Journal of Human Lactation http://jhl.sagepub.com/
Risk Factors for Delayed Lactogenesis among Women with Gestational Diabetes Mellitus Donna J. Chapman J Hum Lact 2014 30: 134 DOI: 10.1177/0890334414525566 The online version of this article can be found at: http://jhl.sagepub.com/content/30/2/134
Published by: http://www.sagepublications.com
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>> Version of Record - Apr 15, 2014 What is This?
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525566
research-article2014
JHLXXX10.1177/0890334414525566Journal of Human LactationChapman
Research Spotlight
Risk Factors for Delayed Lactogenesis among Women with Gestational Diabetes Mellitus
Journal of Human Lactation 2014, Vol. 30(2) 134–135 © The Author(s) 2014 Reprints and permissions: sagepub.com/journalsPermissions.nav DOI: 10.1177/0890334414525566 jhl.sagepub.com
Donna J. Chapman, PhD, RD Matias SL, Dewey KG, Quesenberry CP, Gunderson EP. Maternal prepregnancy obesity and insulin treatment during pregnancy are independently associated with delayed lactogenesis in women with recent gestational diabetes mellitus. Am J Clin Nutr. 2014;99(1): 115-121.
Gestational diabetes mellitus (GDM) has been associated with an increased risk for delayed lactogenesis, yet many women with GDM do not experience this problem. Wouldn’t it be useful to have some solid evidence to help you determine which of your patients with GDM are at greater risk for delayed lactogenesis? In this issue, the Research Spotlight highlights the results of a clinically relevant study that sought to determine the incidence of and risk factors associated with delayed lactogenesis among women with GDM. In this observational study, Dr Susana Matias and colleagues analyzed a subset of the data from the Study of Women, Infant Feeding and Type 2 Diabetes after GDM Pregnancy (SWIFT), in a collaboration between Kaiser Permanente of Northern California and the University of California, Davis. Women were enrolled into the SWIFT study 6 to 9 weeks postpartum, between September 2008 and December 2011. To participate in the SWIFT study, women had to have been diagnosed with GDM before 32 weeks of gestation in their recent pregnancy, receive medical care through Kaiser Permanente of Northern California, deliver a live, healthy singleton born at ≥ 35 weeks gestation, be 18 to 42 years old at the time of delivery, be free of serious medical conditions, require no postpartum medications that affect glucose tolerance or inhibit lactation, complete baseline questionnaires, and plan to breastfeed. For inclusion in the analyses by Matias and colleagues, participants were also required to have initiated breastfeeding and provide data on the timing of lactogenesis stage II. The dependent variable in this study was the timing of lactogenesis stage II. At 6 to 9 weeks postpartum, women were asked to recall the day postpartum (ie, day 1 pp, day 2 pp) on which they first noticed that their breasts were noticeably fuller than during their pregnancy. Maternal perception of breast fullness is a commonly used proxy for the timing of lactogenesis stage II. Delayed lactogenesis was defined as maternal report of breast fullness occurring after 72 hours pp (vs timely lactogenesis, occurring ≤ 72 hours pp). Data on independent variables were collected from medical records, telephone calls, and participant interviews.
These included maternal prepregnancy body mass index (BMI) and gestational weight gain (both categorized according to the 2009 Institute of Medicine categories), age, ethnicity, participation in the Special Supplemental Nutrition Program for Women, Infants and Children (WIC), and labor and delivery characteristics. Gestational diabetes mellitus treatment status was categorized as requiring diet only, oral hypoglycemic agents, or insulin. Infant variables included gestational age, birth weight, infant size (large vs appropriate vs small for gestational age), Apgar score, and sex. The average LATCH score during the first 24 hours postpartum was calculated for each infant. For their statistical analyses, Matias and colleagues used chi-square analyses, Fisher’s exact test, and t tests to evaluate bivariate associations between women with timely versus delayed lactogenesis. Variables that were significant in their bivariate analyses, along with variables supported by scientific literature, were then included in a series of logistic regression models designed to evaluate the independent effect of these variables on the timing of lactogenesis. Model 1 simply evaluated the relationship between maternal prepregnancy BMI (healthy, overweight, or obese) on the timing of lactogenesis. In model 2, they added maternal sociodemographic variables (age and race/ethnicity) as predictors of the timing of lactogenesis. In model 3, they retained the independent variables from model 2 and added covariates describing labor and delivery (parity, delivery mode), infant characteristics (gestational age), and early feedings (LATCH score). Model 4 included all variables from the previous models plus GDM treatment (diet only, oral hypoglycemic agents, insulin). They also tested to see if the relationship between parity and timing of lactogenesis was modified by other variables and found that the interaction between parity and gestational age was significant. Thus, in model 5, they included the variables in model 4 but also added an interaction term for parity and gestational age. These analyses included 883 SWIFT participants, all of whom had GDM. Participants were ethnically diverse, with 77% from minority groups. At 6 to 9 weeks postpartum, BMI
Downloaded from jhl.sagepub.com at HUNTER COLLEGE LIB on June 6, 2014
135
Chapman distribution for the group was 24% healthy weight, 35% overweight, and 41% obese. Twenty-nine percent of the births were by cesarean delivery. One-third of the participants reported delayed lactogenesis (> 72 hours pp). Key risk factors for delayed lactogenesis were identified in the series of logistic regression models. The most clinically relevant finding was the identification of insulin treatment for GDM as a risk factor (adjusted odds ratio [AOR] = 3.11; 95% confidence interval [CI], 1.37-7.05). Other significant predictors of delayed lactogenesis identified in the final model were maternal obesity (AOR = 1.56; 95% CI, 1.07-2.29), increased maternal age (AOR = 1.05; 95% CI, 1.01-1.08), and average LATCH score ≤ 7.5 in the first 24 hours of life (AOR = 1.65; 95% CI, 1.20-2.26). In addition, there was a significant interaction between gestational age and parity, such that increased gestational age was associated with a decreased risk of delayed lactogenesis, but only among multiparous women (AOR = 0.79; 95% CI, 0.67-0.94). This study has identified novel predictors of delayed lactogenesis among a diverse sample of women with a GDMaffected pregnancy. Some unique contributions of this study include the identification of GDM severity (based on the requirement for insulin therapy), lower LATCH scores on the first day of life, and increased maternal age as risk factors for
delayed lactogenesis among a diverse sample of women with GDM. The identification of insulin treatment as an independent risk factor for delayed lactogenesis has important clinical implications and suggests that GDM patients requiring insulin should be given high priority for lactation consultant services. Regarding maternal age, the authors found that a 5-year increase in maternal age was associated with a relatively large (26%) increase in the risk of delayed lactogenesis. Some of the strengths of this study include the large sample size of women with GDM, the ethnically diverse sample, and the standardized procedures for electronic medical record documentation, GDM screening, and treatment within the Kaiser Permanente health care system. As the authors noted, 1 potential limitation of the study is that the timing of lactogenesis stage II was reported at 6 to 9 weeks postpartum, introducing the possibility of recall bias. Given that maternal recall of the timing of lactogenesis has been validated at approximately 6 months pp, the potential for recall bias seems small. This study provides key data to support evidence-based practice in the identification of GDM women at high risk for delayed lactogenesis. Further research is clearly needed to understand the mechanisms behind these risk factors.
Downloaded from jhl.sagepub.com at HUNTER COLLEGE LIB on June 6, 2014
Risk Factors for Delayed Lactogenesis among Women with Gestational Diabetes Mellitus Donna J. Chapman J Hum Lact 2014 30: 134 DOI: 10.1177/0890334414525566 The online version of this article can be found at: http://jhl.sagepub.com/content/30/2/134
Published by: http://www.sagepublications.com
Additional services and information for Journal of Human Lactation can be found at: Email Alerts: http://jhl.sagepub.com/cgi/alerts Subscriptions: http://jhl.sagepub.com/subscriptions Reprints: http://www.sagepub.com/journalsReprints.nav Permissions: http://www.sagepub.com/journalsPermissions.nav
>> Version of Record - Apr 15, 2014 What is This?
Downloaded from jhl.sagepub.com at HUNTER COLLEGE LIB on June 6, 2014
525566
research-article2014
JHLXXX10.1177/0890334414525566Journal of Human LactationChapman
Research Spotlight
Risk Factors for Delayed Lactogenesis among Women with Gestational Diabetes Mellitus
Journal of Human Lactation 2014, Vol. 30(2) 134–135 © The Author(s) 2014 Reprints and permissions: sagepub.com/journalsPermissions.nav DOI: 10.1177/0890334414525566 jhl.sagepub.com
Donna J. Chapman, PhD, RD Matias SL, Dewey KG, Quesenberry CP, Gunderson EP. Maternal prepregnancy obesity and insulin treatment during pregnancy are independently associated with delayed lactogenesis in women with recent gestational diabetes mellitus. Am J Clin Nutr. 2014;99(1): 115-121.
Gestational diabetes mellitus (GDM) has been associated with an increased risk for delayed lactogenesis, yet many women with GDM do not experience this problem. Wouldn’t it be useful to have some solid evidence to help you determine which of your patients with GDM are at greater risk for delayed lactogenesis? In this issue, the Research Spotlight highlights the results of a clinically relevant study that sought to determine the incidence of and risk factors associated with delayed lactogenesis among women with GDM. In this observational study, Dr Susana Matias and colleagues analyzed a subset of the data from the Study of Women, Infant Feeding and Type 2 Diabetes after GDM Pregnancy (SWIFT), in a collaboration between Kaiser Permanente of Northern California and the University of California, Davis. Women were enrolled into the SWIFT study 6 to 9 weeks postpartum, between September 2008 and December 2011. To participate in the SWIFT study, women had to have been diagnosed with GDM before 32 weeks of gestation in their recent pregnancy, receive medical care through Kaiser Permanente of Northern California, deliver a live, healthy singleton born at ≥ 35 weeks gestation, be 18 to 42 years old at the time of delivery, be free of serious medical conditions, require no postpartum medications that affect glucose tolerance or inhibit lactation, complete baseline questionnaires, and plan to breastfeed. For inclusion in the analyses by Matias and colleagues, participants were also required to have initiated breastfeeding and provide data on the timing of lactogenesis stage II. The dependent variable in this study was the timing of lactogenesis stage II. At 6 to 9 weeks postpartum, women were asked to recall the day postpartum (ie, day 1 pp, day 2 pp) on which they first noticed that their breasts were noticeably fuller than during their pregnancy. Maternal perception of breast fullness is a commonly used proxy for the timing of lactogenesis stage II. Delayed lactogenesis was defined as maternal report of breast fullness occurring after 72 hours pp (vs timely lactogenesis, occurring ≤ 72 hours pp). Data on independent variables were collected from medical records, telephone calls, and participant interviews.
These included maternal prepregnancy body mass index (BMI) and gestational weight gain (both categorized according to the 2009 Institute of Medicine categories), age, ethnicity, participation in the Special Supplemental Nutrition Program for Women, Infants and Children (WIC), and labor and delivery characteristics. Gestational diabetes mellitus treatment status was categorized as requiring diet only, oral hypoglycemic agents, or insulin. Infant variables included gestational age, birth weight, infant size (large vs appropriate vs small for gestational age), Apgar score, and sex. The average LATCH score during the first 24 hours postpartum was calculated for each infant. For their statistical analyses, Matias and colleagues used chi-square analyses, Fisher’s exact test, and t tests to evaluate bivariate associations between women with timely versus delayed lactogenesis. Variables that were significant in their bivariate analyses, along with variables supported by scientific literature, were then included in a series of logistic regression models designed to evaluate the independent effect of these variables on the timing of lactogenesis. Model 1 simply evaluated the relationship between maternal prepregnancy BMI (healthy, overweight, or obese) on the timing of lactogenesis. In model 2, they added maternal sociodemographic variables (age and race/ethnicity) as predictors of the timing of lactogenesis. In model 3, they retained the independent variables from model 2 and added covariates describing labor and delivery (parity, delivery mode), infant characteristics (gestational age), and early feedings (LATCH score). Model 4 included all variables from the previous models plus GDM treatment (diet only, oral hypoglycemic agents, insulin). They also tested to see if the relationship between parity and timing of lactogenesis was modified by other variables and found that the interaction between parity and gestational age was significant. Thus, in model 5, they included the variables in model 4 but also added an interaction term for parity and gestational age. These analyses included 883 SWIFT participants, all of whom had GDM. Participants were ethnically diverse, with 77% from minority groups. At 6 to 9 weeks postpartum, BMI
Downloaded from jhl.sagepub.com at HUNTER COLLEGE LIB on June 6, 2014
135
Chapman distribution for the group was 24% healthy weight, 35% overweight, and 41% obese. Twenty-nine percent of the births were by cesarean delivery. One-third of the participants reported delayed lactogenesis (> 72 hours pp). Key risk factors for delayed lactogenesis were identified in the series of logistic regression models. The most clinically relevant finding was the identification of insulin treatment for GDM as a risk factor (adjusted odds ratio [AOR] = 3.11; 95% confidence interval [CI], 1.37-7.05). Other significant predictors of delayed lactogenesis identified in the final model were maternal obesity (AOR = 1.56; 95% CI, 1.07-2.29), increased maternal age (AOR = 1.05; 95% CI, 1.01-1.08), and average LATCH score ≤ 7.5 in the first 24 hours of life (AOR = 1.65; 95% CI, 1.20-2.26). In addition, there was a significant interaction between gestational age and parity, such that increased gestational age was associated with a decreased risk of delayed lactogenesis, but only among multiparous women (AOR = 0.79; 95% CI, 0.67-0.94). This study has identified novel predictors of delayed lactogenesis among a diverse sample of women with a GDMaffected pregnancy. Some unique contributions of this study include the identification of GDM severity (based on the requirement for insulin therapy), lower LATCH scores on the first day of life, and increased maternal age as risk factors for
delayed lactogenesis among a diverse sample of women with GDM. The identification of insulin treatment as an independent risk factor for delayed lactogenesis has important clinical implications and suggests that GDM patients requiring insulin should be given high priority for lactation consultant services. Regarding maternal age, the authors found that a 5-year increase in maternal age was associated with a relatively large (26%) increase in the risk of delayed lactogenesis. Some of the strengths of this study include the large sample size of women with GDM, the ethnically diverse sample, and the standardized procedures for electronic medical record documentation, GDM screening, and treatment within the Kaiser Permanente health care system. As the authors noted, 1 potential limitation of the study is that the timing of lactogenesis stage II was reported at 6 to 9 weeks postpartum, introducing the possibility of recall bias. Given that maternal recall of the timing of lactogenesis has been validated at approximately 6 months pp, the potential for recall bias seems small. This study provides key data to support evidence-based practice in the identification of GDM women at high risk for delayed lactogenesis. Further research is clearly needed to understand the mechanisms behind these risk factors.
Downloaded from jhl.sagepub.com at HUNTER COLLEGE LIB on June 6, 2014
