, meaning the tests conducted on this population might have high markers for IDDM regardless of diet. Knipp et al. reports that the case-control studies conducted to study the effects of milk may be biased; Children at risk of diabetes are reported to have a higher milk intake in New South Wales, Australia while a Swedish survey found pre-diabetic children to have a lower milk intake. This discrepancy in scientific reports contributes to bias and the studies conducted cannot be used to prove that milk affects the pathogenesis of type-1 diabetes. Unfortunately, it is difficult to truly regulate a human being's diet completely because of ethical reasons, especially when the individual is still only an infant. Other foods may be consumed during childhood and could possibly be the cause of increased antibodies. Any article that goes against my argument does not clearly make a stand against milk's harmful effects completely because, despite pointing out bias, all of the studies conducted do show that consumption of milk, especially in children at risk, increases antibody production that targets insulin producing beta-pancreas cells. Some of the antibodies created target meat proteins that exist in milk and the presence of the said antibodies are positively correlated to increased risk of type-1 diabetes. The only article I found to truly oppose my argument is another study conducted by Ziegler et al. in "Early Infant Feeding and Risk of Developing Type-1 Diabetes-Associated Antibodies" compares breastfed children with children who eat gluten-included and milk-based food supplementation. The author finds that breastfed children do not have increased risk of islet-cell antibodies, and milk-based food supplementation even decreases the incidences of islet-cell antibodies. Only gluten-based food supplementation increased the chances of islet-cell antibodies. The article states that "these findings would argue against a role is cow's milk in promoting islet autoimmunity, and even suggest that early exposure may be beneficial in selected individuals." (Ziegler et al. 1727) The article suggests that further examination of other foods besides milk should be studied to try and exact the correct agent for type-1 diabetes. While Ziegler's findings do promote milk rather than debase it, the study is only one of many. There is still plenty of experiments conducted that can prove milk to be detrimental to one's heath. 

Despite several studies supporting a link of milk being connected to type-1 diabetes, there is just equally as much articles and commentaries that disagree. It is, unfortunately, not a concrete topic to work with because the more milk's detrimental causes are brought up, the more backlash and opposition exists to disprove the research. The most common argument against milk is that it stimulates the production of antibodies against pancreas cells that produces insulin. This autoimmune response to an outside antigen results in the disease known as type-1 diabetes. 

