The benefits of breastfeeding are so well recognized that pointing out a flaw usually meets with considerable doubt, if not with outright hostility. Yet what holds true for other areas of physiology and medicine holds true here: What is "natural" is not necessarily flawless. Breast milk is a case in point.
Maternal immunoglobulins and leukocytes transferred to the infant by colostrum or milk generally bolster the infant's poorly developed immune response.1 However, in some instances the wisdom of breastfeeding is questionable, as when mother and child are not Rh or ABO blood group compatible or when the mother carries a microorganism, such as the human T-cell lymphotropic virus Type I (HTLV-I). It seems appropriate to question whether the transfer of lymphocytes, especially allotypic lymphocytes, from mother to infant by breast milk, is wise.
Colostrum contains about 10,000 lymphocytes per mm; approximately 2,000 of those are T lymphocytes. Because newborns have low gastric acidity and peptic enzyme secretion, lymphocytes survive the gastrointestinal tract and traverse the mucosal wall. Therefore, breastfed infants are likely to be tolerized to maternal antigens. Infants breastfed by tuberculin-positive mothers become tuberculin-positive, whereas no such sensitization occurs when the infants of tuberculin-positive mothers are not breastfed. Maternal renal allografts have a better survival rate in individuals who were breastfed than in patients who were not.2
The transmission of intracellular microorganisms such as HTLV-I provides another example. HTLV-I is an intracellular virus and causes leukemias, lymphomas, tropical spastic paraparesis, and many inflammatory diseases. In Japan, where HTLV-I is endemic, breastfeeding by mothers who have antibodies to the virus has been interdicted since 1985.
In the United States, the prevalence of HTLV-I infection based on antibody studies is less than 1%. However, about 8% of New York City blood donors carry the HTLV-I Tax DNA sequence in their lymphocytes without having such antibodies.3 The Tax sequence is known to be the "engine" of HTLV-I, which transactivates numerous genes responsible for the elaboration of cytokines and growth factors likely to play a role in the development of various inflammatory and neoplastic diseases.
Could such lymphocytes play a role in the development of autoimmune diseases? A study conducted on patients with rheumatoid arthritis showed that the prevalence of HTLV-I Tax positivity is at least three times higher in such patients than in healthy individuals.4 None of the participants in the study had ever been transfused, so it must be assumed that the HTLV-I Tax was acquired transplacentally or by breast milk. (An accurate breastfeeding history is difficult, if not impossible, to obtain from middle-aged patients.)
Recently, the prevalence and incidence of 24 autoimmune diseases in the United States was assessed.5 The authors estimated that 1 in 31 Americans is afflicted, but the etiology has remained obscure. It is safe to assume that a breastfeeding history was not obtained. It may be important to compare the allotype of lymphocytes infiltrating organs, such as the thyroid in Hashimoto disease or the thymus in myasthenia gravis, with the allotype of lymphocytes in the circulation of the same individual. Animal models of autoimmune diseases exist in which such studies could be carried out.
Eliminating lymphocytes from breast milk may be prudent. Removing these cells could be accomplished by placing leukocyte reduction filters (routinely used to eliminate leukocytes from blood used for transfusion) into nipple shields, which are used by many women who have cracked or otherwise painful nipples. Such filters also could be placed into the nipples of bottles containing milk collected by breast pumps. The efficacy of these devices is under current investigation. The benefit of this measure may far outweigh its drawbacks.
Dorothea Zucker-Franklin, MD, is a professor of medicine at the New York University School of Medicine.
1. S.S. Ogra, P.L. Ogra, "Components of immunologic reactivity in human colostrum and milk," In: Immunology of Breast Milk; New York: Raven Press, 1979.
2. L. Zhang et al., "Influence of breast feeding on the cytotoxic T cell allorepertoire in man," Transplantation, 52:914, 1991.
3. D. Zucker-Franklin, B.A. Pancake, "Human T cell lymphotropic virus Type I (HTLV-I) tax among American blood donors," Clin Diagn Lab Immun, 5:831, 1998.
4. D. Zucker-Franklin et al., "Prevalence of HTLV-I tax in a subset of patients with rheumatoid arthritis," Clin Exp Rheumatol, 20:161, 2002.
5. D.L. Jacobson et al., "Epidemiology and estimated population burden of selected autoimmune diseases in the United States," Clin Immunol Immunopathol, 84:223, 1997.