Early Infant Diet and Risk of IDDM in Blacks and Whites: A Matched Case-Control Study

Kostraba, Jill N; Dorman, Janice S.; LaPorte, Ronald E.; Scott, Fraser W.; Steenkiste, Ann R.; Gloninger, Margaret F.; Drash, Allan L.

doi:10.2337/diacare.15.5.626

Cited by 45 publications

(46 citation statements)

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“…The results suggest that young age at introduction of dairy products and high milk consumption during childhood increase the levels of cow's milk antibodies and that high IgA antibodies to cow's milk formula are independently associated with increased risk of IDDM. [Diabetologia (1994) 37: 381-387] early introduction of dairy products or other foods could be related to an increased risk of IDDM [3][4][5][6][7]. A detailed study of infant feeding patterns indicated that the age at introduction of dairy products had the closest association with the risk of IDDM when the duration of both overall and exclusive breast-feeding was taken into account [8].…”

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confidence: 99%

Diet, cow's milk protein antibodies and the risk of IDDM in Finnish children

et al. 1994

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Summary Associations of infant feeding patterns and milk consumption with cow's milk protein antibody titres were studied in 697 newly-diagnosed diabetic children, 415 sibling-control children and 86 birth-dateand sex-matched population-based control children in the nationwide "Childhood Diabetes in Finland" study. IgA and IgG antibody titres to the proteins of cow's milk formula, BLG and BSA, and IgM antibody titres to cow's milk formula proteins were measured by ELISA. Several inverse correlations were observed between the duration of breast-feeding or age at introduction of dairy products and antibody titres, and positive correlations were observed between milk consumption and antibody titres in all three populations studied. Multivariate analyses which included the infant feeding variables, milk consumption and current age simultaneously showed that the earlier the introduction of dairy products and the greater the consumption of milk was, the higher several antibody titres were. High IgA antibody titres to cow's milk formula were associated with a greater risk of IDDM both among diabeticpopulation-control and diabetic-sibling-control pairs when adjusted for other cow's milk antibody titres, dietary variables and in diabetic-sibling-control pairs also for ICA. The results suggest that young age at introduction of dairy products and high milk consumption during childhood increase the levels of cow's milk antibodies and that high IgA antibodies to cow's milk formula are independently associated with increased risk of IDDM. [Diabetologia (1994) 37: 381-387]

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confidence: 99%

Diet, cow's milk protein antibodies and the risk of IDDM in Finnish children

et al. 1994

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“…The higher abundance of transporter mRNA indicates a potential for increased nutrient uptake from the intestine at this "critical" time, suggested by this study to be from 44 days of age, at which time the pups may begin consuming the dams' diet through to 21 days of age when weaning occurs. In human infants, many retrospective studies have shown a negative correlation between breast feeding as an infant and IDDM occurrence in adolescence [32,33]. Breast feeding may confer protection by decreasing exposure to foreign antigens via solid food or formula.…”

Section: Discussionmentioning

confidence: 99%

Ontogenic changes in proglucagon mRNA in BB diabetes prone and normal rats weaned onto a chow diet

1997

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The bio-breeding (BB) rat is a useful animal model of human insulin-dependent diabetes mellitus (IDDM) [1,2]. The BB rat displays many of the immune irregularities associated with the human disease. As in human IDDM the syndrome is spontaneous and results in the autoimmune destruction of the insulinproducing beta cells of the pancreas [3,4]. It is well established that both forms of diabetes, human and BB are autoimmune.Investigations into the aetiology of IDDM suggest that both genetic and environmental factors are involved [5]. It is now well recognized that diet is an important factor influencing development of diabetes in the BB rat [6,7]. Studies suggest that semi-purified diet may be protective whereas laboratory chow may be more diabetogenic in nature [8,9].Whether the protective effect of a semi-purified diet is due to the presence of a specific protective component or conversely the absence of a diabetogenic component is yet unknown. It is known, however, that the timing of initial exposure and duration of Diabetologia (1997) Summary Weaning onto chow diets causes the highest incidence of diabetes in the BB rat. Changes in gut development and absorption of nutrients in the diabetes prone rat and the subsequent effect on pancreatic function may play a role in the ultimate development of the disease. BB diabetes prone (dp) and BB normal (n) dams were fed chow diets. Pups were killed at various ages ranging from 7 to 30 days. BBdp rats had higher small intestine and colon weights expressed per body weight at all ages (p < 0.0001). RNA content (mg/g) in the jejunum, ileum and colon was higher in the BBdp rats beginning at the critical period at 21 days and maintained at 24 days and 30 days (p < 0.0001). Proglucagon message decreased with age in both BBdp and BBn animals (p < 0.0001). Levels of proglucagon mRNA were higher in BBdp compared to BBn animals only in the ileum at 10 days (p < 0.01). Adjusting for total ileal and colonic RNA content resulted in BBdp animals having higher total colonic proglucagon mRNA at 21, 24 and 30 days (p < 0.0001). Plasma GLP-1(7-36) amide was more than doubled in BBdp compared to BBn animals (p < 0.0005) at 30 days. Expressing sodium-dependent D-glucose co-transporter (SGLT-1), GLUT2 and GLUT5 mRNA per total jejunal RNA shows increased transporter mRNA in BBdp compared to BBn rats at weaning (21 days) (p < 0.05). Radical differences exist between BBdp and BBn animals at 'critical periods' in both proglucagon and glucose transporter gene expression. These differences may help explain altered growth and diseases incidence between these two strains [Diabetologia (1997) 40: 871-878].

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“…[7][8][9] A number of earlier hypotheses with some supporting evidence have been put forward to explain the possible mechanism of action of the environmental trigger including b-cell death secondary to virally triggered inflammation, molecular mimicry, superantigens and diet. [10][11][12][13][14][15][16][17][18][19] What is certain is that at some point postnatally, the immune system of a genetically predisposed individual is activated to infiltrate chronically the islets of Langerhans. While the initial phase of infiltration may not involve b-cell destruction, a number of studies in vivo and in vitro suggest that immune cells become able to render b-cells dysfunctional through the actions of cytokines they produce such as interleukin-1b.…”

Section: Type I Diabetes Mellitus: the Autoimmune Processmentioning

confidence: 99%