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Higher breastfeeding intensity associated with improved postpartum glucose metabolism in women with recent gestational diabetes
  1. Carla A Borgoño,
  2. Ravi Retnakaran
  1. Department of Medicine, University of Toronto, Toronto, Canada
  1. Correspondence to Ravi Retnakaran
    Leadership Sinai Centre for Diabetes, Mount Sinai Hospital, 60 Murray Street, Suite-L5-039, Mail Box 21, Toronto, ON M5T 3L9, Canada; rretnakaran{at}mtsinai.on.ca

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Context

WHO recommends that all babies should be exclusively breastfed for the first 6 months after birth.1 In the general population, breastfeeding has been associated with short-term improvement in postpartum maternal glucose metabolism and long-term reduction in risk of cardiometabolic disease including type 2 diabetes (T2DM) and myocardial infarction.2 ,3 Women diagnosed with gestational diabetes mellitus (GDM), defined as glucose intolerance of varying severity with onset and first recognition in pregnancy, have an increased lifetime risk of developing both T2DM and cardiovascular disease.4 However, the relationship between breastfeeding and maternal glucose metabolism has not been clearly established in this high-risk population. It is in this context that Gunderson et al have explored the association between lactation intensity and postpartum metabolism in women with recent GDM.

Methods

The authors analysed 522 women with recent GDM recruited between September 2008 and March 2011, who underwent a 2-h 75 g oral glucose tolerance test (OGTT) at 6–9 weeks postpartum within the Kaiser Permanente Northern California integrated healthcare system. Eligibility criteria included a diagnosis of GDM on 3-h 100 g OGTT at 24–32 weeks gestation, delivery of a live, singleton neonate at term and availability of information on infant feeding.

Participants were categorised into four groups based on infant feeding practices: exclusive breastfeeding, mostly breastfeeding (≤6 oz of formula/24 h), mixed/inconsistent feeding of breast milk and formula (7–17 oz/24 h), and exclusive/mostly formula feeding (>17 oz/24 h). Maternal glucose tolerance (fasting and 2-h glucose) and insulin resistance (fasting insulin, homeostasis model assessment of insulin resistance (HOMA-IR)) were compared between the four groups by multiple linear regression. Covariates for adjustment included race/ethnicity, maternal body mass index, education, parity, age, and time spent fasting and breastfeeding prior to the OGTT.

Findings

Women with the highest lactation intensity (exclusively and primarily breastfeeding groups) displayed better glucose metabolism than those with the lowest intensity (exclusively/mainly formula-fed group). Specifically, as compared with the exclusive/mostly formula-fed group, the exclusive and mostly breastfeeding groups, respectively, had lower adjusted mean fasting glucose levels (by −4.3 and −5.0 mg/dl), fasting insulin levels (by −6.3 and −7.5 mU/ml), and HOMA-IR (by −1.79 and −2.18) (all p<0.05). Moreover, the most intensive lactation groups had the lowest proportion of women with diabetes or pre-diabetes (p=0.02) (eg, 45.2% for those exclusively or mostly formula feeding vs 28% for those exclusively breastfeeding).

Commentary

The key advance in this study is its demonstration that intensive lactation in the early puerperium correlates with a beneficial metabolic profile in the high-risk population of women with prior GDM. While prior reports have described a similar relationship between breastfeeding and glucose tolerance at 4 to 12 weeks postpartum following GDM,5 ,6 these studies did not address the intensity of lactation. Thus, the current observation of a dose-dependent relationship between lactation and maternal metabolic parameters offers support for the biological plausibility of breastfeeding conferring metabolic benefits in this high-risk population. Indeed, it is known that the high energy demands required for lactogenesis lead to changes in maternal fuel metabolism, including alterations in glucose handling, increased lipolysis and greater energy expenditure overall.7 Although not assessed in the current study, these effects could underlie the observed metabolic benefits.

Despite biological plausibility and the observed dose-dependent association, it is possible that the link between lactation intensity and maternal glucose metabolism found in this observational study may not be causal. This is in particular because of the possibility of residual confounding by factors not included in the adjusted analyses. These potential confounders include lifestyle factors that may accompany breastfeeding, such as healthy dietary habits and physical activity.

The question as to whether the early beneficial effects associated with lactation can translate into a reduced incidence of cardiometabolic disease in the long-term (postlactation) in the high-risk population of women with GDM currently remains unanswered. If demonstrated through further prospective follow-up, such data could identify breastfeeding as a potential modifier of cardiometabolic risk in this at-risk population. In the mean time, the observations in this study significantly strengthen the need to follow WHO recommendations for breastfeeding in the postpartum management of women with GDM.

References

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Footnotes

  • Competing interests None.