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Breastfeeding Curbs Type 2 Diabetes Later in Life
Renewed efforts to encourage breastfeeding in populations at risk for the development of type 2 diabetes may be useful.
Reviewed by Elizabeth J. Mayer-Davis, PhD
The increasing prevalence of childhood obesity,1 coupled with the appearance of type 2 diabetes in youth,2,3 has led to research into lifestyle approaches that can prevent these conditions. Breastfeeding is associated with a reduced risk of developing type 2 diabetes in adulthood;4 however, little is known about the effect of breastfeeding on type 2 diabetes when the child reaches adolescence.
The protective effect of breastfeeding on the development of type 2 diabetes in youth is centered around its potential to reduce the risk of childhood obesity. Conducted among primarily white populations, recent meta-analyses have concluded that a child having been breastfed is associated with 13% to 22% reduced odds for overweight or obesity in childhood or later in life.5-7 A study including more than 73,000 white and black, low-income children8 revealed that breastfeeding was protective against obesity at age 4 years among offspring of white mothers only. Another analysis, based on breastfeeding duration, found a protective dose-response relationship with the risk of overweight only among non-Hispanic white participants.9 A study of high-risk Latino youth showed no association of breastfeeding with adiposity or glucose and insulin metabolism.10 It is possible that differential effects exist due to race/ethnicity.
We hypothesized that young people with type 2 diabetes would be less likely to have been breastfed compared with nondiabetic control youth and that this finding would be consistent across three race/ethnic groups of non-Hispanic whites, African Americans, and Hispanics and be independent of maternal diabetes status. We also looked into whether current body mass index (BMI) would account for any of the protective association seen. The full results of our work appeared in Diabetes Care;11 the following is a summary of those findings.
SEARCH CC
The SEARCH CC study, an ancillary study to the multicenter SEARCH for Diabetes in Youth, was conducted at two of six SEARCH clinical sites.12
We included 80 youth who had type 2 diabetes and were aged 10 to 21 years, and we also recruited 167 nondiabetic control participants from primary care providers. At the South Carolina and Colorado clinical sites, African American and Hispanic control participants were overrecruited relative to non-Hispanic white participants. This was to ensure adequate numbers among each race/ethnic group for statistical analyses.
Breastfeeding history was obtained from the participants' biological mothers, including duration of breastfeeding and timing of introduction of formula and other foods and beverages. We generated two measures of breastfeeding exposure: breastfeeding (yes/no) and breastfeeding duration. From the biological mother, we also gathered information with regard to diabetes status during pregnancy, prepregnancy height and weight, smoking and alcohol use during pregnancy and lactation, the offspring's birth weight and length, and approximate gestational age. Family history of diabetes was obtained as well.
Unadjusted and adjusted odds ratios (ORs) and 95% confidence intervals (CIs) were generated from logistic regression to calculate the association of breastfeeding with type 2 diabetes. An interaction term between breastfeeding and race/ethnicity was used to determine whether the association differed depending on race/ethnicity. Two models were developed so that potential confounders could be addressed. These included a partially adjusted model with design variables and a fully adjusted model that included all variables from the partially adjusted model, plus additional variables to address any chance of residual confounding. Current weight status (BMI z-score) was added to the adjusted models to evaluate potential mediation of the association between breastfeeding and type 2 diabetes by obesity.
RESULTS
Our study found that the prevalence of any duration of breastfeeding was lower among youth who had type 2 diabetes versus control individuals (19.5% vs 27.1% for African Americans, 50.0% vs 83.8% for Hispanics, and 39.1% vs 77.6% for non-Hispanic whites). Unadjusted characteristics of case and control participants are as follows; 31.3% of youth with type 2 diabetes were breastfed, compared with 63.5% of nondiabetic control youth. Duration of breastfeeding was longer among control than case individuals (P<.0001), and current BMI z-score was higher among case compared with control participants (P<.0001).
The overall crude OR for the association of breastfeeding and type 2 diabetes was 0.26 (95% CI, 0.15–0.46). Results were similar by race/ethnic group, with a P value for interaction of 0.17. The OR for the association, after the adjustment for 12 potential confounders, was 0.43 (0.19–0.99). The OR was attenuated when the current BMI z-score was added to the model (0.82 [0.30–2.30]), which suggests possible mediation through current childhood weight status. When we conducted analyses that included duration of breastfeeding—adjusted for potential confounders—there was evidence for a dose response (test for trend, P<.001) even after inclusion of the BMI z-score.
A partially adjusted model included eight variables that were statistically significantly associated with both case-control status and breastfeeding. We evaluated the dose response based on breastfeeding duration as well.
IMPLICATIONS AND MECHANISMS
Our findings provide evidence for a protective association of breastfeeding against the development of type 2 diabetes in youth in a dose-response fashion, independent of other potentially confounding variables. The attenuation of ORs when BMI z-score was added were consistent with a causal pathway in which breastfeeding may lower the risk for overweight in childhood, in turn possibly reducing the risk for type 2 diabetes. With multiple potential confounders accounted for, however, a statistically significant trend (P<.0001) for breastfeeding duration was observed that was not fully accounted for by current weight status in childhood.
In our study, the protective association of breastfeeding on type 2 diabetes development was seen for all race/ethnicity categories, with higher proportions of breastfed infants having a lower risk of diabetes. The statistical test for interaction by race/ethnicity was not statistically significant, and we believe further research in larger samples is required to better understand potential differences in associations of breastfeeding and type 2 diabetes.
A lower prevalence of breastfeeding among African American infants than among infants of other race/ethnicities13 and among infants of low-income families and low maternal education13 has been previously documented. Although we considered these characteristics as potential confounding variables in our analyses, the finding of a protective association persisted. We believe that targeting population subgroups at high risk both for type 2 diabetes and low prevalence of breastfeeding (including African American, low-income, and low-education populations) may offer an important opportunity for primary prevention of type 2 diabetes.
Prior to this study, we hypothesized that the analyses would find that a child's current weight status would at least partially mediate any protective association of breastfeeding with type 2 diabetes that we observed. Some potential mechanisms for an association of breastfeeding with a reduction in childhood obesity include a satiety signal in response to breast milk's nutritional makeup14 and overfeeding of bottle-fed infants who have higher levels of plasma insulin levels and a prolonged insulin response compared with breastfed infants.15 Still, a statistically significant protective dose-response association was observed.
Aside from weight status, potential mechanisms accounting for a protective association between breastfeeding and type 2 diabetes could include environmental toxins as potential contributors to obesity and related metabolic disorders.16-19
Because the development of type 2 diabetes requires inadequate insulin secretion relative to insulin resistance, we considered possible mechanisms for protection related to this. Vitamins E and D20,21 have been associated with improved beta-cell function; however, both are likely to be sufficient in infant formula.22,23 Nitrate exposure may have a negative impact on beta-cell function,24 and it is possible that increased intake of tap water, mixed with formula powders, raises nitrate exposure in formula-fed infants compared with breastfed infants.
Breastfeeding may be protective against type 2 diabetes development in youth regardless of race/ethnicity and is mediated, at least in part, by current weight status in childhood. Further work is needed to confirm this finding and evaluate both obesity-related and obesity-independent mechanisms. Given other well-established reasons for breastfeeding (see accompanying sidebar, Breastfeeding Linked to Higher Intelligence Scores), efforts to encourage the practice in at-risk populations may be useful.
Elizabeth J. Mayer-Davis, PhD, is from the Center for Research in Nutrition and Health Disparities and Epidemiology and Biostatistics, University of South Carolina, Columbia. She may be reached at ejmayer@gwm.sc.edu.
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