<?xml version="1.0" encoding="utf-8"?>
<recommendedContent xmlns="http://api.mspoke.com">
    <recommendedItem id="20100101_19_430"
                     title="HRT Linked to Asthma Risk (CME/CE)"
                     score="0.01"
                     href="http://www.medpagetoday.com/Endocrinology/Menopause/tb/18342?impressionId=1265797940809"
                     
      &lt;p&gt;Estrogen-only hormone replacement therapy is associated with an increased risk of asthma in postmenopausal women, a large prospective observational cohort study showed.&lt;/p&gt;
&lt;p&gt;Recent and current users of estrogen had a 54% increase in the risk of being diagnosed with asthma, according to Isabelle Romieu, MD, ScD, of the National Institute of Public Health in Cuernavaca, Mexico, and colleagues.&lt;/p&gt;
&lt;p&gt;The risk was even higher in nonsmokers or those who reported an allergic disease before they developed asthma, the researchers reported online in &lt;em&gt;Thorax&lt;/em&gt;.&lt;/p&gt;
&lt;p&gt;Epidemiological studies suggest that an endocrine mechanism  --  perhaps endogenous estrogen synthesis  --  is involved in asthma in women and girls, the researchers wrote.&lt;/p&gt;
&lt;p&gt;It&apos;s plausible that hormone replacement therapy &quot;might therefore play a role in asthma onset,&quot; they theorized in the journal.&lt;/p&gt;
&lt;p&gt;To delve into the question, Romieu and colleagues turned to the E3N cohort study, which is the French component of the continuing European Prospective Investigation into Cancer and Nutrition (EPIC) study.&lt;/p&gt;
&lt;p&gt;The study started in 1990 and includes 98,995 French women born between 1925 and 1950. The participants complete self-administered questionnaires every two years, giving details of their medical history, menopausal status, and a variety of lifestyle characteristics.&lt;/p&gt;
&lt;p&gt;Women were deemed to have a new case of asthma if  --  after being free of the disease at baseline  --  they later reported both that they had suffered asthma attacks and that the diagnosis had been confirmed by a physician.&lt;/p&gt;
&lt;p&gt;Among the participants, Romieu and colleagues found 57,664 women who were free of asthma at menopause. In that group, the researchers found, there were 569 incident cases of asthma during a total of 495,448 years of follow-up.&lt;/p&gt;
&lt;p&gt;Analysis showed that hormone replacement therapy in general was related to an increased risk of asthma onset among recent users, with a hazard ratio of 1.20. But the 95% confidence interval ranged from 0.98 to 1.46, so the finding was not statistically significant.&lt;/p&gt;
&lt;p&gt;Instead, the researchers found, the association only reached significance among women reporting the use of estrogen alone, where the hazard ratio was 1.54, with a 95% confidence interval from 1.13 to 2.09.&lt;/p&gt;
&lt;p&gt;The risk was particularly great in estrogen-using women who had never smoked or who had reported allergic disease before the asthma onset. Those hazard ratios were 1.80 and 1.84, respectively, and both reached significance.&lt;/p&gt;
&lt;p&gt;The increased risk among never smokers might reflect an anti-estrogen effect of tobacco smoke, the researchers speculated, or difficulty isolating the additional effect of the therapy in smokers.&lt;/p&gt;
&lt;p&gt;The strengths of the study include its large size, prospective design, and relatively low loss to follow-up of 3.8%, Romieu and colleagues said.&lt;/p&gt;
&lt;p&gt;They added that the results might be biased if users of hormone replacement therapy reported more asthma attacks or were diagnosed more often because of more frequent visits to the doctor.&lt;/p&gt;
&lt;p&gt;Indeed, hormone therapy users had more mammograms than nonusers, they noted, but added that the participants all had free medical care and &quot;there is no reason to believe&quot; that hormone users had more medical visits for non-gynecological reasons than nonusers.&lt;/p&gt;
&lt;p&gt;Hormone therapy has been controversial  --  and on the decline  --  since the landmark Women&apos;s Health Initiative study was stopped in 2002 when the researchers found that participants taking estrogen plus progestin had a greater incidence of coronary heart disease, breast cancer, stroke, and pulmonary embolism than those receiving placebo.&lt;/p&gt;
&lt;p&gt;In the current study, the combination hormone therapy was not associated with an increase in asthma incidence.&lt;/p&gt;
&lt;div style=&quot;float:left;border-style:solid;border-width:1px;border-color:#8dabbc;font-family:arial;font-size:12px;background-color:#DBE9F2;padding:5px;&quot;&gt;&lt;p&gt;The study and researchers had support from Mutuelle G&amp;#233;n&amp;#233;rale de l&apos;Education Nationale, the Institut de Canc&amp;#233;rologie Gustave Roussy, the Institut National de la Sant&amp;#233; et de la Recherche M&amp;#233;dicale, the CDC, the Canc&amp;#233;rop&amp;#244;le R&amp;#233;gion Ile de France, and the GA&lt;sup&gt;2&lt;/sup&gt;LEN project.&lt;/p&gt;&lt;p&gt;The authors did not report any potential conflicts.&lt;/p&gt;&lt;/div&gt;&lt;div style=&quot;clear:both;&quot;&gt;&lt;/div&gt;
    </recommendedItem>
    <recommendedItem id="20100101_19_412"
                     title="Depression During Pregnancy Linked to Kids&apos; Behavior Problems (CME/CE)"
                     score="0.009"
                     href="http://www.medpagetoday.com/Psychiatry/Depression/tb/18321?impressionId=1265797940809"
                     
      &lt;p&gt;Children born to mothers who were depressed during pregnancy were more than twice as likely to display antisocial behavior by age 16 as children whose mothers had not been depressed, researchers found.&lt;/p&gt;
&lt;p&gt;Of 120 mothers from South London who were followed from pregnancy through their children&apos;s teen years, 31% had depression during pregnancy, according to Dale Hay, PhD, of Cardiff University in Wales, and colleagues.&lt;/p&gt;
&lt;p&gt;Children born to these women were significantly more likely to display antisocial behavior (OR 2.46, 95% CI 1.10 to 5.48) and commit violent acts (OR 4.36, 95% CI 1.54 to 12.41) before age 16, the researchers reported in the January/February issue of &lt;em&gt;Child Development&lt;/em&gt;.&lt;/p&gt;
&lt;p&gt;The associations were magnified in women who also had a history of behavior problems when they were children.&lt;/p&gt;
&lt;p&gt;&quot;A focus on mothers&apos; history of conduct problems and depression during pregnancy, as opposed to broader measures of the social environment, would hold promise for more targeted early interventions to prevent the development of serious antisocial behavior,&quot; Hay&apos;s group wrote.&lt;/p&gt;
&lt;p&gt;Previous studies have linked mothers&apos; mental health problems in pregnancy with disruptive behaviors in their children, but it&apos;s unclear what explains the relationship, according to the researchers.&lt;/p&gt;
&lt;p&gt;To explore the issue, they turned to the South London Child Development Study, which prospectively followed 120 pregnant women and their children into the teenage years.&lt;/p&gt;
&lt;p&gt;All families came from a relatively disadvantaged urban area. These families were more likely to belong to the working class and to be from ethnic minority groups than the general U.K. population.&lt;/p&gt;
&lt;p&gt;One-third of the children had been arrested or diagnosed with a conduct disorder by age 16. Of these 88.9% had been arrested and 45% had committed violent acts, including theft from a person, violent disorder, fighting, carrying a weapon, and assault.&lt;/p&gt;
&lt;p&gt;The association between maternal depression during pregnancy and risk of antisocial behavior remained relatively constant in analyses controlling for family environment, a child&apos;s exposure to maternal depression after birth, mothers&apos; substance use during pregnancy, and parental antisocial behavior.&lt;/p&gt;
&lt;p&gt;None of the factors fully explained the relationship. Neither did the arrest history of the biological father.&lt;/p&gt;
&lt;p&gt;But, the researchers wrote in the paper, &quot;it would be unwise to conclude that paternal risk factors are unimportant, given that we did not have more detailed information about the father&apos;s own history of conduct disorders.&quot;&lt;/p&gt;
&lt;p&gt;They explored several potential mechanisms for the link between maternal depression and a child&apos;s behavior problems: &lt;ul&gt; &lt;li&gt;Direct effects on the fetus from biological correlates of the mothers&apos; depressive symptoms&lt;/li&gt; &lt;li&gt;Depression in pregnancy as a sign of environmental adversity&lt;/li&gt; &lt;li&gt;Re-exposure to maternal depression after birth&lt;/li&gt; &lt;li&gt;Indirect effects of depression on the developing fetus driven by mothers&apos; smoking, drinking, and drug taking during pregnancy &lt;/li&gt; &lt;li&gt;A genetic explanation whereby women who experience depression in pregnancy may also have a greater genetic risk for antisocial behavior, which they pass on to their offspring &lt;/li&gt; &lt;/ul&gt;&lt;/p&gt;
&lt;p&gt;Hay and her colleagues noted that these explanations are not necessarily mutually exclusive.&lt;/p&gt;
&lt;p&gt;They also acknowledged some limitations of the study, including the lack of information about fetal growth and neuroendocrine measures on the mother and child and the relatively small sample size.&lt;/p&gt;
&lt;div style=&quot;float:left;border-style:solid;border-width:1px;border-color:#8dabbc;font-family:arial;font-size:12px;background-color:#DBE9F2;padding:5px;&quot;&gt;&lt;p&gt;The SLCDS has been funded by U.K. project grants from the Medical Research Council, by the Psychiatric Research Trust, and by the South West G.P. Trust. The current analysis was partially supported by an Economic and Social Research Council studentship to one of Hay&apos;s co-authors and by a Medical Research Council U.K. Program Grant.&lt;/p&gt;&lt;p&gt;The authors did not report any conflicts of interest.&lt;/p&gt;&lt;/div&gt;&lt;div style=&quot;clear:both;&quot;&gt;&lt;/div&gt;
    </recommendedItem>
    <recommendedItem id="20100101_19_405"
                     title="Difficult Childhood Lingers in the Mind (CME/CE)"
                     score="0.008"
                     href="http://www.medpagetoday.com/Psychiatry/GeneralPsychiatry/tb/18312?impressionId=1265797940809"
                     
      &lt;p&gt;Adversities faced in childhood have effects on mental health far into the future, researchers affirmed.&lt;/p&gt;
&lt;p&gt;Mental illness in adulthood was increasingly likely the more traumas faced in childhood, Ronald C. Kessler, PhD, of Harvard, and colleagues reported in the February issue of the &lt;em&gt;Archives of General Psychiatry&lt;/em&gt;.&lt;/p&gt;
&lt;p&gt;Childhood difficulties potentially explained 32.4% of all the psychiatric disorders examined, they said, based on analyses of the National Comorbidity Survey Replication.&lt;/p&gt;
&lt;p&gt;Adversities relating to family dysfunction  --  substance-abusing parents, sexual or physical abuse in the home, neglect, etc.  --  appeared to have the strongest link to onset and persistence of psychiatric disorders, they reported.&lt;/p&gt;
&lt;p&gt;These findings match folk wisdom and decades of research into the negative effects of child maltreatment, commented John McGrath, MD, PhD, of the Queensland Centre for Mental Health Research in Wacol, Australia, and colleagues in an accompanying editorial.&lt;/p&gt;
&lt;p&gt;But the lack of specificity between certain exposures to particular mental health outcomes  --  such as the death of one&apos;s mother leading to depression  --  was notable, the editorialists said.&lt;/p&gt;
&lt;p&gt;&quot;Thus, childhood trauma upsets the orderly psychological and biological cascades of development, leaving the affected individual at increased risk of a wide range of adverse mental health outcomes,&quot; they wrote.&lt;/p&gt;
&lt;p&gt;Rather than continue to rehash the epidemiology, it&apos;s time to focus on prevention and intervention, McGrath&apos;s group emphasized.&lt;/p&gt;
&lt;p&gt;&quot;It is unrealistic to think that we could protect all children from all adversities, but can we identify factors that bolster resilience and focus our efforts on the most vulnerable subgroups?&quot; they asked.&lt;/p&gt;
&lt;p&gt;The researchers examined joint associations of 12 retrospectively reported childhood adversities with lifetime incidence of disorders meeting Diagnostic and Statistical Manual of Mental Disorders (DSM-IV) criteria in the National Comorbidity Survey Replication I, a cross-sectional survey of a nationally-representative sample of adults in 9,282 American households.&lt;/p&gt;
&lt;p&gt;Among the respondents, 53.4% reported at least one childhood adversity, most commonly parental divorce (17.5%), family violence (14.0%), family economic problems (10.6%), and parental mental illness (10.3%).&lt;/p&gt;
&lt;p&gt;These adversities were all individually and significantly linked to first onset of psychiatric disorders with odds ratios of 1.5 to 1.9 for dysfunctional family factors (physical abuse, sexual abuse, neglect, parental mental illness, parental substance abuse, parental criminality, or family violence) and 1.0 to 1.5 for other factors like life-threatening childhood physical illness, extreme poverty, parental divorce, or loss of or separation from parents.&lt;/p&gt;
&lt;p&gt;Despite some apparent but not significantly meaningful variation in type of adversity with type of psychiatric disorder, the researchers said they could rule out that all types were the same for future mental health risk (&lt;em&gt;P&lt;/em&gt;&amp;lt;0.001).&lt;/p&gt;
&lt;p&gt;Problems tended to cluster, though. Among people who faced one adversity in childhood, 51.2% to 95.1% faced others as well, depending on the adversity.&lt;/p&gt;
&lt;p&gt;Risk of mental illness rose with number of issues faced in childhood from an odds ratio of 1.3 for one up to 3.4 for six and 3.2 for seven or more adversities.&lt;/p&gt;
&lt;p&gt;&quot;This subadditive pattern has important implications for intervention because it means that prevention or amelioration of only a single childhood adversity in youths exposed to many childhood adversities is unlikely to have important preventive effects,&quot; the researchers wrote.&lt;/p&gt;
&lt;p&gt;Overall, childhood adversities were projected to account for 44.6% of childhood-onset disorders, 32.0% of adolescent-onset disorders, and 28.6% of adult-onset disorders.&lt;/p&gt;
&lt;p&gt;The researchers also looked at persistence through the second part of the National Comorbidity Survey Replication which went beyond just core diagnostic assessment in 5,692 respondents.&lt;/p&gt;
&lt;p&gt;In a complex multivariate interactive analysis, childhood adversity from dysfunctional family factors appeared significantly linked to persistence in a given year (&lt;em&gt;P&lt;/em&gt;&amp;lt;0.001) whereas the number of factors was not significant.&lt;/p&gt;
&lt;p&gt;These significant factors were parental mental illness, physical abuse, sexual abuse, and neglect, but they carried modest effects individually with odds ratios of 1.2.&lt;/p&gt;
&lt;p&gt;But in one simulation, not being exposed to childhood trauma would only increase the time since the most recent episode of psychiatric illness by 1.6%, suggesting &quot;quite modest&quot; substantive importance in determining persistence.&lt;/p&gt;
&lt;p&gt;&quot;These results indirectly suggest that the public health implications of childhood adversities are greater for primary than for secondary prevention because the associations of childhood adversities with disorder onset are much stronger than the associations with persistence,&quot; Kessler&apos;s group wrote.&lt;/p&gt;
&lt;p&gt;The researchers cautioned that recall bias may have limited their study such that the results could be considered an &quot;upper bound&quot; for the real association and that the study could not prove causality.&lt;/p&gt;
&lt;div style=&quot;float:left;border-style:solid;border-width:1px;border-color:#8dabbc;font-family:arial;font-size:12px;background-color:#DBE9F2;padding:5px;&quot;&gt;&lt;p&gt;The National Comorbidity Survey Replication is supported by a grant from the National Institute of Mental Health with supplemental support from the National Institute on Drug Abuse, the Substance Abuse and Mental Health Services Administration, a grant from the Robert Wood Johnson Foundation, and the John W. Alden Trust.&lt;/p&gt;&lt;p&gt;The analyses were supported by a grant from the NIMH; the John D. and Catherine T. MacArthur Foundation; the Pfizer Foundation; grants from the U.S. Public Health Service; an award from the Fogarty International Center; the Pan American Health Organization; Eli Lilly; Ortho-McNeil Pharmaceutical; GlaxoSmithKline; and Bristol-Myers Squibb.&lt;/p&gt;&lt;p&gt;Kessler reported financial conflicts of interest with GlaxoSmithKline, Kaiser Permanente, Pfizer, sanofi-aventis, Shire Pharmaceuticals, Wyeth-Ayerst, Eli Lilly, Bristol-Myers Squibb, Johnson &amp;amp; Johnson Pharmaceuticals, and Ortho-McNeil Pharmaceutical.&lt;/p&gt;&lt;p&gt;The editorialists reported no conflicts of interest.&lt;/p&gt;&lt;/div&gt;&lt;div style=&quot;clear:both;&quot;&gt;&lt;/div&gt;
    </recommendedItem>
    <recommendedItem id="20100101_19_355"
                     title="Obesity Delays Puberty in Boys (CME/CE)"
                     score="0.006"
                     href="http://www.medpagetoday.com/Pediatrics/Obesity/tb/18235?impressionId=1265797940809"
                     
      &lt;p&gt;Unlike overweight girls, who tend to enter puberty early, overweight and obese boys in the U.S. may begin puberty later than thin boys, according to one of the first longitudinal studies of weight and timing of puberty in males.&lt;/p&gt;
&lt;p&gt;At 11.5 years, boys with the highest body mass index (mean BMI z score=1.84) were 165% more likely to be prepubertal than the thinnest boys (95% CI 1.05 to 6.61; &lt;em&gt;P&lt;/em&gt;=0.04), researchers reported online in the Feb. 1 &lt;em&gt;Archives of Pediatrics and Adolescent Medicine&lt;/em&gt;.&lt;/p&gt;
&lt;p&gt;&quot;This longitudinal study provides further evidence that higher BMI during early and middle childhood is not associated with earlier pubertal onset in boys, contrary to what is seen in girls,&quot; Joyce M. Lee, MD, MPH, of the University of Michigan, and colleagues wrote.&lt;/p&gt;
&lt;p&gt;&quot;In fact, higher BMI in earlier childhood may be associated with and precede later onset of puberty among a population-based sample of U.S. boys.&quot;&lt;/p&gt;
&lt;p&gt;Rates of obesity among American girls and boys have nearly tripled since the 1960s, prompting concerns about the effect of excess weight on growth and development. Most research has focused on obese girls, who appear to reach puberty earlier than thin girls. A recent cross-sectional study suggested that, unlike their female counterparts, overweight boys may develop later.&lt;/p&gt;
&lt;p&gt;To further explore this relationship, Lee and colleagues analyzed the records of 401 boys from diverse socioeconomic backgrounds in ten regions of the U.S., using data from the National Institute of Child Health and Human Development Study of Early Child Care and Youth Development. The participants were full-term, only children born in 1991.&lt;/p&gt;
&lt;p&gt;The data included height and weight measurements of the children from ages 2 to 12 years and a visual assessment of whether the children had begun puberty, using Tanner genitalia staging, at 9.5, 10.5, and 11.5 years. Boys were defined as prepubertal if they were Tanner stage 1 at 11.5 years old and were otherwise categorized as pubertal.&lt;/p&gt;
&lt;p&gt;Among the participants, 14.4% were overweight (BMI &amp;#8805; 85th and &amp;lt;95th percentiles) and 19.4% were obese (BMI&amp;#8805;95th percentile) at age 11.5. Overall, 49 boys (12.2%) were prepubertal at age 11.5 years by Tanner genitalia staging.&lt;/p&gt;
&lt;p&gt;The authors wrote that their findings have important implications for understanding sex differences in physiological mechanisms of puberty.&lt;/p&gt;
&lt;p&gt;They noted that puberty is regulated by the gonadotropin-releasing hormone axis for both girls and boys, but it&apos;s unclear why such different associations between body fat and the timing of pubertal onset would exist between the sexes.&lt;/p&gt;
&lt;p&gt;&quot;Given the recent childhood obesity epidemic, additional studies are needed to further investigate the epidemiological link between body fat and pubertal initiation and progression in boys as well as the physiological mechanisms responsible,&quot; they concluded.&lt;/p&gt;
&lt;p&gt;The authors were unable to analyze the data based on race, because most of the children in the study were white. They also noted that BMI is a surrogate measure of overall body fat, and that study has found that the relationship between body fat and BMI varies depending on race. They also recommended that future studies use multiple methods of determining whether children have entered puberty.&lt;/p&gt;
&lt;div style=&quot;float:left;border-style:solid;border-width:1px;border-color:#8dabbc;font-family:arial;font-size:12px;background-color:#DBE9F2;padding:5px;&quot;&gt;&lt;p&gt;The study was funded by the National Institute of Child Health and Human Development and the American Heart Association.&lt;/p&gt;&lt;p&gt;The authors reported no financial conflicts of interest.&lt;/p&gt;&lt;/div&gt;&lt;div style=&quot;clear:both;&quot;&gt;&lt;/div&gt;
    </recommendedItem>
    <recommendedItem id="20100101_19_288"
                     title="SSRIs Affect Breast Milk Production (CME/CE)"
                     score="0"
                     href="http://www.medpagetoday.com/Endocrinology/GeneralEndocrinology/tb/18149?impressionId=1265797940809"
                     
      &lt;p&gt;Women taking selective serotonin reuptake inhibitor (SSRI) antidepressants may experience delays in postpartum breast milk production, researchers said.&lt;/p&gt;
&lt;p&gt;Delayed secretory activation occurred in 87.5% of a small group of women taking SSRIs, compared with 43.5% of those not taking the drugs (RR 2, 95% CI 1.51 to 2.67, &lt;em&gt;P&lt;/em&gt;=0.02), according to Aaron M. Marshall, PhD, of the University of Cincinnati.&lt;/p&gt;
&lt;p&gt;The relative risk of delayed activation remained significantly higher (&lt;em&gt;P&lt;/em&gt;&amp;lt;0.05) among SSRI users after adjustment for maternal age, obesity, cesarean delivery, infant gestational age, and infant breastfeeding behavior, the researchers reported online in the &lt;em&gt;Journal of Clinical Endocrinology and Metabolism&lt;/em&gt;.&lt;/p&gt;
&lt;p&gt;An early breastfeeding difficulty faced by many women, particularly those who are primiparous, is milk secretion delayed beyond 72 hours postpartum.&lt;/p&gt;
&lt;p&gt;These women also are at risk of early cessation of breastfeeding. In fact, only 11% of mothers in the U.S. breastfeed exclusively for the recommended six months.&lt;/p&gt;
&lt;p&gt;Studies in animal models and cell cultures suggested that serotonin (5-HT) is an important local regulator of lactation homeostasis, and the 5-HT transporter is expressed in mammary tissue at the apical membrane of epithelial cells.&lt;/p&gt;
&lt;p&gt;Serotonin is controlled intracellularly by a balance between synthesis and degradation, while extracellularly its availability is controlled through recycling by the 5-HT transporter.&lt;/p&gt;
&lt;p&gt;The 5-HT transporter also is the target for the most commonly prescribed class of antidepressants in the U.S. and other developed countries. These SSRI antidepressants are typically used to treat postpartum depression.&lt;/p&gt;
&lt;p&gt;The investigators conducted in vitro and animal studies to establish that the 5-HT transporter is expressed in breast tissue, particularly in the apical membranes of mammary epithelial cells, and that pharmacologic inhibition of the transporter disrupts tight junctures leading to a local involution-like effect.&lt;/p&gt;
&lt;p&gt;To examine the potential effect of SSRI inhibition on milk production in women, Marshall and colleagues enrolled 431 mothers as part of a longitudinal cohort study examining barriers to early lactation success.&lt;/p&gt;
&lt;p&gt;All were expecting their first live-born infants, had no known absolute contraindication to breastfeeding, and were at least 19 years old.&lt;/p&gt;
&lt;p&gt;Women taking SSRIs were more likely to have scored higher on a depressive symptom scale (as expected), and were somewhat more likely to be obese or to have had a cesarean delivery.&lt;/p&gt;
&lt;p&gt;Participating mothers were visited between 72 and 96 hours after giving birth to assess their breastfeeding experience and to determine the timing of secretory activation, and then seen again one week later.&lt;/p&gt;
&lt;p&gt;Delayed secretory activation was defined as initiation more than 72 hours postpartum.&lt;/p&gt;
&lt;p&gt;Median onset of secretory activation among the SSRI-treated mothers was 85.8 hours compared with 69.1 hours in mothers not using the drugs (&lt;em&gt;P&lt;/em&gt;=0.004).&lt;/p&gt;
&lt;p&gt;Eight women reported regular use of an SSRI medication. Seven experienced definite delayed secretory activation, and the eighth reported activation at 72 hours and therefore did not meet the defined cutoff for delayed activation.&lt;/p&gt;
&lt;p&gt;All women taking SSRIs had experienced secretory activation by their second visit a week after the first interview.&lt;/p&gt;
&lt;p&gt;The researchers noted that most studies on the effects of SSRI use during pregnancy and lactation have focused on the risks for developmental defects or whether the drugs passed into milk during lactation.&lt;/p&gt;
&lt;p&gt;This study, they said, is the first to report data on another important aspect of SSRI use during the peripartum, the effect on milk production.&lt;/p&gt;
&lt;p&gt;They concluded that the risk of delayed secretory activation was twice as great among primiparous women using an SSRI medication, and although the fraction of women taking the drugs was small, the risk was significant and remained so after adjustment for potential confounding factors.&lt;/p&gt;
&lt;p&gt;Further examination of this relationship is needed in larger groups of mothers, the researchers said, and in studies to determine if there are differences among the antidepressant medications.&lt;/p&gt;
&lt;div style=&quot;float:left;border-style:solid;border-width:1px;border-color:#8dabbc;font-family:arial;font-size:12px;background-color:#DBE9F2;padding:5px;&quot;&gt;&lt;p&gt;This work was supported by the National Institutes of Health, the USDA Cooperative State Research, Education, and Extension Service, and the Department of Health and Human Services.&lt;/p&gt;&lt;/div&gt;&lt;div style=&quot;clear:both;&quot;&gt;&lt;/div&gt;
    </recommendedItem>
</recommendedContent>