Expert Commentary

EXPERT COMMENTARY

 A 2013 report from the Women’s Health Initiative (WHI), the large National Institutes of Health–funded placebo-controlledrandomized trial of postmenopausal hormone therapy (HT) with oral estrogen (for women with hysterectomy) or estrogen-progestin (for women with an intact uterus), with 13 years of cumulative follow-up, documented the safety of systemic HT when initiated by women younger than 60 years of age or within 10 years of menopause onset.¹ Now, with 18 years of cumulative follow-up data available (intervention and extended postintervention phases), the WHI investigators present all-cause and cause-specific mortality outcomes from the 2 HT trials.

Related article:
2017 Update on menopause

Details of the study

A total of 27,347 WHI participants (baseline mean age, 63.4 years; 80.6% white) used oral estrogen-progestin therapy (EPT) or placebo for a median of 5.6 years (n = 16,608) or estrogen-only therapy (ET) or placebo for a median of 7.2 years (n = 10,739). Each hazard ratio (HR) reported below refers to 18-year cumulative follow-up.

All-cause mortality. In the overall pooled cohort (EPT and ET groups), all-cause mortality was similar, with a rate of 27.1% in the HT group and 27.6% in the placebo group (HR, 0.99; 95% confidence interval [CI], 0.94–1.03). The mortality end points included deaths from all causes; cardiovascular disease (coronary heart disease, stroke, and other cardiovascular diseases); cancer (breast, colorectal, and other cancers); and other (Alzheimer disease, other dementia, chronic obstructive pulmonary disease, injuries and accidents, and other).

Stratifying by baseline participant age (comparing women aged 50–59 years with those aged 70–79 years), the HR for all-cause mortality in the pooled cohort during the intervention phase was 0.61 (95% CI, 0.43–0.87), and during the cumulative 18-year follow-up, the HR was 0.87 (95% CI, 0.76–1.00).

Cause-specific mortality. Neither cardiovascular disease mortality nor total cancer mortality was significantly impacted by HT use. In the pooled cohort, cardiovascular disease mortality was 8.9% in the HT group and 9.0% in the placebo group (HR, 1.00; 95% CI, 0.92–1.08), with no differences between the EPT and the ET trials. Cancer mortality rates in the pooled cohort also were similar, with 8.2% in the HT group and 8.0% in the placebo group (HR, 1.03; 95% CI, 0.95–1.12).

With respect to breast cancer mortality, the impact of HT diverged for EPT and ET. For the EPT group, the HR for breast cancer mortality was 1.44 (95% CI, 0.97–2.15; P = .07), while for the ET group the HR was 0.55 (95% CI, 0.33–0.92; P = .02).

Related articles:
Does the discontinuation of menopausal hormone therapy affect a woman’s cardiovascular risk?

Study strengths and weaknesses

The WHI represents the largest randomized placebo-controlled trials of HT. The current WHI trials report provides new, cumulative 18-year follow-up data on all-cause and cause-specific mortality in women treated with HT or placebo.

The authors noted, however, that the use of only one HT dose, formulation, and route of administration in each trial may limit the generalizability of the study results to other HT preparations. For example, the WHI did not examine the transdermal route of estrogen administration. Likewise, the WHI did not examine use of progestational agents other than medroxyprogesterone acetate. In addition, while almost all cohort deaths were captured through the National Death Index for the data analyses, specificity of cause of death may vary across outcomes. Further, since multiple outcomes and subgroups were examined, clinicians should interpret cause-specific mortality rates with caution.

Share your thoughts! Send your Letter to the Editor to rbarbieri@frontlinemedcom.com. Please include your name and the city and state in which you practice.

EXPERT COMMENTARY

 A 2013 report from the Women’s Health Initiative (WHI), the large National Institutes of Health–funded placebo-controlledrandomized trial of postmenopausal hormone therapy (HT) with oral estrogen (for women with hysterectomy) or estrogen-progestin (for women with an intact uterus), with 13 years of cumulative follow-up, documented the safety of systemic HT when initiated by women younger than 60 years of age or within 10 years of menopause onset.¹ Now, with 18 years of cumulative follow-up data available (intervention and extended postintervention phases), the WHI investigators present all-cause and cause-specific mortality outcomes from the 2 HT trials.

Related article:
2017 Update on menopause

Details of the study

A total of 27,347 WHI participants (baseline mean age, 63.4 years; 80.6% white) used oral estrogen-progestin therapy (EPT) or placebo for a median of 5.6 years (n = 16,608) or estrogen-only therapy (ET) or placebo for a median of 7.2 years (n = 10,739). Each hazard ratio (HR) reported below refers to 18-year cumulative follow-up.

All-cause mortality. In the overall pooled cohort (EPT and ET groups), all-cause mortality was similar, with a rate of 27.1% in the HT group and 27.6% in the placebo group (HR, 0.99; 95% confidence interval [CI], 0.94–1.03). The mortality end points included deaths from all causes; cardiovascular disease (coronary heart disease, stroke, and other cardiovascular diseases); cancer (breast, colorectal, and other cancers); and other (Alzheimer disease, other dementia, chronic obstructive pulmonary disease, injuries and accidents, and other).

Stratifying by baseline participant age (comparing women aged 50–59 years with those aged 70–79 years), the HR for all-cause mortality in the pooled cohort during the intervention phase was 0.61 (95% CI, 0.43–0.87), and during the cumulative 18-year follow-up, the HR was 0.87 (95% CI, 0.76–1.00).

Cause-specific mortality. Neither cardiovascular disease mortality nor total cancer mortality was significantly impacted by HT use. In the pooled cohort, cardiovascular disease mortality was 8.9% in the HT group and 9.0% in the placebo group (HR, 1.00; 95% CI, 0.92–1.08), with no differences between the EPT and the ET trials. Cancer mortality rates in the pooled cohort also were similar, with 8.2% in the HT group and 8.0% in the placebo group (HR, 1.03; 95% CI, 0.95–1.12).

With respect to breast cancer mortality, the impact of HT diverged for EPT and ET. For the EPT group, the HR for breast cancer mortality was 1.44 (95% CI, 0.97–2.15; P = .07), while for the ET group the HR was 0.55 (95% CI, 0.33–0.92; P = .02).

Related articles:
Does the discontinuation of menopausal hormone therapy affect a woman’s cardiovascular risk?

Study strengths and weaknesses

The WHI represents the largest randomized placebo-controlled trials of HT. The current WHI trials report provides new, cumulative 18-year follow-up data on all-cause and cause-specific mortality in women treated with HT or placebo.

The authors noted, however, that the use of only one HT dose, formulation, and route of administration in each trial may limit the generalizability of the study results to other HT preparations. For example, the WHI did not examine the transdermal route of estrogen administration. Likewise, the WHI did not examine use of progestational agents other than medroxyprogesterone acetate. In addition, while almost all cohort deaths were captured through the National Death Index for the data analyses, specificity of cause of death may vary across outcomes. Further, since multiple outcomes and subgroups were examined, clinicians should interpret cause-specific mortality rates with caution.

Share your thoughts! Send your Letter to the Editor to rbarbieri@frontlinemedcom.com. Please include your name and the city and state in which you practice.

EXPERT COMMENTARY

 A 2013 report from the Women’s Health Initiative (WHI), the large National Institutes of Health–funded placebo-controlledrandomized trial of postmenopausal hormone therapy (HT) with oral estrogen (for women with hysterectomy) or estrogen-progestin (for women with an intact uterus), with 13 years of cumulative follow-up, documented the safety of systemic HT when initiated by women younger than 60 years of age or within 10 years of menopause onset.¹ Now, with 18 years of cumulative follow-up data available (intervention and extended postintervention phases), the WHI investigators present all-cause and cause-specific mortality outcomes from the 2 HT trials.

Related article:
2017 Update on menopause

Details of the study

A total of 27,347 WHI participants (baseline mean age, 63.4 years; 80.6% white) used oral estrogen-progestin therapy (EPT) or placebo for a median of 5.6 years (n = 16,608) or estrogen-only therapy (ET) or placebo for a median of 7.2 years (n = 10,739). Each hazard ratio (HR) reported below refers to 18-year cumulative follow-up.

All-cause mortality. In the overall pooled cohort (EPT and ET groups), all-cause mortality was similar, with a rate of 27.1% in the HT group and 27.6% in the placebo group (HR, 0.99; 95% confidence interval [CI], 0.94–1.03). The mortality end points included deaths from all causes; cardiovascular disease (coronary heart disease, stroke, and other cardiovascular diseases); cancer (breast, colorectal, and other cancers); and other (Alzheimer disease, other dementia, chronic obstructive pulmonary disease, injuries and accidents, and other).

Stratifying by baseline participant age (comparing women aged 50–59 years with those aged 70–79 years), the HR for all-cause mortality in the pooled cohort during the intervention phase was 0.61 (95% CI, 0.43–0.87), and during the cumulative 18-year follow-up, the HR was 0.87 (95% CI, 0.76–1.00).

Cause-specific mortality. Neither cardiovascular disease mortality nor total cancer mortality was significantly impacted by HT use. In the pooled cohort, cardiovascular disease mortality was 8.9% in the HT group and 9.0% in the placebo group (HR, 1.00; 95% CI, 0.92–1.08), with no differences between the EPT and the ET trials. Cancer mortality rates in the pooled cohort also were similar, with 8.2% in the HT group and 8.0% in the placebo group (HR, 1.03; 95% CI, 0.95–1.12).

With respect to breast cancer mortality, the impact of HT diverged for EPT and ET. For the EPT group, the HR for breast cancer mortality was 1.44 (95% CI, 0.97–2.15; P = .07), while for the ET group the HR was 0.55 (95% CI, 0.33–0.92; P = .02).

Related articles:
Does the discontinuation of menopausal hormone therapy affect a woman’s cardiovascular risk?

Study strengths and weaknesses

The WHI represents the largest randomized placebo-controlled trials of HT. The current WHI trials report provides new, cumulative 18-year follow-up data on all-cause and cause-specific mortality in women treated with HT or placebo.

The authors noted, however, that the use of only one HT dose, formulation, and route of administration in each trial may limit the generalizability of the study results to other HT preparations. For example, the WHI did not examine the transdermal route of estrogen administration. Likewise, the WHI did not examine use of progestational agents other than medroxyprogesterone acetate. In addition, while almost all cohort deaths were captured through the National Death Index for the data analyses, specificity of cause of death may vary across outcomes. Further, since multiple outcomes and subgroups were examined, clinicians should interpret cause-specific mortality rates with caution.

Share your thoughts! Send your Letter to the Editor to rbarbieri@frontlinemedcom.com. Please include your name and the city and state in which you practice.

EXPERT COMMENTARY

Preeclampsia is a disorder of impaired placentation. ELABELA (ELA) encodes an endogenous ligand for the apelin receptor and is detected in preimplantation human blastocysts and in 2 organs in adults: the placenta and kidney. Recently, an international team of researchers described their study findings on ELA and its role in placental vascular development and preeclampsia in mice.

Details of the study

To delineate the contribution of ELA to mammalian development, Ho and colleagues generated Ela knockout mice. The investigators showed that during development, the ELA protein is first detected in the early placenta and becomes abundant later in placenta formation. They also demonstrated that ELA is a pregnancy hormone that circulates in the blood of pregnant, but not nonpregnant, mice.

Placental structure. The Ela knockout mice had placentas that demonstrated thin labyrinths, with poor vascularization, increased apoptosis, and reduced proliferation. Further, RNA analysis of ELA-lacking placentas revealed a gene expression profile indicative of hypoxia, including the upregulation of certain genes involved in blood vessel building. Placental vessels showed overall stunted architecture characterized by little or no extension and branching of angiogenic sprouts and impaired formation of the adequate labyrinth network required for proper perfusion in the placenta.

Given these gene expression findings and the fact that placental and vascular abnormalities have long been suspected to underlie preeclampsia, the investigators sought to determine if ELA-lacking mice exhibit preeclampsia. Evidence indicated they do.

Indicators of preeclampsia. Pregnant ELA-lacking mice had significantly higher levels of proteinuria and significantly higher blood pressure than either pregnant wild-type mice or nonpregnant ELA-lacking mice. Further, at the end of pregnancy, histology and transmission electron microscopy of kidney glomerular sections from ELA-lacking pregnant mice revealed signs of endotheliosis, a unique renal pathology that is also observed in women with preeclampsia. Pups of ELA-lacking mothers tended to weigh less than those of wild-type mothers, a situation that may be similar to the fetal intrauterine growth restriction commonly seen in women with preeclampsia.

Angiogenic factors. The authors then looked at levels of angiogenic proteins implicated in the pathogenesis of preeclampsia to determine if ELA is upstream. They found that ELA-lacking mice placentas had increased levels of sFlt1, Vegfa, and Plgf mRNA; these transcriptional changes, however, did not translate into significantly elevated plasma levels of the respective proteins. Thus, these findings indicate that ELA acts independently of, and possibly earlier than, angiogenic factors in the pathogenesis of preeclampsia.

Experimental treatment. The authors further showed that infusing recombinant ELA protein could alleviate symptoms of preeclampsia in mice. Injection of ELA protein in ELA-lacking mice led to reduction of blood pressure, reversal of glomerular endotheliosis, and rescue of fetal growth restriction.

Study strengths and weaknesses

This animal study contributes compelling molecular evidence of ELA’s role in mammalian placental development and angiogenesis, revealing that ELA deficiency leads to preeclampsia and placental abnormalities in pregnant mice. How ELA acts in humans and human pregnancy, however, has yet to be explored.

Share your thoughts! Send your Letter to the Editor to rbarbieri@frontlinemedcom.com. Please include your name and the city and state in which you practice.

EXPERT COMMENTARY

Preeclampsia is a disorder of impaired placentation. ELABELA (ELA) encodes an endogenous ligand for the apelin receptor and is detected in preimplantation human blastocysts and in 2 organs in adults: the placenta and kidney. Recently, an international team of researchers described their study findings on ELA and its role in placental vascular development and preeclampsia in mice.

Details of the study

To delineate the contribution of ELA to mammalian development, Ho and colleagues generated Ela knockout mice. The investigators showed that during development, the ELA protein is first detected in the early placenta and becomes abundant later in placenta formation. They also demonstrated that ELA is a pregnancy hormone that circulates in the blood of pregnant, but not nonpregnant, mice.

Placental structure. The Ela knockout mice had placentas that demonstrated thin labyrinths, with poor vascularization, increased apoptosis, and reduced proliferation. Further, RNA analysis of ELA-lacking placentas revealed a gene expression profile indicative of hypoxia, including the upregulation of certain genes involved in blood vessel building. Placental vessels showed overall stunted architecture characterized by little or no extension and branching of angiogenic sprouts and impaired formation of the adequate labyrinth network required for proper perfusion in the placenta.

Given these gene expression findings and the fact that placental and vascular abnormalities have long been suspected to underlie preeclampsia, the investigators sought to determine if ELA-lacking mice exhibit preeclampsia. Evidence indicated they do.

Indicators of preeclampsia. Pregnant ELA-lacking mice had significantly higher levels of proteinuria and significantly higher blood pressure than either pregnant wild-type mice or nonpregnant ELA-lacking mice. Further, at the end of pregnancy, histology and transmission electron microscopy of kidney glomerular sections from ELA-lacking pregnant mice revealed signs of endotheliosis, a unique renal pathology that is also observed in women with preeclampsia. Pups of ELA-lacking mothers tended to weigh less than those of wild-type mothers, a situation that may be similar to the fetal intrauterine growth restriction commonly seen in women with preeclampsia.

Angiogenic factors. The authors then looked at levels of angiogenic proteins implicated in the pathogenesis of preeclampsia to determine if ELA is upstream. They found that ELA-lacking mice placentas had increased levels of sFlt1, Vegfa, and Plgf mRNA; these transcriptional changes, however, did not translate into significantly elevated plasma levels of the respective proteins. Thus, these findings indicate that ELA acts independently of, and possibly earlier than, angiogenic factors in the pathogenesis of preeclampsia.

Experimental treatment. The authors further showed that infusing recombinant ELA protein could alleviate symptoms of preeclampsia in mice. Injection of ELA protein in ELA-lacking mice led to reduction of blood pressure, reversal of glomerular endotheliosis, and rescue of fetal growth restriction.

Study strengths and weaknesses

This animal study contributes compelling molecular evidence of ELA’s role in mammalian placental development and angiogenesis, revealing that ELA deficiency leads to preeclampsia and placental abnormalities in pregnant mice. How ELA acts in humans and human pregnancy, however, has yet to be explored.

Share your thoughts! Send your Letter to the Editor to rbarbieri@frontlinemedcom.com. Please include your name and the city and state in which you practice.

EXPERT COMMENTARY

Preeclampsia is a disorder of impaired placentation. ELABELA (ELA) encodes an endogenous ligand for the apelin receptor and is detected in preimplantation human blastocysts and in 2 organs in adults: the placenta and kidney. Recently, an international team of researchers described their study findings on ELA and its role in placental vascular development and preeclampsia in mice.

Details of the study

To delineate the contribution of ELA to mammalian development, Ho and colleagues generated Ela knockout mice. The investigators showed that during development, the ELA protein is first detected in the early placenta and becomes abundant later in placenta formation. They also demonstrated that ELA is a pregnancy hormone that circulates in the blood of pregnant, but not nonpregnant, mice.

Placental structure. The Ela knockout mice had placentas that demonstrated thin labyrinths, with poor vascularization, increased apoptosis, and reduced proliferation. Further, RNA analysis of ELA-lacking placentas revealed a gene expression profile indicative of hypoxia, including the upregulation of certain genes involved in blood vessel building. Placental vessels showed overall stunted architecture characterized by little or no extension and branching of angiogenic sprouts and impaired formation of the adequate labyrinth network required for proper perfusion in the placenta.

Given these gene expression findings and the fact that placental and vascular abnormalities have long been suspected to underlie preeclampsia, the investigators sought to determine if ELA-lacking mice exhibit preeclampsia. Evidence indicated they do.

Indicators of preeclampsia. Pregnant ELA-lacking mice had significantly higher levels of proteinuria and significantly higher blood pressure than either pregnant wild-type mice or nonpregnant ELA-lacking mice. Further, at the end of pregnancy, histology and transmission electron microscopy of kidney glomerular sections from ELA-lacking pregnant mice revealed signs of endotheliosis, a unique renal pathology that is also observed in women with preeclampsia. Pups of ELA-lacking mothers tended to weigh less than those of wild-type mothers, a situation that may be similar to the fetal intrauterine growth restriction commonly seen in women with preeclampsia.

Angiogenic factors. The authors then looked at levels of angiogenic proteins implicated in the pathogenesis of preeclampsia to determine if ELA is upstream. They found that ELA-lacking mice placentas had increased levels of sFlt1, Vegfa, and Plgf mRNA; these transcriptional changes, however, did not translate into significantly elevated plasma levels of the respective proteins. Thus, these findings indicate that ELA acts independently of, and possibly earlier than, angiogenic factors in the pathogenesis of preeclampsia.

Experimental treatment. The authors further showed that infusing recombinant ELA protein could alleviate symptoms of preeclampsia in mice. Injection of ELA protein in ELA-lacking mice led to reduction of blood pressure, reversal of glomerular endotheliosis, and rescue of fetal growth restriction.

Study strengths and weaknesses

This animal study contributes compelling molecular evidence of ELA’s role in mammalian placental development and angiogenesis, revealing that ELA deficiency leads to preeclampsia and placental abnormalities in pregnant mice. How ELA acts in humans and human pregnancy, however, has yet to be explored.

Share your thoughts! Send your Letter to the Editor to rbarbieri@frontlinemedcom.com. Please include your name and the city and state in which you practice.

Visit the NAMS annual meetings website

Share your thoughts! Send your Letter to the Editor to rbarbieri@frontlinemedcom.com. Please include your name and the city and state in which you practice.

Visit the NAMS annual meetings website

Share your thoughts! Send your Letter to the Editor to rbarbieri@frontlinemedcom.com. Please include your name and the city and state in which you practice.

Visit the NAMS annual meetings website

Share your thoughts! Send your Letter to the Editor to rbarbieri@frontlinemedcom.com. Please include your name and the city and state in which you practice.

Click here to download

Click here to download

Click here to download

EXPERT COMMENTARY

Influenza can be a serious, even life-threatening infection, especially in pregnant women and their newborn infants.¹ For that reason, the Centers for Disease Control and Prevention (CDC) and the American College of Obstetricians and Gynecologists (ACOG) strongly recommend that all pregnant women receive the inactivated influenza vaccine at the start of each flu season, regardless of trimester of exposure.

The most widely-used vaccine in the United States is the inactivated quadrivalent vaccine, which is intended for intramuscular administration in a single dose. The 2017-2018 version of this vaccine includes 2 influenza A antigens and 2 influenza B antigens. The first of the A antigens differs from last year's vaccine. The other 3 antigens are the same as in the 2016-2017 vaccine:

• A/Michigan/45/2015 (H1N1) pdm09-like virus
• A/Hong Kong/4801/2014 (H3N2)-like virus  
• B/Brisbane/60/2008-like virus
• B/Phuket/3073/2013-like virus (B/Yamagota)

Several recent reports in large, diverse populations^2-5 have demonstrated that the vaccine does not increase the risk of spontaneous abortion, stillbirth, preterm delivery, or congenital anomalies. Therefore, a recent report by Donahue and colleagues⁶ is surprising and is certainly worthy of our attention. 

Related article:
Does influenza immunization during pregnancy confer flu protection to newborns?

Details of the study

Donahue and colleagues, experienced investigators, were tasked by the CDC with using information from the Vaccine Safety Datalink to specifically assess the safety of the influenza vaccine when administered early in pregnancy. They evaluated 485 women who had experienced a spontaneous abortion in 1 of 2 time periods: September 1, 2010 to April 28, 2011 and September 1, 2011 to April 28, 2012. These women were matched by last menstrual period with controls who subsequently had a liveborn infant or stillbirth at greater than 20 weeks of gestation. The exposure of interest was receipt of the monovalent H1N1 vaccine (H1N1pdm09), the inactivated trivalent vaccine (A/California/7/2009 H1N1 pdm09-like, A/Perth/16/2009 H3N2-like, and B/Brisbane/60/2008-like), or both in the 28 days immediately preceding the spontaneous abortion. The investigators also considered 2 other windows of exposure: 29 to 56 days and greater than 56 days. In addition, they controlled for the following potential confounding variables: maternal age, smoking history, presence of type 1 or 2 diabetes, prepregnancy BMI, and previous health care utilization. 

Cases were significantly older than controls. They also were more likely to be African-American, to have had a history of greater than or equal to 2 spontaneous abortions, and to have smoked during pregnancy. The median gestational age at the time of spontaneous abortion was 7 weeks. Overall, the adjusted odds ratio (aOR) of spontaneous abortion within the 1- to 28-day window was 2.0 (95% confidence interval [CI], 1.1-3.6). There was not even a weak association in the other 2 windows of exposure. However, in women who received the pH1N1 vaccine in the previous flu season, the aOR was 7.7 (95% CI, 2.2-27.3). When women who had experienced 2 or more spontaneous abortions were excluded, the aOR remained significantly elevated at 6.5 (95% CI, 1.7-24.3). The aOR was 1.3 (95% CI, 0.7-2.7) in women who were not vaccinated with the pH1N1 vaccine in the previous flu season.

Donahue and colleagues⁶ offered several possible explanations for their observations. They noted that the pH1N1 vaccine seemed to cause at least mild increases in pro-inflammatory cytokines, particularly in pregnant compared with nonpregnant women. In addition, infection with the pH1N1 virus or vaccination with the pH1N1 vaccine induces an increase in T helper type-1 cells, which exert a pro-inflammatory effect. Excessive inflammation, in turn, may cause spontaneous abortion.

Related article:
5 ways to reduce infection risk during pregnancy

Study limitations

This study has several important limitations. First, the vaccine used in the investigation is not identical to the one used most commonly today. Second, although the number of women with spontaneous abortions is relatively large, the number who received the pH1N1-containing vaccine in consecutive years was relatively small. Third, this case-control study was able to estimate an odds ratio for the adverse outcome, but it could not prove causation, nor could it provide a precise estimate of absolute risk for a spontaneous miscarriage following the influenza vaccine. Finally, the authors, understandably,were unable to control for all the myriad factors that may increase the risk for spontaneous abortion.

Share your thoughts! Send your Letter to the Editor to rbarbieri@frontlinemedcom.com. Please include your name and the city and state in which you practice.

EXPERT COMMENTARY

Influenza can be a serious, even life-threatening infection, especially in pregnant women and their newborn infants.¹ For that reason, the Centers for Disease Control and Prevention (CDC) and the American College of Obstetricians and Gynecologists (ACOG) strongly recommend that all pregnant women receive the inactivated influenza vaccine at the start of each flu season, regardless of trimester of exposure.

The most widely-used vaccine in the United States is the inactivated quadrivalent vaccine, which is intended for intramuscular administration in a single dose. The 2017-2018 version of this vaccine includes 2 influenza A antigens and 2 influenza B antigens. The first of the A antigens differs from last year's vaccine. The other 3 antigens are the same as in the 2016-2017 vaccine:

• A/Michigan/45/2015 (H1N1) pdm09-like virus
• A/Hong Kong/4801/2014 (H3N2)-like virus  
• B/Brisbane/60/2008-like virus
• B/Phuket/3073/2013-like virus (B/Yamagota)

Several recent reports in large, diverse populations^2-5 have demonstrated that the vaccine does not increase the risk of spontaneous abortion, stillbirth, preterm delivery, or congenital anomalies. Therefore, a recent report by Donahue and colleagues⁶ is surprising and is certainly worthy of our attention. 

Related article:
Does influenza immunization during pregnancy confer flu protection to newborns?

Details of the study

Donahue and colleagues, experienced investigators, were tasked by the CDC with using information from the Vaccine Safety Datalink to specifically assess the safety of the influenza vaccine when administered early in pregnancy. They evaluated 485 women who had experienced a spontaneous abortion in 1 of 2 time periods: September 1, 2010 to April 28, 2011 and September 1, 2011 to April 28, 2012. These women were matched by last menstrual period with controls who subsequently had a liveborn infant or stillbirth at greater than 20 weeks of gestation. The exposure of interest was receipt of the monovalent H1N1 vaccine (H1N1pdm09), the inactivated trivalent vaccine (A/California/7/2009 H1N1 pdm09-like, A/Perth/16/2009 H3N2-like, and B/Brisbane/60/2008-like), or both in the 28 days immediately preceding the spontaneous abortion. The investigators also considered 2 other windows of exposure: 29 to 56 days and greater than 56 days. In addition, they controlled for the following potential confounding variables: maternal age, smoking history, presence of type 1 or 2 diabetes, prepregnancy BMI, and previous health care utilization. 

Cases were significantly older than controls. They also were more likely to be African-American, to have had a history of greater than or equal to 2 spontaneous abortions, and to have smoked during pregnancy. The median gestational age at the time of spontaneous abortion was 7 weeks. Overall, the adjusted odds ratio (aOR) of spontaneous abortion within the 1- to 28-day window was 2.0 (95% confidence interval [CI], 1.1-3.6). There was not even a weak association in the other 2 windows of exposure. However, in women who received the pH1N1 vaccine in the previous flu season, the aOR was 7.7 (95% CI, 2.2-27.3). When women who had experienced 2 or more spontaneous abortions were excluded, the aOR remained significantly elevated at 6.5 (95% CI, 1.7-24.3). The aOR was 1.3 (95% CI, 0.7-2.7) in women who were not vaccinated with the pH1N1 vaccine in the previous flu season.

Donahue and colleagues⁶ offered several possible explanations for their observations. They noted that the pH1N1 vaccine seemed to cause at least mild increases in pro-inflammatory cytokines, particularly in pregnant compared with nonpregnant women. In addition, infection with the pH1N1 virus or vaccination with the pH1N1 vaccine induces an increase in T helper type-1 cells, which exert a pro-inflammatory effect. Excessive inflammation, in turn, may cause spontaneous abortion.

Related article:
5 ways to reduce infection risk during pregnancy

Study limitations

This study has several important limitations. First, the vaccine used in the investigation is not identical to the one used most commonly today. Second, although the number of women with spontaneous abortions is relatively large, the number who received the pH1N1-containing vaccine in consecutive years was relatively small. Third, this case-control study was able to estimate an odds ratio for the adverse outcome, but it could not prove causation, nor could it provide a precise estimate of absolute risk for a spontaneous miscarriage following the influenza vaccine. Finally, the authors, understandably,were unable to control for all the myriad factors that may increase the risk for spontaneous abortion.

Share your thoughts! Send your Letter to the Editor to rbarbieri@frontlinemedcom.com. Please include your name and the city and state in which you practice.

EXPERT COMMENTARY

Influenza can be a serious, even life-threatening infection, especially in pregnant women and their newborn infants.¹ For that reason, the Centers for Disease Control and Prevention (CDC) and the American College of Obstetricians and Gynecologists (ACOG) strongly recommend that all pregnant women receive the inactivated influenza vaccine at the start of each flu season, regardless of trimester of exposure.

The most widely-used vaccine in the United States is the inactivated quadrivalent vaccine, which is intended for intramuscular administration in a single dose. The 2017-2018 version of this vaccine includes 2 influenza A antigens and 2 influenza B antigens. The first of the A antigens differs from last year's vaccine. The other 3 antigens are the same as in the 2016-2017 vaccine:

• A/Michigan/45/2015 (H1N1) pdm09-like virus
• A/Hong Kong/4801/2014 (H3N2)-like virus  
• B/Brisbane/60/2008-like virus
• B/Phuket/3073/2013-like virus (B/Yamagota)

Several recent reports in large, diverse populations^2-5 have demonstrated that the vaccine does not increase the risk of spontaneous abortion, stillbirth, preterm delivery, or congenital anomalies. Therefore, a recent report by Donahue and colleagues⁶ is surprising and is certainly worthy of our attention. 

Related article:
Does influenza immunization during pregnancy confer flu protection to newborns?

Details of the study

Donahue and colleagues, experienced investigators, were tasked by the CDC with using information from the Vaccine Safety Datalink to specifically assess the safety of the influenza vaccine when administered early in pregnancy. They evaluated 485 women who had experienced a spontaneous abortion in 1 of 2 time periods: September 1, 2010 to April 28, 2011 and September 1, 2011 to April 28, 2012. These women were matched by last menstrual period with controls who subsequently had a liveborn infant or stillbirth at greater than 20 weeks of gestation. The exposure of interest was receipt of the monovalent H1N1 vaccine (H1N1pdm09), the inactivated trivalent vaccine (A/California/7/2009 H1N1 pdm09-like, A/Perth/16/2009 H3N2-like, and B/Brisbane/60/2008-like), or both in the 28 days immediately preceding the spontaneous abortion. The investigators also considered 2 other windows of exposure: 29 to 56 days and greater than 56 days. In addition, they controlled for the following potential confounding variables: maternal age, smoking history, presence of type 1 or 2 diabetes, prepregnancy BMI, and previous health care utilization. 

Cases were significantly older than controls. They also were more likely to be African-American, to have had a history of greater than or equal to 2 spontaneous abortions, and to have smoked during pregnancy. The median gestational age at the time of spontaneous abortion was 7 weeks. Overall, the adjusted odds ratio (aOR) of spontaneous abortion within the 1- to 28-day window was 2.0 (95% confidence interval [CI], 1.1-3.6). There was not even a weak association in the other 2 windows of exposure. However, in women who received the pH1N1 vaccine in the previous flu season, the aOR was 7.7 (95% CI, 2.2-27.3). When women who had experienced 2 or more spontaneous abortions were excluded, the aOR remained significantly elevated at 6.5 (95% CI, 1.7-24.3). The aOR was 1.3 (95% CI, 0.7-2.7) in women who were not vaccinated with the pH1N1 vaccine in the previous flu season.

Donahue and colleagues⁶ offered several possible explanations for their observations. They noted that the pH1N1 vaccine seemed to cause at least mild increases in pro-inflammatory cytokines, particularly in pregnant compared with nonpregnant women. In addition, infection with the pH1N1 virus or vaccination with the pH1N1 vaccine induces an increase in T helper type-1 cells, which exert a pro-inflammatory effect. Excessive inflammation, in turn, may cause spontaneous abortion.

Related article:
5 ways to reduce infection risk during pregnancy

Study limitations

This study has several important limitations. First, the vaccine used in the investigation is not identical to the one used most commonly today. Second, although the number of women with spontaneous abortions is relatively large, the number who received the pH1N1-containing vaccine in consecutive years was relatively small. Third, this case-control study was able to estimate an odds ratio for the adverse outcome, but it could not prove causation, nor could it provide a precise estimate of absolute risk for a spontaneous miscarriage following the influenza vaccine. Finally, the authors, understandably,were unable to control for all the myriad factors that may increase the risk for spontaneous abortion.

Share your thoughts! Send your Letter to the Editor to rbarbieri@frontlinemedcom.com. Please include your name and the city and state in which you practice.

To date, efforts to translate exciting laboratory findings into clinical trials for Parkinson’s disease have not met with much success. However, the latest exenatide study results offer another chance for improving this situation. This randomized, placebo-controlled trial also highlights how a medication already in human use might be repurposed for a novel application.

Whether this study actually proved its concept will require confirmation by further clinical investigation. The biggest challenge presented by this study has to do with studying patients with Parkinson’s disease who already are receiving symptomatic therapy with dopaminergic drugs. The study plan was to eliminate this effect by an overnight washout of Parkinson’s disease drugs. But waiting for a day or two after stopping medication, even for a short-acting drug like levodopa, does not necessarily abolish all of its symptomatic effects. If exenatide acted by enhancing the temporary relief of parkinsonism offered by medications rather than by protecting against further neurodegeneration, study ratings would not be able to discern this difference. Similarly, if exenatide exerts a trophic effect on striatal dopamine transporters, the observed reduction of decline in dopamine transporter (DAT) scan readings would not necessarily reflect sparing of further dopaminergic neuron loss.

Another potentially confounding factor was that during the course of the trial, the exenatide group increased its concomitant dopaminergic therapy more than the placebo-treated controls did. In a study of only 62 subjects who were already advanced in the course of Parkinson’s disease and experiencing motor fluctuations, any imbalance between treatment and placebo groups might impart uncertainties for which it may be difficult to correct.

Despite all the reasonable objections that might detract from a definitive interpretation of this study, its results make a credible argument for a neuroprotection outcome. The happenstance of two seemingly independent indicators of disease modification—in this case, the washout ratings of parkinsonian features and the DAT scan results—provides grounds for optimism. In the quest for halting the advance of Parkinson’s disease, the perfect study has yet to emerge. The exenatide investigators’ careful attention to detail and collection of other study information and biomarker specimens will serve well the next researchers who explore the potential for glucagon-like peptide-1 treatments.

—Peter A. LeWitt, MD
Professor of Neurology
Wayne State University School of Medicine
Director, Parkinson's Disease and Movement Disorders Program
Henry Ford Hospital West Bloomfield
West Bloomfield, Michigan

To date, efforts to translate exciting laboratory findings into clinical trials for Parkinson’s disease have not met with much success. However, the latest exenatide study results offer another chance for improving this situation. This randomized, placebo-controlled trial also highlights how a medication already in human use might be repurposed for a novel application.

Whether this study actually proved its concept will require confirmation by further clinical investigation. The biggest challenge presented by this study has to do with studying patients with Parkinson’s disease who already are receiving symptomatic therapy with dopaminergic drugs. The study plan was to eliminate this effect by an overnight washout of Parkinson’s disease drugs. But waiting for a day or two after stopping medication, even for a short-acting drug like levodopa, does not necessarily abolish all of its symptomatic effects. If exenatide acted by enhancing the temporary relief of parkinsonism offered by medications rather than by protecting against further neurodegeneration, study ratings would not be able to discern this difference. Similarly, if exenatide exerts a trophic effect on striatal dopamine transporters, the observed reduction of decline in dopamine transporter (DAT) scan readings would not necessarily reflect sparing of further dopaminergic neuron loss.

Another potentially confounding factor was that during the course of the trial, the exenatide group increased its concomitant dopaminergic therapy more than the placebo-treated controls did. In a study of only 62 subjects who were already advanced in the course of Parkinson’s disease and experiencing motor fluctuations, any imbalance between treatment and placebo groups might impart uncertainties for which it may be difficult to correct.

Despite all the reasonable objections that might detract from a definitive interpretation of this study, its results make a credible argument for a neuroprotection outcome. The happenstance of two seemingly independent indicators of disease modification—in this case, the washout ratings of parkinsonian features and the DAT scan results—provides grounds for optimism. In the quest for halting the advance of Parkinson’s disease, the perfect study has yet to emerge. The exenatide investigators’ careful attention to detail and collection of other study information and biomarker specimens will serve well the next researchers who explore the potential for glucagon-like peptide-1 treatments.

—Peter A. LeWitt, MD
Professor of Neurology
Wayne State University School of Medicine
Director, Parkinson's Disease and Movement Disorders Program
Henry Ford Hospital West Bloomfield
West Bloomfield, Michigan

To date, efforts to translate exciting laboratory findings into clinical trials for Parkinson’s disease have not met with much success. However, the latest exenatide study results offer another chance for improving this situation. This randomized, placebo-controlled trial also highlights how a medication already in human use might be repurposed for a novel application.

Whether this study actually proved its concept will require confirmation by further clinical investigation. The biggest challenge presented by this study has to do with studying patients with Parkinson’s disease who already are receiving symptomatic therapy with dopaminergic drugs. The study plan was to eliminate this effect by an overnight washout of Parkinson’s disease drugs. But waiting for a day or two after stopping medication, even for a short-acting drug like levodopa, does not necessarily abolish all of its symptomatic effects. If exenatide acted by enhancing the temporary relief of parkinsonism offered by medications rather than by protecting against further neurodegeneration, study ratings would not be able to discern this difference. Similarly, if exenatide exerts a trophic effect on striatal dopamine transporters, the observed reduction of decline in dopamine transporter (DAT) scan readings would not necessarily reflect sparing of further dopaminergic neuron loss.

Another potentially confounding factor was that during the course of the trial, the exenatide group increased its concomitant dopaminergic therapy more than the placebo-treated controls did. In a study of only 62 subjects who were already advanced in the course of Parkinson’s disease and experiencing motor fluctuations, any imbalance between treatment and placebo groups might impart uncertainties for which it may be difficult to correct.

Despite all the reasonable objections that might detract from a definitive interpretation of this study, its results make a credible argument for a neuroprotection outcome. The happenstance of two seemingly independent indicators of disease modification—in this case, the washout ratings of parkinsonian features and the DAT scan results—provides grounds for optimism. In the quest for halting the advance of Parkinson’s disease, the perfect study has yet to emerge. The exenatide investigators’ careful attention to detail and collection of other study information and biomarker specimens will serve well the next researchers who explore the potential for glucagon-like peptide-1 treatments.

—Peter A. LeWitt, MD
Professor of Neurology
Wayne State University School of Medicine
Director, Parkinson's Disease and Movement Disorders Program
Henry Ford Hospital West Bloomfield
West Bloomfield, Michigan

Photo: Shutterstock

Many hospitals across the country have received designation as “Baby Friendly”; many other hospitals are in the process of seeking this designation. In order to be Baby Friendly, a hospital or birth center must prove they have implemented a set of 10 rules to encourage breastfeeding. As Baby Friendly USA puts it in their byline, it has become the gold standard of care.

Importantly, Baby Friendly fails to recognize that there is another equally crucial participant in any childbirth experience—the woman. Although childbirth is natural and usually healthy, it is not easy. Women commonly lose up to 1 L of blood during childbirth.¹ Labor can take 18 to 24 hours for a first-timer and about 12 to 18 hours for an encore performance, often disrupting at least1 entire night of sleep. The minimally invasive cesarean delivery continues to elude us, and women undergoing cesarean delivery must contend with a sizable incision and the additional pain and associated recovery.

Hospitals adopting the Baby Friendly rules must not allow formula, must prohibit pacifier use, and must go to great lengths to encourage rooming-in. Rooming-in means that the baby shares the same room as the new mother around-the-clock, which is reported to help the new mother distinguish sounds that indicate “feed me” from those that indicate a cool breeze. Rooming-in has been shown to be associated with a modest increase in breastfeeding²; however, women who are committed to breastfeeding likely room-in more often than women less committed to breastfeeding. Whether or not forcing the woman who is less committed to breastfeeding or the woman highly committed to breastfeeding who just wants a good night’s rest to room-in with her baby has a meaningful impact on breastfeeding remains unknown.

Are we violating ethics rules?

When hospitals adopt the Baby Friendly rules—policies that limit women’s choices for themselves and for their baby—we violate medical ethics principles regarding respect for autonomy, beneficence, and truthfulness. For instance, women are told that if they breastfeed their babies will be smarter, healthier, and have stronger emotional bonds. However, when research studies control for factors such as mothers’ education level or the amount of time spent talking to the baby, the effect of breastfeeding on intelligence “washes out.”³ Babies who are formula-fed but cuddled experience the same degree of bonding with their mothers as breast-fed babies.^4,5

Although breast is best, the reported benefits that underlie Baby Friendly are overblown and oversold. When we explain to a woman why her newborn cannot spend a few hours in the nursery or why we cannot allow a pacifier, we are denying her the right to parent and make choices for herself and her baby, not acting in the best interest of the woman. We are in fact misrepresenting the truth. We are also acting paternalistic, propagating the long tradition of telling women that we know better about their reproductive health and choices.

Related article:
Women’s Preventive Services Initiative Guidelines provide consensus for practicing ObGyns

Breastfeeding still not fully accepted outside the hospital

The Baby Friendly rules restrict autonomy and prod women to breastfeed for the few days that they remain in the hospital postpartum. However, these women go home to societal and institutional systems that are deeply unsupportive of breastfeeding. In addition to being the birthplace for 98% of babies born in the United States, the health care industry is the single largest employer of US women.^6,7 There are 5 academic hospitals in the Boston area. After contacting the human resources department at each, I found that only 1 has a policy for their breastfeeding employees.

Women should not be forced to choose between breastfeeding and working, between taking a longer maternity leave (often unpaid and professionally detrimental) and shelving the breast pump. What we invest in reveals our values. When we require women to room-in without respecting their choices or needs, and when workplaces fail to provide reasonable flexibility and private space for breast-pumping employees, our values as a society are revealed.

Women and men, hospital users and hospital employees, need to insist that the principles of autonomy, respect for persons, truthfulness, and justice guide breastfeeding policy both within our hospitals and within our workplaces. We need to respect women and the choices that they make for themselves and their families. We need to allow women to decide to recover from their delivery without their baby constantly in arms’ reach. We need to ensure that our counseling and our policies are rooted in sound science and not influenced by passionate but biased perspectives.

Share your thoughts! Send your Letter to the Editor to rbarbieri@frontlinemedcom.com. Please include your name and the city and state in which you practice.

Photo: Shutterstock

Many hospitals across the country have received designation as “Baby Friendly”; many other hospitals are in the process of seeking this designation. In order to be Baby Friendly, a hospital or birth center must prove they have implemented a set of 10 rules to encourage breastfeeding. As Baby Friendly USA puts it in their byline, it has become the gold standard of care.

Importantly, Baby Friendly fails to recognize that there is another equally crucial participant in any childbirth experience—the woman. Although childbirth is natural and usually healthy, it is not easy. Women commonly lose up to 1 L of blood during childbirth.¹ Labor can take 18 to 24 hours for a first-timer and about 12 to 18 hours for an encore performance, often disrupting at least1 entire night of sleep. The minimally invasive cesarean delivery continues to elude us, and women undergoing cesarean delivery must contend with a sizable incision and the additional pain and associated recovery.

Hospitals adopting the Baby Friendly rules must not allow formula, must prohibit pacifier use, and must go to great lengths to encourage rooming-in. Rooming-in means that the baby shares the same room as the new mother around-the-clock, which is reported to help the new mother distinguish sounds that indicate “feed me” from those that indicate a cool breeze. Rooming-in has been shown to be associated with a modest increase in breastfeeding²; however, women who are committed to breastfeeding likely room-in more often than women less committed to breastfeeding. Whether or not forcing the woman who is less committed to breastfeeding or the woman highly committed to breastfeeding who just wants a good night’s rest to room-in with her baby has a meaningful impact on breastfeeding remains unknown.

Are we violating ethics rules?

When hospitals adopt the Baby Friendly rules—policies that limit women’s choices for themselves and for their baby—we violate medical ethics principles regarding respect for autonomy, beneficence, and truthfulness. For instance, women are told that if they breastfeed their babies will be smarter, healthier, and have stronger emotional bonds. However, when research studies control for factors such as mothers’ education level or the amount of time spent talking to the baby, the effect of breastfeeding on intelligence “washes out.”³ Babies who are formula-fed but cuddled experience the same degree of bonding with their mothers as breast-fed babies.^4,5

Although breast is best, the reported benefits that underlie Baby Friendly are overblown and oversold. When we explain to a woman why her newborn cannot spend a few hours in the nursery or why we cannot allow a pacifier, we are denying her the right to parent and make choices for herself and her baby, not acting in the best interest of the woman. We are in fact misrepresenting the truth. We are also acting paternalistic, propagating the long tradition of telling women that we know better about their reproductive health and choices.

Related article:
Women’s Preventive Services Initiative Guidelines provide consensus for practicing ObGyns

Breastfeeding still not fully accepted outside the hospital

The Baby Friendly rules restrict autonomy and prod women to breastfeed for the few days that they remain in the hospital postpartum. However, these women go home to societal and institutional systems that are deeply unsupportive of breastfeeding. In addition to being the birthplace for 98% of babies born in the United States, the health care industry is the single largest employer of US women.^6,7 There are 5 academic hospitals in the Boston area. After contacting the human resources department at each, I found that only 1 has a policy for their breastfeeding employees.

Women should not be forced to choose between breastfeeding and working, between taking a longer maternity leave (often unpaid and professionally detrimental) and shelving the breast pump. What we invest in reveals our values. When we require women to room-in without respecting their choices or needs, and when workplaces fail to provide reasonable flexibility and private space for breast-pumping employees, our values as a society are revealed.

Women and men, hospital users and hospital employees, need to insist that the principles of autonomy, respect for persons, truthfulness, and justice guide breastfeeding policy both within our hospitals and within our workplaces. We need to respect women and the choices that they make for themselves and their families. We need to allow women to decide to recover from their delivery without their baby constantly in arms’ reach. We need to ensure that our counseling and our policies are rooted in sound science and not influenced by passionate but biased perspectives.

Share your thoughts! Send your Letter to the Editor to rbarbieri@frontlinemedcom.com. Please include your name and the city and state in which you practice.

Photo: Shutterstock

Many hospitals across the country have received designation as “Baby Friendly”; many other hospitals are in the process of seeking this designation. In order to be Baby Friendly, a hospital or birth center must prove they have implemented a set of 10 rules to encourage breastfeeding. As Baby Friendly USA puts it in their byline, it has become the gold standard of care.

Importantly, Baby Friendly fails to recognize that there is another equally crucial participant in any childbirth experience—the woman. Although childbirth is natural and usually healthy, it is not easy. Women commonly lose up to 1 L of blood during childbirth.¹ Labor can take 18 to 24 hours for a first-timer and about 12 to 18 hours for an encore performance, often disrupting at least1 entire night of sleep. The minimally invasive cesarean delivery continues to elude us, and women undergoing cesarean delivery must contend with a sizable incision and the additional pain and associated recovery.

Hospitals adopting the Baby Friendly rules must not allow formula, must prohibit pacifier use, and must go to great lengths to encourage rooming-in. Rooming-in means that the baby shares the same room as the new mother around-the-clock, which is reported to help the new mother distinguish sounds that indicate “feed me” from those that indicate a cool breeze. Rooming-in has been shown to be associated with a modest increase in breastfeeding²; however, women who are committed to breastfeeding likely room-in more often than women less committed to breastfeeding. Whether or not forcing the woman who is less committed to breastfeeding or the woman highly committed to breastfeeding who just wants a good night’s rest to room-in with her baby has a meaningful impact on breastfeeding remains unknown.

Are we violating ethics rules?

When hospitals adopt the Baby Friendly rules—policies that limit women’s choices for themselves and for their baby—we violate medical ethics principles regarding respect for autonomy, beneficence, and truthfulness. For instance, women are told that if they breastfeed their babies will be smarter, healthier, and have stronger emotional bonds. However, when research studies control for factors such as mothers’ education level or the amount of time spent talking to the baby, the effect of breastfeeding on intelligence “washes out.”³ Babies who are formula-fed but cuddled experience the same degree of bonding with their mothers as breast-fed babies.^4,5

Although breast is best, the reported benefits that underlie Baby Friendly are overblown and oversold. When we explain to a woman why her newborn cannot spend a few hours in the nursery or why we cannot allow a pacifier, we are denying her the right to parent and make choices for herself and her baby, not acting in the best interest of the woman. We are in fact misrepresenting the truth. We are also acting paternalistic, propagating the long tradition of telling women that we know better about their reproductive health and choices.

Related article:
Women’s Preventive Services Initiative Guidelines provide consensus for practicing ObGyns

Breastfeeding still not fully accepted outside the hospital

The Baby Friendly rules restrict autonomy and prod women to breastfeed for the few days that they remain in the hospital postpartum. However, these women go home to societal and institutional systems that are deeply unsupportive of breastfeeding. In addition to being the birthplace for 98% of babies born in the United States, the health care industry is the single largest employer of US women.^6,7 There are 5 academic hospitals in the Boston area. After contacting the human resources department at each, I found that only 1 has a policy for their breastfeeding employees.

Women should not be forced to choose between breastfeeding and working, between taking a longer maternity leave (often unpaid and professionally detrimental) and shelving the breast pump. What we invest in reveals our values. When we require women to room-in without respecting their choices or needs, and when workplaces fail to provide reasonable flexibility and private space for breast-pumping employees, our values as a society are revealed.

Women and men, hospital users and hospital employees, need to insist that the principles of autonomy, respect for persons, truthfulness, and justice guide breastfeeding policy both within our hospitals and within our workplaces. We need to respect women and the choices that they make for themselves and their families. We need to allow women to decide to recover from their delivery without their baby constantly in arms’ reach. We need to ensure that our counseling and our policies are rooted in sound science and not influenced by passionate but biased perspectives.

Share your thoughts! Send your Letter to the Editor to rbarbieri@frontlinemedcom.com. Please include your name and the city and state in which you practice.