<?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="0.014"
                     href="http://www.medpagetoday.com/Endocrinology/Menopause/tb/18342?impressionId=1265761574068"
                     
      &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_393"
                     title="SMFM: Gene Variants Linked to Preterm Labor (CME/CE)"
                     score="0.013"
                     href="http://www.medpagetoday.com/MeetingCoverage/SMFM/tb/18295?impressionId=1265761574068"
                     
      Genetic variants involved in regulating inflammation and the extracellular matrix may increase the risk of preterm birth, researchers say.&lt;br&gt;
&lt;br&gt;A single nucleotide polymorphism (SNP) in fetal interleukin-6 (&lt;em&gt;ILR6&lt;/em&gt;) and another in maternal tissue inhibitor of metalloproteinase 2 (&lt;em&gt;TIMP2&lt;/em&gt;) were each associated with a twofold increased risk of spontaneous preterm birth.&lt;br&gt;
&lt;br&gt;Roberto Romero, MD, of the National Institute of Child Health and Human Development, and colleagues reported the findings at the Society for Maternal-Fetal Medicine meeting in Chicago.&lt;/p&gt;
&lt;p&gt;&quot;The genetic makeup of both mother and fetus can contribute to the risk of premature labor,&quot; Romero told &lt;em&gt;MedPage Today&lt;/em&gt;. &quot;Our discovery . . . helps explain why some mothers have premature labor and delivery despite having optimal prenatal care.&quot;&lt;/p&gt;
&lt;p&gt;Inflammatory hormones have been shown to play a role in the labor process, and previous studies have found that a third of preterm infants are born to mothers with a silent amniotic infection.&lt;/p&gt;
&lt;p&gt;Now, the findings suggest that individual genetic variation involved in that inflammatory response may account for discrepancies in preterm births.&lt;/p&gt;
&lt;p&gt;&quot;We have a large body of evidence that proves silent infections are a frequent and important cause of premature labor,&quot; Romero said. &quot;These infections can also attack the fetus before it is born.&quot;&lt;/p&gt;
&lt;p&gt;He explained that the mother&apos;s hormones initiate the onset of labor to get rid of the infected tissue, and the fetus seeks to exit a hostile intrauterine environment that threatens its survival.&lt;/p&gt;
&lt;p&gt;To look at the mechanisms by which this process occurs, Romero and colleagues conducted a case-control study of mothers in Chile to assess genetic factors that could predispose women to spontaneous preterm labor and delivery.&lt;/p&gt;
&lt;p&gt;Patients who delivered prior to 37 weeks gestation served as cases, while women who delivered a normal neonate at term served as controls. There were 223 mothers and 179 fetuses in the case group, and 599 mothers and 628 fetuses in the control group.&lt;/p&gt;
&lt;p&gt;The researchers subsequently examined 190 candidate genes and 775 SNPs.&lt;/p&gt;
&lt;p&gt;They found that the strongest fetal single-locus association with risk of spontaneous preterm birth was in &lt;em&gt;ILR6&lt;/em&gt;, (OR 2.07, 95% CI 1.42 to 3.02,&lt;em&gt; P&lt;/em&gt;=0.0001).&lt;/p&gt;
&lt;p&gt;The strongest maternal single-locus association with spontaneous preterm labor and delivery was in tissue inhibitor of metalloproteinase &lt;em&gt;TIMP2&lt;/em&gt; (OR 1.98, 95% CI 1.38 to 2.83, &lt;em&gt;P&lt;/em&gt;=0.0002). This gene is involved in regulating the extracellular matrix, which holds cells within tissues.&lt;/p&gt;
&lt;p&gt;The associations remained significant after controlling for multiple comparisons, Romero said.&lt;/p&gt;
&lt;p&gt;Global haplotype analysis also indicated an association between a fetal DNA variant in insulin-like growth factor 2 (&lt;em&gt;P&lt;/em&gt;=0.004) as well as maternal alpha 3 type IV collagen isoform 1 (&lt;em&gt;COL4A3&lt;/em&gt;) (&lt;em&gt;P&lt;/em&gt;=0.007).&lt;/p&gt;
&lt;p&gt;&quot;Some women and fetuses carry gene variants that predispose them to the early onset of labor,&quot; Romero said.&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 researchers 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_391"
                     title="Rare Genetic Deletion Linked to Morbid Obesity (CME/CE)"
                     score="0.012"
                     href="http://www.medpagetoday.com/Genetics/GeneralGenetics/tb/18286?impressionId=1265761574068"
                     
      &lt;p&gt;Missing sections of DNA may have a powerful impact on weight for a small segment of the population, researchers said.&lt;/p&gt;
&lt;p&gt;Nearly all teens and adults found to have a particular deletion of roughly 30-genes on chromosome 16p11.2 were obese  --  most morbidly so  --  with a body mass index of at least 40 kg/m&lt;sup&gt;2&lt;/sup&gt;, Philippe Froguel, MD, PhD, of Imperial College London, and colleagues reported in &lt;em&gt;Nature&lt;/em&gt;.&lt;/p&gt;
&lt;p&gt;While the variant appeared to explain only a small proportion of morbid obesity  --  0.7% in the study population  --  it was never present in healthy, normal-weight controls.&lt;/p&gt;
&lt;p&gt;&quot;Although the recent rise in obesity in the developed world is down to an unhealthy environment, with an abundance of unhealthy food and many people taking very little exercise, the difference in the way people respond to this environment is often genetic,&quot; Froguel said in a prepared statement.&lt;/p&gt;
&lt;p&gt;But with further findings like these, it may be possible to identify such individuals through genetic testing, he said.&lt;/p&gt;
&lt;p&gt;If so, &quot;We can then offer them appropriate support and medical interventions, such as the option of weight-loss surgery, to improve their long-term health,&quot; Froguel declared.&lt;/p&gt;
&lt;p&gt;Although researchers speculate that one in 20 cases of obesity may have a genetic cause, the genetic component remains largely elusive.&lt;/p&gt;
&lt;p&gt;Even accounting for such a small fraction of cases, the newly discovered 16p11.2 variant would be the second most frequent known genetic cause of obesity, Froguel&apos;s group said.&lt;/p&gt;
&lt;p&gt;Extensive genome-wide association studies have linked numerous single nucleotide polymorphisms (SNPs) to obesity, but added all together they account for only a small fraction of the known heritable component, the researchers said.&lt;/p&gt;
&lt;p&gt;&quot;The &apos;common disease, common variant&apos; hypothesis is increasingly coming under challenge,&quot; they wrote.&lt;/p&gt;
&lt;p&gt;Their team first identified the genetic deletion in teen and adults with learning difficulties or delayed development.&lt;/p&gt;
&lt;p&gt;Because the 31 individuals who had the nearly identical deletions of at least 593 kilobases at chromosome 16p11.2 in one copy of their DNA all had a BMI of over 30 kg/m&lt;sup&gt;2&lt;/sup&gt;, the researchers decided to dig a little deeper.&lt;/p&gt;
&lt;p&gt;&quot;Cohorts with extreme phenotypes that include obesity may be enriched for rare but very potent risk variants,&quot; making them easier to discover, they wrote.&lt;/p&gt;
&lt;p&gt;So they undertook a case-control study among 312 patients at three centers in Britain and France who presented with congenital malformations, developmental delay, or both, in addition to obesity.&lt;/p&gt;
&lt;p&gt;The same deletions were seen in 2.9% of these individuals.&lt;/p&gt;
&lt;p&gt;The function of the missing genes are not well known, but some have previously been associated with delayed development, autism, and schizophrenia.&lt;/p&gt;
&lt;p&gt;Notably, though, the frequency of deletion of these genes in the obese case-control cohort was &quot;appreciably higher&quot; than the less than 1% seen in the autism and other studies that didn&apos;t include obesity as an inclusion criteria, the researchers said.&lt;/p&gt;
&lt;p&gt;A second independent survey of genetic data at eight cytogenetic centers in France, Switzerland, and Estonia turned up a 0.6% rate among 3,947 people with developmental delay, malformations, or both, but who were not selected for obesity (&lt;em&gt;P&lt;/em&gt;=0.00022 versus the cohort selected for obesity).&lt;/p&gt;
&lt;p&gt;Analysis of those with the missing genes revealed an age-dependent link to weight: All four teens and adults were obese. Children were often obese (four of 15) or overweight (two of 15). Children under 2 years all had normal weight.&lt;/p&gt;
&lt;p&gt;So to see whether the deletion was independent of neurodevelopmental problems, Froguel&apos;s group examined genome-wide association study data from general population cohorts totaling 11,856 individuals along with 2,772 from childhood obesity and adult morbid obesity case-control studies, 931 in an extreme early-onset obesity study, and 141 who had bariatric weight-loss surgery.&lt;/p&gt;
&lt;p&gt;All adult carriers of the deletion were obese with the exception of one who was apparently diabetic. Each of the seven children and adolescents who carried the variant had a BMI in the top 0.1% for their age and gender.&lt;/p&gt;
&lt;p&gt;None had any reported developmental or cognitive problems. Four had reported hyperphagia with excessive hunger and food intake.&lt;/p&gt;
&lt;p&gt;Altogether, the 16p11.2 deletions predicted 29.8-fold elevated risk of obesity (&lt;em&gt;P&lt;/em&gt;=0.00000058) and 43.0-fold elevated risk of morbid obesity (&lt;em&gt;P&lt;/em&gt;=0.000000064) compared with lean or normal weight.&lt;/p&gt;
&lt;p&gt;By extrapolation, the researchers extrapolated that about 0.4% of all morbidly obese cases are attributable to an inherited 16p11.2 deletion, with 0.3% arising from a de novo deletion in the same genetic region.&lt;/p&gt;
&lt;p&gt;&quot;Although they may be heterogeneous in nature, these deletions are highly likely to be the causal variants,&quot; they wrote.&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 supported by &quot;Le Conseil Regional Nord Pas de Calais/FEDER&quot; along with various governmental and industry supporters for the various component studies.&lt;/p&gt;&lt;p&gt;The researchers 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_299"
                     title="Teen Pregnancies, Births, and Abortions Increase"
                     score="0.005"
                     href="http://www.medpagetoday.com/OBGYN/Pregnancy/tb/18162?impressionId=1265761574068"
                     
      &lt;p&gt;After a decade of decline, the rate of teenage pregnancies increased by 3% in 2006 as 750,000 women younger than 20 became pregnant, according to a report released by the Guttmacher Institute.&lt;/p&gt;
&lt;p&gt;And as pregnancies increased, so did births  --  41.9 births per 1,000 U.S. teenage girls, which was 4% higher than in 2005  --  and abortions, which increased by 1% from 2005 to 2006.&lt;/p&gt;
&lt;p&gt;In a prepared statement, Planned Parenthood blamed abstinence-only sex education programs for the uptick.&lt;/p&gt;
&lt;p&gt;&quot;It is a tragedy that after a decade of progress in reducing the rate of teenage pregnancy we are witnessing a substantial increase in the number of teens who are getting pregnant,&quot; Planned Parenthood said.&lt;/p&gt;
&lt;p&gt;In a statement released last May in conjunction with the &quot;National Day to Prevent Teen Pregnancy&quot; the American College of Obstetricians and Gynecologists (ACOG), agreed that comprehensive sex education was likely to be more effective than abstinence-only programs.&lt;/p&gt;
&lt;p&gt;&quot;Abstinence works for some teens, but the idea that most teens will wait to have sex indefinitely is rigid and impractical,&quot; said Richard S. Guido, MD, chair of the ACOG&apos;s Committee on Adolescent Health Care.&lt;/p&gt;
&lt;p&gt;But the Guttmacher report suggested that the reasons for increase may be more complex, including &quot;shifts in the racial and ethnic composition of the population, increases in poverty, the growth of abstinence-only sex education programs at the expense of comprehensive programs, and changes in public perception and attitudes toward both teenage and unintended pregnancy.&quot;&lt;/p&gt;
&lt;p&gt;Among black teenagers the pregnancy rate was 126.3 per 1,000 versus 44 per 1,000 non-Hispanic white teenagers.&lt;/p&gt;
&lt;p&gt;A breakdown by state revealed that New Mexico had the highest teenage pregnancy rate, followed by Nevada, Arizona, Texas, and Mississippi.&lt;/p&gt;
&lt;p&gt;Conversely, the lowest teenage pregnancy rate was in New Hampshire  --  33 pregnancies per 1,000  --  followed by Vermont, Maine, Minnesota, and North Dakota.&lt;/p&gt;
&lt;p&gt;Texas had the highest rate of births to teenage mothers  --  62 per 1,000  --  and New York had the highest rate of abortions among teenagers, 41 per 1,000.&lt;/p&gt;
&lt;p&gt;The report was based on data from the National Center for Health Statistics of the U.S. Department of Health and Human Services (number of births), the Guttmacher Institute (total number of abortions), the U.S. Centers for Disease Control and Prevention (age and race/ethnicity distribution of women obtaining abortions), and the Population Estimates Program of the U.S. Bureau of the Census in collaboration with NCHS (population estimates).&lt;/p&gt;
&lt;p&gt;Among other findings in the report: &lt;ul&gt; &lt;li&gt;The pregnancy rate was 71.5 pregnancies per 1,000 girls ages 15-19 and pregnancies occurred among 7% of females in this age group.&lt;/li&gt; &lt;li&gt;Although teenage abortions increased by 1% from 2005 to 2006, the overall teenage abortion rate declined by about a third over the two decades from 1986 to 2006.&lt;/li&gt; &lt;li&gt;The increase in teen pregnancies and births to teenage mothers was observed across all racial and ethnic groups.&lt;/li&gt; &lt;/ul&gt;&lt;/p&gt;
&lt;p&gt;The authors said that additional research was needed to determine if the disparities in rates by both race and region carry over to adult women.&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 report was prepared by Kathryn Kost, Stanley Henshaw, and Liz Carlin of the Guttmacher Institute.&lt;/p&gt;&lt;p&gt;Lawrence Finer, Rebecca Wind, Susheela Singh, and Laura Lindberg provided comments on early drafts.&lt;/p&gt;&lt;p&gt;The report was funded by grants from the Brush Foundation, The California Wellness Foundation (TCWF) and the Annie E. Casey Foundation. The Guttmacher Institute also gratefully acknowledges the general support it receives from individuals and foundations, including major grants from The William and Flora Hewlett Foundation, The David and Lucile Packard Foundation, and the Ford Foundation, which undergirds all of the Institute&apos;s work.&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="0.005"
                     href="http://www.medpagetoday.com/Endocrinology/GeneralEndocrinology/tb/18149?impressionId=1265761574068"
                     
      &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>