Title: Does the introduction of cows milk in early infancy lead to type 1 diabetes?
Key words: type 1, diabetes, cow’s milk, genetics, infant diet, obesity, sensitisation, sensitization, diabetogenic, insulin, bovine, anti-bovine, antibodies, bottle-fed, breast fed, breast feeding, prediabetic, tolerance, islet cell, pancreas, pancreatic, gluten, viral proteins, autoimmunity, sensitizing,
Date: Sept 2006
Category: Specific conditions
Author: Morgan, G
Does the introduction of cows milk in early infancy lead to type 1 diabetes?
Type 1 diabetes is a multifactorial disease typically developing during childhood. Several factors have been implicated as aetiological agents, including genetics (Couper 2001), viral exposure (Gale 2004), maternal age (Bingley 2000) and vitamin D status (Harris 2002). The role played by the early introduction of cow’s milk into the infant diet will be considered in this review.
The role of obesity in the aetiology of type 2 diabetes has been well described. Rapid early growth in infancy has also been associated with the later onset of type 1 diabetes (EURODIAS 2002). In a Finnish study (Hypponen 1999), exposure to cow’s milk in infants less than 3 months old was linked to the later onset of obesity and type 1 diabetes. Two further studies in children up to 15 years of age in European populations (Virtanen 2000, Thorsdottir 2003) showed a higher consumption of cow’s milk and saturated fat and a higher incidence of type 1 diabetes.
Unanswered by such cross-sectional studies is the question as to whether early sensitization to cow’s milk in early infancy determines the later onset of type 1 diabetes or whether higher cow’s milk consumption throughout infancy and childhood is the major promotional factor. More detailed cross-sectional and prospective studies in this younger age group have helped to shed light on the immunological issues involved whilst failing to isolate a determinant diabetogenic factor. Thus, although up to 100% of children with type 1 diabetes possess anti-bovine insulin antibodies that cross-react with human insulin (Vaarala 2002, Perez-Bravo 2003), and antibodies against bovine insulin may be detected in bottle fed babies by the age of 3 months (Paronen 2000), antibody titres are not related to the duration of breast feeding or the time of introduction of cow’s milk (Perez-Bravo 2003). Both elevated bovine and human insulin antibodies serve as prediabetic markers in at risk genetic groups (Vaarala 1999), but tolerance to the bovine antibodies appears to develop between 3 and 18 months of age (Vaarala 1999, Paronen 2000a), and the human insulin antibodies, though appearing early, have a high rate of disappearance (Kimpimaki 2002). A causal relationship with diabetes has not been established for these antibodies.
The development of islet cell antibodies appears more specific in determining pancreatic islet cell destruction and the evolution of type 1 diabetes (Kimpimaki 2002). However, there again appears to be no relation between the length of breast feeding, early introduction of cow’s milk into the diet, and the development of islet cell antibodies and diabetes (Harrison 1999, Couper 1999, Ziegler 2003). Studies on other dietary proteins, notably gluten (Ziegler 2003), when consumed before 3 months of age, have shown more significant associations with type 1 diabetes. Beta-casein, the major protein found in cow’s milk, is associated with higher antibody titres in bottle fed and in children with type 1 diabetes (Monetini 2001).
Many researchers believe that diabetes in children has its roots in altered gut function secondary to a genetically determined sensitivity of the gut mucosa to dietary and viral proteins, leading to the dysfunctional cytokine and immunological response associated with type 1 diabetes (Vaarala 2002, Akerblom 2002). Population variations in the incidence of genetic, infective, dietary and other factors have rendered the interpretation of disparate data difficult. Thus, for example, the extensive Finnish studies have been carried out on a population with the highest incidence of type 1 diabetes in the world but with a relatively low rate of enteroviral infection (Viskari 2004) - proposed as precipitating islet cell autoimmunity in this population (Couper2001). The relative contributions of environmental triggering factors in type 1 diabetes has proven difficult to qualify and quantify in practice.
With respect to cow’s milk as a sensitizing agent, though some studies have shown prolonged breast feeding and late introduction of cow’s milk to be protective (Sadauskaite-Kuehne 2004), the majority of such studies have shown no such association (Wasmuth 2000). In particular, early introduction of cow’s milk in young infants does not appear to affect either the immunological profile or the evolution of diabetes in the at risk group (Harrison 1999, Couper 1999).
In conclusion, given the methodological difficulties in conducting long-term prospective trials for a multifactorial disease such as type 1 diabetes, with a peak incidence in children at age 10-15, it is difficult to isolate causal from confounding factors. Thus, with respect to the aetiological role of cow’s milk in type 1 diabetes, although there is much observational data linking immunological sensitization and consumption with the development of this disease in childhood, there is a dearth of conclusive interventionist studies proving a causal relationship. More specifically there is no evidence to link the earlier introduction of cow’s milk into the diet in early infancy and the later development of type 1 diabetes.
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