<?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=1265819390750"
                     
      &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_431"
                     title="Down a Beer to Improve Bone Health? Not So Fast"
                     score="0.013"
                     href="http://www.medpagetoday.com/PrimaryCare/DietNutrition/tb/18347?impressionId=1265819390750"
                     
      &lt;p&gt;A flagon of ale may indeed be a good source of dietary silicon, a recent study showed, but experts say any attempt to link beer drinking to bone health is not based on scientific data.&lt;/p&gt;
&lt;p&gt;The study of 100 commercial beers in the February issue of the &lt;em&gt;Journal of the Science of Food and Agriculture&lt;/em&gt;, by Charles Bamforth, PhD, DSc, and Troy Casey, of the University of California Davis, examined the silicon content that results from different ingredients and brewing processes.&lt;/p&gt;
&lt;p&gt;Although a press release issued with the study prominently mentioned the link between silicon and bone health, the study itself did not look at bone mineral density or analyze any patient data at all, according to several researchers contacted by &lt;em&gt;MedPage Today&lt;/em&gt; and ABC News.&lt;/p&gt;
&lt;p&gt;The authors wrote that they explored the silicon content in beer because the popular beverage has been identified as one of the richest potential sources of dietary silicon in the Western diet. The average intake is 20 to 50 mg/day.&lt;/p&gt;
&lt;p&gt;The beers sampled contained an average of 29.4 mg/L of silicon, with a range of 6.4 to 56.4 mg/L. Beers made from a barley-based grist (as opposed to wheat-based beers ) and brews containing more hops had the highest silicon levels.&lt;/p&gt;
&lt;p&gt;The beer type with the overall highest silicon level was India Pale Ale, with an average of 41.2 mg/L. Other ales came in second with 32.8 mg/L.&lt;/p&gt;
&lt;p&gt;Nonalcoholic beers, light lagers, and wheat beers had the least silicon.&lt;/p&gt;
&lt;p&gt;In the end, the authors concluded that &quot;beer is a substantial source of silicon in the diet&quot; and that &quot;beers containing high levels of malted barley and hops are richest in silicon,&quot; but they did not attempt to establish a link between beer drinking and bone health.&lt;/p&gt;
&lt;p&gt;Experts contacted for comment on the study also cautioned the public against establishing any such connection.&lt;/p&gt;
&lt;p&gt;&quot;To conclude any bone health benefits from this study would require a great leap,&quot; Tim Byers, MD, MPH, deputy director of the University of Colorado Cancer Center in Aurora, wrote in an e-mail.&lt;/p&gt;
&lt;p&gt;Other researchers noted that previous studies have shown an association between alcohol consumption and an increased risk of fracture.&lt;/p&gt;
&lt;p&gt;That&apos;s probably because of a greater chance of falling after drinking, according to Walter Willett, MD, DrPH, of the Harvard School of Public Health.&lt;/p&gt;
&lt;p&gt;In fact, Stephen Richardson, MD, an endocrinologist at NYU Langone Medical Center, noted that &quot;alcohol consumption is a risk factor for osteoporosis.&quot;&lt;/p&gt;
&lt;p&gt;Still, there is some evidence supporting a positive link between overall dietary silicon and bone health.&lt;/p&gt;
&lt;p&gt;A 2004 cross-sectional study in the &lt;em&gt;Journal of Bone and Mineral Research&lt;/em&gt; that used data from the Framingham Offspring cohort found a significant association between greater dietary silicon intake, including that from beer, and higher bone mineral density in the hip in men and premenopausal women.&lt;/p&gt;
&lt;p&gt;The researchers concluded: &quot;These findings suggest that higher dietary silicon intake in men and younger women may have salutary effects on skeletal health, especially cortical bone health, that has not been previously recognized.&quot;&lt;/p&gt;
&lt;p&gt;Another study by the same group published last year in the &lt;em&gt;American Journal of Clinical Nutrition&lt;/em&gt; found that moderate consumption of alcohol, including beer, wine, and liquor, was associated with higher bone mineral density in men and postmenopausal women.&lt;/p&gt;
&lt;p&gt;However, it also showed that men who drank too much liquor were more likely to have lower spine and hip bone mineral density.&lt;/p&gt;
&lt;p&gt;The relationship between beer and bone mineral density appeared to be mediated by silicon, the researchers concluded.&lt;/p&gt;
&lt;p&gt;Bottom line: considering the increased fracture risk and the various other problems associated with drinking too much alcohol, experts agree that guzzling beer is not strategy for improving bone health.&lt;/p&gt;
&lt;p&gt;&quot;In the absence of bone density values or preferably fracture incidence, it would be premature to tout beer as a preventative or treatment,&quot; Richardson said.&lt;/p&gt;
&lt;p&gt;David Katz, MD, MPH, of the Yale School of Public Health, agreed.&lt;/p&gt;
&lt;p&gt;&quot;This is NOT a reason to drink beer,&quot; he said in an e-mail. &quot;This is simply a bit of good news for those who do drink beer already  --  yours truly among them!&quot;&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 authors did not make any financial disclosures.&lt;/p&gt;&lt;/div&gt;&lt;div style=&quot;clear:both;&quot;&gt;&lt;/div&gt;&lt;p&gt;&lt;em&gt;This article was developed in collaboration with ABC News. &lt;/em&gt;&lt;img src=&quot;http://www.medpagetoday.com/upload/2009/10/1/14357_1.jpg&quot; mce_src=&quot;http://www.medpagetoday.com/upload/2009/10/1/14357_1.jpg&quot; alt=&quot;&quot;&gt;&lt;/p&gt;
    </recommendedItem>
    <recommendedItem id="20100101_19_428"
                     title="Blocking Serotonin in Gut Reverses Osteoporosis in Mice (CME/CE)"
                     score="0.013"
                     href="http://www.medpagetoday.com/Endocrinology/Osteoporosis/tb/18346?impressionId=1265819390750"
                     
      &lt;p&gt;Blocking serotonin production in the intestine might help restore lost bone mass, rather than just preventing further loss like most current osteoporosis treatments, an animal study suggested.&lt;/p&gt;
&lt;p&gt;Once daily treatment with a novel serotonin inhibitor prevented development of osteoporosis and also fully reversed existing low bone mass in mice, according Gerard Karsenty, MD, PhD, of Columbia University in New York City, and colleagues.&lt;/p&gt;
&lt;p&gt;These proof-of-principle findings came without any impact on serotonin levels in the brain, the researchers reported in the Feb. 7 issue of &lt;em&gt;Nature Medicine&lt;/em&gt;.&lt;/p&gt;
&lt;p&gt;Just two years ago, Karsenty&apos;s group discovered that the vast majority of serotonin in the body acts to regulate bone formation.&lt;/p&gt;
&lt;p&gt;Only 5% plays the chemical&apos;s better-known role as a brain neurotransmitter. The rest comes from the gut for circulation below the blood-brain barrier which, in this regard, Karsenty called &quot;more hermetic than the Berlin Wall was.&quot;&lt;/p&gt;
&lt;p&gt;So the gut treatment is unlikely to affect mood and other critical functions serotonin plays in the brain, he emphasized in an interview. But he acknowledged that much more proof is needed on the way to the clinic.&lt;/p&gt;
&lt;p&gt;The tip-off to bone effects of serum serotonin came from a group of patients with a syndrome that produced high bone mass when they were into their 60s.&lt;/p&gt;
&lt;p&gt;Usually, bone destruction outpaces formation after menopause, eventually leading to osteoporosis. But something different was happening in these patients, who never developed the condition.&lt;/p&gt;
&lt;p&gt;&quot;The only cause we could find was that it was due to a decrease in the synthesis of serotonin in the gut,&quot; Karsenty told &lt;em&gt;MedPage Today&lt;/em&gt;.&lt;/p&gt;
&lt;p&gt;After their initial experiments showed serotonin did indeed boost the pace of bone formation, the researchers found that a biotech company had already developed a compound that would reduce gut synthesis of the hormone. It had been tested in women with irritable bowel syndrome.&lt;/p&gt;
&lt;p&gt;So Karsenty&apos;s group examined its effects on bone in mice and found a dose-dependent reduction in serum serotonin.&lt;/p&gt;
&lt;p&gt;Mice that got 250 mg/kg body weight per day of this compound  --  known as LP533401, a small molecule inhibitor of Tph1, the initial enzyme in gut serotonin synthesis  --  produced 30% less serotonin than controls, without a change in brain serotonin levels.&lt;/p&gt;
&lt;p&gt;Then the researchers tested the compound on mice whose ovaries had been excised to simulate the dramatic drop-off in hormones women experience after menopause. That condition, in turn, leads to an imbalance in bone resorption versus formation.&lt;/p&gt;
&lt;p&gt;Mice given the experimental drug at doses up to 10 mg/kg, starting the day after surgery, had elevated bone resorption but maintained higher bone mass than those that got placebo. The placebo group all developed osteopenia.&lt;/p&gt;
&lt;p&gt;Treated mice had a &quot;major&quot; increase in bone formation markers, including osteoblast numbers, bone formation rate, and osteocalcin serum levels. But again, brain serotonin remained unaffected.&lt;/p&gt;
&lt;p&gt;These benefits were achieved with a modest, roughly 30% reduction in serum serotonin  --  which appeared to be the threshold beyond which skeletal response increased only marginally.&lt;/p&gt;
&lt;p&gt;Some mice were left untreated for two weeks  --  &quot;a long time for a rodent,&quot; Karsenty noted  --  to develop osteopenia. Subsequently treated with a daily 250 mg/kg dose of LP533401, they had such an increase in bone formation over four weeks that it normalized their bone mass, the researchers noted.&lt;/p&gt;
&lt;p&gt;The same thing happened when researchers began treatment even longer after surgery, six or 12 weeks, when bone loss was already severe. Bone mass rose with serotonin inhibition in the vertebrae and long bones, but without a change in bone length or width.&lt;/p&gt;
&lt;p&gt;Nor were there effects on platelets, coagulation, or the GI tract with regard to the key measures of transit, colonic mobility, and gastric emptying.&lt;/p&gt;
&lt;p&gt;Serotonin inhibition in the gut as a potential anabolic treatment for osteopenia and osteoporosis appeared to work as well as the only currently available treatment that can increase bone formation sufficiently to compensate for the increased resorption caused by menopause  --  parathyroid hormone injections.&lt;/p&gt;
&lt;p&gt;Since serum serotonin inhibitors could be given in pill form, this pathway is much more attractive, Karsenty said.&lt;/p&gt;
&lt;p&gt;The specific agent used in this trial was designed for proof-of-principle and wouldn&apos;t necessarily be what is developed for clinical use, he cautioned.&lt;/p&gt;
&lt;p&gt;&quot;Although the data presented here are promising we remain fully aware that, since rodents do not remodel bones as much as humans do, our results will have to be confirmed in other species,&quot; the researchers also warned in the paper.&lt;/p&gt;
&lt;p&gt;Karsenty said the group plans to continue animal model studies for the time being, with no plans to move into clinical trials.&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 grants from the National Institutes of Health and a Gideon and Sevgi Rodan fellowship from the International Bone and Mineral Society.&lt;/p&gt;&lt;p&gt;The researchers reported no conflicts of interest or industry involvement in the study.&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="0.003"
                     href="http://www.medpagetoday.com/Endocrinology/GeneralEndocrinology/tb/18149?impressionId=1265819390750"
                     
      &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>
    <recommendedItem id="20100101_19_235"
                     title="Congenital Anomalies Linked to Mom&apos;s Diabetes (CME/CE)"
                     score="-0.002"
                     href="http://www.medpagetoday.com/OBGYN/Pregnancy/tb/18065?impressionId=1265819390750"
                     
      &lt;p&gt;Pregestational maternal diabetes was associated with an increased risk of a major congenital anomaly, but obesity itself was not, a cross-sectional study found.&lt;/p&gt;
&lt;p&gt;In a multivariable logistic model, the major contributor to a rising rate of congenital anomalies was maternal pregestational diabetes (OR 3.8, 95% CI 2.1 to 6.6), according to Joseph R. Biggio, Jr., MD, and colleagues from the University of Alabama at Birmingham.&lt;/p&gt;
&lt;p&gt;&quot;Because hyperglycemia is a major contributor to developmental malformations, interventions to address obesity and identify women at risk for diabetes and hyperglycemia should be considered in efforts to reduce the occurrence of congenital anomalies,&quot; they wrote in the February issue of &lt;em&gt;Obstetrics &amp;amp; Gynecology.&lt;/em&gt;&lt;/p&gt;
&lt;p&gt;Maternal obesity has been linked with numerous problems, including preeclampsia, gestational diabetes, fetal and neonatal death, and birth trauma, but scientists have disagreed over whether it also contributes to the risk of fetal malformations, the researchers noted.&lt;/p&gt;
&lt;p&gt;To help settle the issue, Biggio and colleagues used a perinatal database in their university health system that included all women with singletons delivered between 1991 and 2004.&lt;/p&gt;
&lt;p&gt;They divided the cohort into three time periods  --  1991 to 1994, 1995 to 1999, and 2000 to 2004, with a total of 41,902 pregnancies.&lt;/p&gt;
&lt;p&gt;For their primary analysis, they defined maternal obesity as a first prenatal visit weight greater than 200 lb, because during the earlier epochs many women did not have body mass index (BMI) calculated. For their secondary analyses they used BMI greater than 29 kg/m&lt;sup&gt;2&lt;/sup&gt; as the criterion for obesity.&lt;/p&gt;
&lt;p&gt;In each epoch, there were increases in mean maternal weight, mean BMI, the proportion of women weighing more than 200 lb, the proportion with a BMI greater than 29 kg/m&lt;sup&gt;2&lt;/sup&gt;, and the prevalence of pregestational diabetes (&lt;em&gt;P&lt;/em&gt;&amp;lt;0.001 for all).&lt;/p&gt;
&lt;p&gt;Univariable analysis determined that the rate of major anomalies, particularly involving the cardiac and pulmonary systems, also increased during each time period.&lt;/p&gt;
&lt;p&gt;But there was no independent association between congenital anomalies and maternal obesity using either definition, during any of the three time periods or during the study overall.&lt;/p&gt;
&lt;p&gt;Although no direct association was seen between congenital malformations and maternal obesity, the investigators reported that the proportion of anomalies that could be attributed to obesity increased from 0% to 23% during the overall study period.&lt;/p&gt;
&lt;p&gt;The proportion of anomalies that could be attributed to diabetes ranged from 58% to 76%.&lt;/p&gt;
&lt;p&gt;Moreover, for obese women with diabetes the proportion of anomalies attributed to diabetes increased sharply, from 48% in the first epoch to 74% in the third epoch.&lt;/p&gt;
&lt;p&gt;In contrast, for the obstetric population as a whole, the population-attributable risk of congenital malformation related to obesity rose from near zero in the first epoch to 6.1% in the third epoch, while that related to diabetes increased from 3.3% to 9.2%, the investigators reported.&lt;/p&gt;
&lt;p&gt;During the course of the study there was a nearly 15-lb increase in maternal weight and a 30% increase in the proportion of women whose BMI exceeded 29 kg/m&lt;sup&gt;2&lt;/sup&gt;.&lt;/p&gt;
&lt;p&gt;There also was a nearly twofold increase in the rate of major anomalies  --  and a 250% increase in the prevalence of diabetes.&lt;/p&gt;
&lt;p&gt;The authors observed that there has been much interest in the effects of maternal obesity on birth defects.&lt;/p&gt;
&lt;p&gt;Although the pathophysiologic basis for this possible association have not been identified, hypotheses have included increased serum insulin, lower levels of folic acid, chronic hypoxia, and increased inflammatory mediators.&lt;/p&gt;
&lt;p&gt;&quot;Our study provides evidence that the defects may not be due solely to the maternal obesity per se but may be due to undiagnosed diabetes,&quot; the investigators wrote.&lt;/p&gt;
&lt;p&gt;From a public health standpoint, the study findings suggest that efforts to reduce the prevalence of congenital anomalies should be focused less on obesity and aimed more closely at correcting hyperglycemia.&lt;/p&gt;
&lt;p&gt;&quot;If euglycemia could be achieved before pregnancy, or at least embryogenesis and organogenesis, the majority of these anomalies could potentially be avoided,&quot; they observed.&lt;/p&gt;
&lt;p&gt;They also suggested that even women of normal weight, but with other diabetes risk factors, could benefit from closer attention to glycemic control.&lt;/p&gt;
&lt;p&gt;A weakness of the study was the fact that detailed data on glycemic control was not available in the perinatal database, &quot;and therefore we cannot comment on the association between glycemic control and anomaly rates,&quot; the investigators 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 in part by the National Institute of Child Health and Human Development.&lt;/p&gt;&lt;p&gt;The authors did not report any potential conflicts of interest.&lt;/p&gt;&lt;/div&gt;&lt;div style=&quot;clear:both;&quot;&gt;&lt;/div&gt;
    </recommendedItem>
</recommendedContent>