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Infant Feeding Practices and Their Possible Relationship to the Etiology of Diabetes Mellitus

American Academy of Pediatrics

Policy Statement

Pediatrics Volume 94,                                 Number 5                             November 1994, p 752-754

Infant Feeding Practices and Their Possible Relationship to the Etiology of Diabetes Mellitus (RE9430)


Work Group on Cow's Milk Protein and Diabetes Mellitus

ABBREVIATIONS. IDDM, insulin-dependent diabetes mellitus; BB, biobreeding.

Insulin-dependent diabetes mellitus (IDDM) is a common serious genetic disorder affecting a large number of children and adolescents around the world. The annual incidence rate in the United States is approximately 15 per 100 000 persons under 19 years of age, with a prevalence of 2.6 per 1000 persons. Accurate statistics on the ultimate development of IDDM in adults are limited but suggest that the annual rate varies by geographic regions. An adolescent peak occurs in most populations, but approximately equal numbers of individuals develop IDDM before and after 19 years of age.[1-10]

The etiology of beta cell damage and destruction appears to involve an interphase between genetic predisposition and environmental insult; IDDM is not inherited. Genetic alterations involving specific HLA antigens located on chromosome 6 (and other possible non-chromosome 6 alterations) result in an increased risk that beta cell damage will occur. It appears, however, that less than 5% of individuals possessing the currently identifiable "diabetic genes" will ever become overtly diabetic.[11-15] The pathologic process that leads to beta cell destruction is autoimmune, involving both T-cell and B-cell responses with cytokine release and free radical accumulation. Nitric oxide seems the likely candidate as the final toxic mediator.[16-19]


There is a long history of attempts to link the expression of diabetes to a variety of environmental events. The assumed relationship between mumps infection and later development of IDDM spans almost a century.[20] The critical unresolved questions include: 1) What triggers the autoimmune process? 2) Is there a single trigger or do many environmental insults accumulate to finally destroy the beta cell mass? 3) Is there a period of special susceptibility and is this correlated with specific environmental agents? 4) What is the duration of the biologic latency period between the triggering insult and the clinical expression of diabetes?

The available evidence supports the contention that several environmental factors may be critically involved in the initiation and continuation of the destructive autoimmune process--viral infections, several specific toxins, nutritional alterations, and emotional stress.[21-24] Furthermore, while single episodes (such as a mumps infection) may rarely lead to diabetes, in most cases multiple and varied insults over time are probably necessary. A recent article has discussed the possible relationship between early exposure to cow's milk protein and the development of IDDM.[25] Although the report provides a conceptual framework, new methodology, and impressive statistics, it is only one of a number of studies over the past 10 years that have attempted to unravel the complexities of infant feeding practices and later development of IDDM.


In 1984 the initial observation published linking infant feeding practices and the later development of IDDM involved an ecological study of breast-feeding practices over several years in Scandinavia. The study showed that children born during years when breast-feeding was common were less likely to develop IDDM compared with those born during years when breast-feeding was less popular. These findings inferred that either the absence of breast-feeding or the early introduction of cow's milk formula to the infant's diet were factors in the development of IDDM in genetically susceptible individuals.[26] Since then over 90 articles have been published, both defending the original concept and presenting arguments against its validity. Gerstein,[27] in a meta-analysis, reviewed all the publications and carefully selected about 20 studies that met stringent scientific criteria. This analysis concluded that there was a modest, but statistically significant association (odds ratio >= 1.5) between the early introduction of cow's milk (and/or early termination of breast-feeding) and the development of IDDM in childhood. The timing, dosage, and duration of the infant's exposure to cow's milk may be important, with some studies suggesting earlier age of onset of IDDM in those who were not breast-fed or had very limited exposure to human milk.[28-45]

A commentary by Kostraba[46] accompanying the Gerstein meta-analysis appropriately broadens the discussion to include other aspects of infant feeding and suggests caution in moving from statistical relationships to causation. If a causal link exists between the ingestion of cow's milk and the onset of diabetes, it seems that milk protein or some subfraction is an active precipitator of the autoimmune process in genetically susceptible subjects, rather than human milk providing a protective influence. There is no evidence that processed milk, such as that found in commercial infant formulas, is in any way more or less harmful than whole cow's milk.

It has been known for several years that children with IDDM have an increased frequency of antibodies to a variety of cow's milk proteins, which is particularly evident in those with early onset IDDM. The recent article by Karjalainen et al[25] extends these observations and may provide additional insight into the initiation of the autoimmune process. These investigators identified antibodies to a 17-amino acid fragment of bovine serum albumin in 100% of a large group of Finnish children with newly diagnosed diabetes. Bovine serum albumin, which is present in cow's milk, is immunologically distinct from human serum albumin with little or no cross-reactivity. Antibodies to the 17-amino acid bovine serum albumin peptide molecule were found in few healthy controls or siblings of diabetic children. These exciting, provocative results have not been fully duplicated in extended studies in the initial laboratory and have yet to be confirmed by other investigators.[47]


To our knowledge, the first documentation of a link between cow's milk protein and diabetes in susceptible animal strains was reported in 1984, shortly after the Scandinavian observations of breast-feeding practices and the development of IDDM.[26,48] The addition of cow's milk protein to routine rat chow increased the frequency of diabetes in genetically susceptible biobreeding (BB) rats up to nearly 100%. Removing all whole protein and replacing it with a protein hydrolysate reduced the expression of diabetes in these animals to nearly zero. Numerous studies of feeding have since been carried out utilizing primarily the genetically susceptible BB rat and nonobese diabetic mouse strains. Although many studies have confirmed a provocative effect of milk proteins and beef proteins on the frequency of diabetes,[49-53] this finding has not been invariably true. Several investigators have been unable to replicate the early findings consistently and have in some cases identified evidence that a number of plant proteins, most notably soy, may also trigger diabetes in susceptible animal strains.[54-59]


1. Insulin-dependent diabetes mellitus develops within a group of individuals who carry specific diabetes susceptibility traits. Because all of the potential diabetes "susceptibility genes" are not known, currently it is not possible to identify all individuals at risk. It appears, however, that a small percentage of such individuals will ever develop clinical diabetes mellitus.

2. The autoimmune destructive process may be triggered by a number of environmental events.

3. Early exposure of infants to cow's milk protein may be an important factor in the initiation of the beta cell destructive process in some individuals. It is not known whether the cow's milk protein in commercially available infant formulas is associated with this process.

4. The avoidance of cow's milk protein for the first several months of life may reduce the later development of IDDM or delay its onset in susceptible individuals.

5. Research directed toward further defining the possible relationship between infant feeding practices and the development of IDDM is needed.


1. Breast-feeding is strongly endorsed as the primary source of nutrition during the first year of life for all infants.

2. In families with a strong history of IDDM, particularly if a sibling has diabetes, breast-feeding and avoidance of commercially available cow's milk and products containing intact cow's milk protein during the first year of life are strongly encouraged.

3. Since the antigenicity of infant formulas and cow's milk may be different and there is no evidence against the use of formula for infants whose mothers do not breast-feed, commercial infant formulas utilizing cow's milk protein remain the approved alternate.

4. The substitution of soy-based formulas for milk-based formulas is not advised for either general or high-risk infant feeding practices because of animal studies linking the ingestion of soy protein intake to the development of diabetes.

5. The substitution of elemental formulas for milk-based formulas has intellectual appeal as potential antigenically harmful large proteins have been replaced by dipeptides, tripeptides, and oligopeptides. However, because no scientific studies in humans confirming their benefit are yet available, this feeding option cannot be endorsed.

6. A prospective randomized trial in which genetically susceptible infants avoid the ingestion of cow's milk should be developed through collaborative national and international arrangements.


Allan L. Drash, MD, Chair

Michael S. Kramer, MD

Jack Swanson, MD

John N. Udall, Jr, MD, PhD


1. LaPorte RE, Fishbein HA, Drash AL, et al. The Pittsburgh insulin-dependent diabetes mellitus (IDDM) registry: the incidence of insulin-dependent diabetes mellitus in Allegheny County, Pennsylvania (1965-1976). Diabetes. 1981;30:279-284

2. LaPorte RE, Tajima N, Akerblom HK, et al. Geographic differences in the risk of insulin dependent diabetes mellitus: the importance of registries. Diabetes Care. 1985;8(suppl 1):101-107

3. Diabetes Epidemiology Research International. Geographic patterns of childhood insulin-dependent diabetes mellitus. Diabetes. 1988;37:1113-1119

4. Rewers M, LaPorte RE, King H, Tuomilehto J. Trends in the prevalence and incidence of diabetes: insulin-dependent diabetes mellitus in childhood. World Health Stat Q. 1988;41:179-189

5. Stone RA. Secular trends in incidence of childhood IDDM in 10 countries. Diabetes Care. 1990;39:858-864

6. WHO DIAMOND Project Group. WHO multinational project for childhood diabetes. Diabetes Care. 1990;13:1062-1068

7. Joner G, Sovik O. The incidence of type I (insulin-dependent) diabetes mellitus 15-29 years in Norway 1978-1982. Diabetologia. 1991;34:271-274

8. Schoenle EJ, Bagot M, Semadeni S, Wiesendanger M, Molinai L. Epidemiology of insulin-dependent diabetes mellitus in Switzerland: increasing incidence rate and rural-urban differences in Swiss men born 1948-1972. Diabetes Care. In press

9. Nystrom L, Dahlquist G, Rewers M, Wall S. The Swedish childhood diabetes study. An analysis of the temporal variation in diabetes incidence 1978-1987. Int J Epidemiol. 1990;19:141-146

10. Tuomilehto J, Rewers M, Reunanen A, et al. Increasing trend in type I (insulin-dependent) diabetes mellitus in childhood in Finland. Analysis of age, calendar time and birth cohort effects during 1965 to 1984. Diabetologia. 1991;34:282-287

11. Todd JA, Bell JI, McDevitt HO. HLA-DQ beta gene contributes to susceptibility resistance to insulin-dependent diabetes mellitus. Nature. 1987;329:599-604

12. Todd JA, Bell JI, McDevitt JA. A molecular basis for genetic susceptibility in insulin dependent diabetes mellitus. Trends Genet. 1988;4:129-134

13. Morel PA, Dorman JS, Todd JA, McDevitt HO, Trucco M. Aspartic acid at position 57 of the HLA-DQ beta chain protects against type I diabetes mellitus: a family study. Proc Natl Acad Sci USA. 1988;85:8111-8115

14. Trucco M. Immunogenetics in insulin-dependent diabetes mellitus: the second-event hypothesis. In: Belfione F, Bergman RN, Molinatti GM, eds. Current Topics in Diabetes Research. Vol 12. Basel: Karger; 1993, pp 135-146

15. Trucco M. To be or not to be ASP 57, that is the question. Diabetes Care. 1992;15:705-715

16. Bottazzo GF. Death of a beta cell: homicide or suicide? Diabetic Med. 1986;3:119-130

17. Eisenbarth GS. Type I diabetes mellitus. A chronic autoimmune disease. N Engl J Med. 1986;314:1360-1368

18. Drell DW, Notkins AL. Multiple immunological abnormalities in patients with type I (insulin dependent) diabetes mellitus. Diabetologia. 1987;30:132-143

19. Kolb H, Kolb-Bachofen V. Nitric oxide: a pathogenic factor in autoimmunity. Immunol Today. 1992;13:157-160

20. Harris HF. A case of diabetes mellitus following mumps. Boston Med Surg J. 1899;140:645-649

21. Orchard TJ, Dorman JS, LaPorte RE, Ferrell RE, Drash AL. Host and environmental interactions in diabetes mellitus. J Chronic Dis. 1986;39:979-999

22. Diabetes Epidemiology Research International. Preventing insulin dependent diabetes mellitus: the environmental challenge. Br Med J. 1987;295:479-481

23. Drash AL, Lipton RB, Dorman JS, et al. The interface between epidemiology and molecular biology in the search for the causes of insulin dependent diabetes mellitus. Ann Med. 1991;23:463-471

24. Laron Z, Karp M, eds. Genetic Environmental Risk Factors for Type I Diabetes (IDDM) Including a Discussion on the Autoimmune Basis. London, England: Freund Publishing House, Ltd; 1992

25. Karjalainen J, Martin JM, Knip M, et al. A bovine albumin peptide as a possible trigger of insulin-dependent diabetes mellitus. N Engl J Med. 1992;327:302-307

26. Borch-Johnsen K, Joner G, Mandrup-Poulsen T, et al. Relation between breast-feeding and incidence rates of insulin-dependent diabetes mellitus. A hypothesis. Lancet. 1984;2:1083-1086

27. Gerstein HC. Cow's milk exposure type I diabetes mellitus. A critical overview of the clinical literature. Diabetes Care. 1994;17:13-19

28. Scott FW. Cow milk and insulin-dependent diabetes mellitus: is there a relationship? Am J Clin Nutr. 1990;51:489-491

29. Dahl-Jorgensen K, Joner G, Hanssen KF. Relationship between cows' milk consumption and incidence of IDDM in childhood. Diabetes Care. 1991;14:1081-1083

30. Virtanen SM, Rasanen L, Aro A, et al. Infant feeding in Finnish children less than 7 yr of age with newly diagnosed IDDM. Childhood Diabetes in Finland Study Group. Diabetes Care. 1991;14:415-417

31. Virtanen SM, Rasanen L, Aro A, et al. Feeding in infancy and the risk of type 1 diabetes mellitus in Finnish children. Childhood Diabetes in Finland Study Group. Diabetic Med. 1992;9:815-819

32. Dahlquist G, Blom L, Lonnberg G. The Swedish childhood diabetes study--a multivariate analysis of risk determinants for diabetes in different age groups. Diabetologia. 1991;34:757-762

33. Blom L, Dahlquist G, Nystrom L, Sandstrom A, Wall S. The Swedish childhood diabetes study--social and perinatal determinants for diabetes in childhood. Diabetologia. 1989;32:7-13

34. Dahlquist G, Savilahti E, Landin-Olsson M. An increased level of antibodies to beta-lactoglobulin is a risk determinant for early-onset type 1 (insulin-dependent) diabetes mellitus independent of islet cell antibodies and early introduction of cow's milk. Diabetologia. 1992;35:980-984

35. Glatthaar C, Whittall DE, Welborn TA, et al. Diabetes in Western Australian children: descriptive epidemiology. Med J Aust. 1988;148:117-123

36. Kostraba JN, Dorman JS, LaPorte RE, et al. Early infant diet and risk of IDDM in blacks and whites--a matched case-control study. Diabetes Care. 1992;15:626-631

37. Siemiatycki J, Colle E, Campbell S, Dewar RA, Belmonte MM. Case-control study of IDDM. Diabetes Care. 1989;12:209-216

38. Mayer EJ, Hamman RF, Gay EC, Lezotte DC, Savitz DA, Klingensmith GJ. Reduced risk of IDDM among breast-fed children. The Colorado IDDM Registry. Diabetes. 1988;37:1625-1632

39. Kostraba JN, Cruikshanks KJ, Lawler-Heavner J, et al. Early exposure to cow's milk and solid foods in infancy, genetic predisposition and risk of IDDM. Diabetes. 1993;42:288-295

40. Fort P, Lanes R, Dahlem S, et al. Breast feeding and insulin-dependent diabetes mellitus in children. J Am Coll Nutr. 1986;5:439-441

41. Kyvik KO, Green A, Svendsen A, Mortensen K. Breast feeding and the development of type 1 diabetes mellitus. Diabetic Med. 1992;9:233-235

42. Metcalfe MA, Baum JD. Family characteristics and insulin dependent diabetes. Arch Dis Child. 1992;67:731-736

43. Nigro G, Campea L, De Novellis A, Orsini M. Breast-feeding and insulin-dependent diabetes mellitus. Lancet. 1985;1:467

44. Bognetti E, Meschi F, Malavasi C, et al. HLA antigens in Italian type 1 diabetic patients: role of DR3/DR4 antigens and breast feeding in the onset of the disease. Acta Diabetol. 1992;28:229-232

45. Virtanen SM, Rasanen L, Ylonen K, et al. Early introduction of dairy products associated with increased risk of IDDM in Finnish children. Childhood in Diabetes in Finland Study Group. Diabetes. 1993;42:1786-1790

46. Kostraba JN. What can epidemiology tell us about the role of infant diet in the etiology of IDDM? Diabetes Care. 1994;17:87-91

47. Atkinson MA, Bowman MA, Kao KJ, et al. Lack of immune responsiveness to bovine serum albumin in insulin-dependent diabetes. N Engl J Med. 1993;329:1853-1858

48. Elliot RB, Martin JM. Dietary protein: a trigger of insulin dependent diabetes in the BB rat? Diabetologia. 1984;26:297-299

49. Daneman D, Fishman L, Clarson C, Martin J. Dietary triggers of insulin-dependent diabetes in the BB rat. Diabetes Res Clin Exp. 1987;5:93-97

50. Coleman DL, Kuzava JE, Leiter EH. Effect of diet on incidence of diabetes in nonobese diabetic mice. Diabetes. 1990;39:432-436

51. Scott FW, Daneman D, Martin JM. Evidence for a critical role of diet in the development of insulin-dependent diabetes mellitus. Diabetes Res Clin Exp. 1988;7:153-157

52. Scott FW, Elliott RB, Kolb H. Diet and autoimmunity: prospects of prevention of type I diabetes. Diabetes Nutr Metabol Clin Exp. 1989;2:61-67

53. Leslie RDG, Elliot RB. Early environmental events as a cause of IDDM: evidence and implications. Diabetes. 1994;43:843-850

54. Scott FW, Sarwar G, Cloutier HE. Diabetogenicity of various protein sources in the diet of the diabetes-prone BB rat. In: Camerini-Davalos RA, Cole HS, eds. Prediabetes. New York: Plenum Publishing Corp; 1988:277-285

55. Scott FW, Cloutier HC, Souligny J, Riley WJ, Hoorfar J, Brogren CH. Diet and antibody production in the diabetes-prone BB rat. In: Larkins R, Zimmet P, Chisholm D, eds. Diabetes 1988. Proceedings of the 13th International Diabetes Federation. The Netherlands: Elsevier Science Publishers BV; 1989:763-767

56. Scott FW, Marliss EB. Conference summary: diet as an environmental factor in development of insulin-dependent diabetes mellitus. Can J Physiol Pharmacol. 1991;69:311-319

57. Hoorfar J, Scott FW, Cloutier HE. Dietary plant materials and development of diabetes in the BB rat. J Nutr. 1991;121:908-916

58. Scott FW. Food, diabetes immunology. In: Forse SA, Kabbash L, Blackburn GL, Bell SJ, eds. Diet, Nutrition and Immunity. Boca Raton, FL: CRC Press. In press.

59. Hoorfar J, Buschard K, Dagnaes-Hansen F. Prophylactic nutritional modification of the incidence of diabetes in autoimmune non-obese diabetic (NOD) mice. Br J Nutr. 1993;69:597-607


The recommendations in this statement do not indicate an exclusive course of treatment or serve as a standard of medical care. Variations, taking into account individual circumstances, may be appropriate.

PEDIATRICS (ISSN 0031 4005). Copyright (c) 1994 by the American Academy of Pediatrics.

No part of this statement may be reproduced in any form or by any means without prior written permission from the American Academy of Pediatrics except for one copy for personal use.



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