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    <recommendedItem id="20100101_19_473"
                     title="AAN: High Intake of Vitamin D Linked to Lower MS Risk (CME/CE)"
                     score="0.014"
                     href="http://www.medpagetoday.com/MeetingCoverage/AAN/tb/18406?impressionId=1265819245048"
                     
      &lt;p&gt;TORONTO  --  Women whose mothers consumed high levels of vitamin D during pregnancy have a lower risk of developing multiple sclerosis, a large, observational study confirmed.&lt;/p&gt;
&lt;p&gt;Mothers who reported the highest intake during pregnancy were 45% less likely to have a daughter who subsequently developed the disease than those who consumed the least vitamin D (RR 0.55, 95% CI 0.35 to 0.88), according to Fariba Mirzaei, MD, MPH, a doctoral student at the Harvard School of Public Health.&lt;/p&gt;
&lt;p&gt;Mirzaei is scheduled to report the findings at the American Academy of Neurology (AAN) meeting in April.&lt;/p&gt;
&lt;p&gt;Lily Jung, MD, a neurologist at Swedish Medical Center in Seattle, said in an interview that the study &quot;adds more fuel to the fire that low vitamin D is important in the genesis of MS,&quot; which has been demonstrated in previous studies. (See &lt;a href=&quot;http://www.medpagetoday.com/Neurology/MultipleSclerosis/4738&quot; mce_href=&quot;http://www.medpagetoday.com/Neurology/MultipleSclerosis/4738&quot; target=&quot;_blank&quot;&gt;High Blood Levels of Vitamin D May Lower MS Risk&lt;/a&gt;)&lt;/p&gt;
&lt;p&gt;She said it&apos;s unclear why vitamin D is associated with risk of multiple sclerosis.&lt;/p&gt;
&lt;p&gt;&quot;There&apos;s an idea that perhaps there might be receptors that are turned on by vitamin D levels that give some form of protection, but that is very preliminary information and we&apos;re still learning a lot about that,&quot; said Jung, who is also a spokeswoman for the AAN.&lt;/p&gt;
&lt;p&gt;Although the link between vitamin D and risk of multiple sclerosis has been demonstrated before, gestational exposure to the vitamin has not been studied.&lt;/p&gt;
&lt;p&gt;To fill that gap, Mirzaei analyzed data from the Nurses&apos; Mothers&apos; Study, which includes a subcohort of the two Nurses&apos; Health Studies that was restricted to nurses whose biological mothers completed a questionnaire in 2001 about their diet during pregnancy.&lt;/p&gt;
&lt;p&gt;The current analysis included 35,794 nurse-mother pairs.&lt;/p&gt;
&lt;p&gt;During the 16-year study period, 199 of the nurses were diagnosed with multiple sclerosis.&lt;/p&gt;
&lt;p&gt;In addition to a lower risk of disease among those whose mothers consumed the largest amounts of vitamin D, those whose mothers had the highest predicted serum 25-hydroxyvitamin D levels also had a reduced risk of having a daughter with the disease (RR 0.58, 95% CI 0.37 to 0.90).&lt;/p&gt;
&lt;p&gt;In an analysis of milk drinking alone, mothers who drank at least four glasses a day had a nonsignificant reduced risk of having a daughter who would develop multiple sclerosis compared with those who drank less than three glasses a month (RR 0.44, 95% CI 0.16 to 1.23).&lt;/p&gt;
&lt;p&gt;However, there was a significant trend for lower risk of multiple sclerosis with increasing milk consumption (&lt;em&gt;P&lt;/em&gt;=0.001).&lt;/p&gt;
&lt;p&gt;Jung noted that the study was limited by the use of questionnaires decades after a pregnancy to determine dietary intake of vitamin D.&lt;/p&gt;
&lt;p&gt;Nevertheless, she said, &quot;this is very consistent with what we&apos;re seeing elsewhere in terms of vitamin D in moms and the risk of MS in kids.&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;Mirzaei did not make any financial disclosures.&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="0.01"
                     href="http://www.medpagetoday.com/Pediatrics/Obesity/tb/18235?impressionId=1265819245048"
                     
      &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_341"
                     title="Doctor&apos;s Orders: Brain&apos;s Wiring Makes Change Hard"
                     score="0.008"
                     href="http://www.medpagetoday.com/Psychiatry/Addictions/tb/18207?impressionId=1265819245048"
                     
      &lt;p&gt;Doctor&apos;s Orders&lt;em&gt; is a feature in the collaboration between &lt;/em&gt;MedPage Today &lt;em&gt;and&lt;/em&gt; ABC News&lt;em&gt;. In this monthly segment we explore medical issues of interest to physicians and their patients alike. This month, we look at addiction and addictive behaviors, and what neuroimaging studies have revealed about why it&apos;s so hard to break bad habits. &lt;/em&gt;&lt;/p&gt;&lt;hr&gt;

&lt;p&gt;&lt;em&gt;&lt;/em&gt;&lt;/p&gt;
&lt;p&gt;&lt;em&gt;&lt;/em&gt;&lt;/p&gt;
&lt;p&gt;&lt;em&gt;&lt;/em&gt;&lt;/p&gt;
&lt;p&gt;&lt;em&gt;&lt;/em&gt;&lt;/p&gt;

&lt;p&gt;By the end of January, many New Year&apos;s resolutions have been tossed out with the leftover holiday cookies. That&apos;s because change is hard  --  and neuroscientists are learning why.&lt;br&gt;
&lt;br&gt;Advances in neuroimaging have enabled researchers to peer inside the brains of addicts and patients with addictive behaviors. They can see in real-time what gets patients hooked: how the brain&apos;s reward system  --  based largely on the neurotransmitter dopamine  --  thirsts for more, while inhibitory control centers experience a system failure.&lt;br&gt;
&lt;br&gt;The pattern is similar across all kinds of behaviors  --  from cocaine and tobacco addiction to overeating. That&apos;s why changing your mind may be the first step toward breaking a habit, but altering the brain&apos;s neural machinery is the real challenge.&lt;/p&gt;
&lt;p&gt;&lt;strong&gt;Hijacked Pathways&lt;/strong&gt;&lt;/p&gt;
&lt;p&gt;Drug-taking and other addictive behaviors &quot;hijack&quot; the brain&apos;s reward system, says Petros Levounis, MD, director of the Addiction Institute of New York at St. Luke&apos;s and Roosevelt Hospitals in Manhattan.&lt;/p&gt;
&lt;p&gt;In normal patients, dopamine plays a major role in motivation and reward, surging before and during a pleasurable activity  --  say, eating or sex  --  to make patients want to repeat a behavior that&apos;s crucial to the survival of the species.&lt;/p&gt;
&lt;p&gt;Dopaminergic pathways connect the limbic system, responsible for emotion, with the hippocampus, etching rewarding behaviors into the brain by creating strong, salient memories.&lt;/p&gt;
&lt;p&gt;The problem arises when the memory and the craving to recapture it takes over a person&apos;s life.&lt;/p&gt;
&lt;p&gt;&quot;Imagine what a strong hold these hijacked reward pathways take on our brains and our whole existence when they&apos;re so closely connected, geographically and anatomically speaking, with our memories and our emotions,&quot; Levounis says.&lt;/p&gt;
&lt;p&gt;As the dopamine surge repeats and repeats, it gains speed, but the brakes begin to fail: Normal function in the brain&apos;s frontal lobes, responsible for inhibitory control and executive functioning (read: willpower), tends to decrease in addicts.&lt;/p&gt;
&lt;p&gt;&quot;Ultimately,&quot; Levounis says, &quot;the war on drugs is a war between the hijacked reward pathways that push the person to want to use, and the frontal lobes, which try to keep the beast at bay. That is the essence of addiction.&quot;&lt;/p&gt;
&lt;p&gt;&lt;strong&gt;Similar Patterns&lt;/strong&gt;&lt;/p&gt;
&lt;p&gt;These neural pathways have been well studied in the brains of hardcore addicts. Now, researchers say they see similar pathways involved in other bad behaviors.&lt;/p&gt;
&lt;p&gt;Gene-Jack Wang, MD, of Brookhaven National Laboratory on New York&apos;s Long Island, has conducted several brain imaging studies of obese patients using PET-CT scans.&lt;/p&gt;
&lt;p&gt;The scans have revealed similarities in brain activity  --  or a lack thereof  --  between patients addicted to cocaine or alcohol, and those &quot;addicted&quot; to eating. Normally, the PET scan lights up when a contrast of radioactive glucose is metabolized, revealing an area of red activity in the center of the brain.&lt;/p&gt;
&lt;p&gt;But in both drug-addicted and obese patients, the scans show very little red activity, because there aren&apos;t enough receptors to which the radioactive glucose can bind. Wang says the decreased availability of dopamine receptors is the brain&apos;s way of coping with a constant dopamine overload.&lt;/p&gt;
&lt;p&gt;&quot;If a person constantly has an excess of dopamine, the brain will down-regulate,&quot; Wang says, explaining the principle commonly referred to as tolerance. &quot;Once the system is down-regulated, we have to do more in order to get the same amount of feeling in our normal state.&quot;&lt;/p&gt;
&lt;p&gt;Thus, obese patients &quot;will want to eat more in order to compensate for their down-regulated system.&quot;&lt;/p&gt;
&lt;p&gt;In other experiments, Wang and his colleagues have also found that a higher body mass index (BMI) correlated with lower prefrontal cortex function  --  the area associated with inhibitory control.&lt;/p&gt;
&lt;p&gt;&quot;If they&apos;re obese,&quot; Wang said, &quot;they have a problem controlling their eating behaviors.&quot;&lt;/p&gt;
&lt;p&gt;Those studies also revealed that a higher BMI was linked to a decrease in memory and executive functioning.&lt;/p&gt;
&lt;p&gt;&lt;strong&gt;Out of Control&lt;/strong&gt;&lt;/p&gt;
&lt;p&gt;Ed Susman was 293 pounds when he decided to join a clinical trial for an investigational weight-loss drug and chronicle his year-long experience for &lt;em&gt;MedPage Today&lt;/em&gt;. (See &lt;a href=&quot;http://www.medpagetoday.com/PrimaryCare/Diabetes/8125&quot; mce_href=&quot;http://www.medpagetoday.com/PrimaryCare/Diabetes/8125&quot; target=&quot;_blank&quot;&gt;Journalist Participant to Present Insider View of Weight-Loss Trial&lt;/a&gt;)&lt;/p&gt;
&lt;p&gt;Eating, to him, was a &quot;compulsion&quot;  --  as was biting his nails, a habit he picked up at age 4.&lt;/p&gt;
&lt;p&gt;Over the course of the trial, not only did Susman lose 52 pounds, he also stopped his nail-biting.&lt;/p&gt;
&lt;p&gt;He doesn&apos;t yet know if he was in the drug arm of the trial, but he strongly suspects he wasn&apos;t experiencing a placebo effect.&lt;/p&gt;
&lt;p&gt;&quot;I believe I was on the drug because it controlled a compulsion that I had had for 50 years,&quot; Susman says of the nail-biting. &quot;This stopped it cold.&quot;&lt;/p&gt;
&lt;p&gt;Unfortunately, he says, the same didn&apos;t happen with his eating habits, but he&apos;s gained back only 10 of those 52 pounds in the year since his participation in the trial ended.&lt;/p&gt;
&lt;p&gt;The still-investigational drug is lorcaserin  --  a combination of benzazepine and hydrochloride, two neurological agents. Susman says it is &quot;supposed to improve your willpower, your ability to overcome compulsions.&quot;&lt;/p&gt;
&lt;p&gt;Lorcaserin is a selective 5-HT&lt;sub&gt;2C&lt;/sub&gt; receptor agonist, working through the serotonin system, which regulates appetite, mood, and motor behavior.&lt;/p&gt;
&lt;p&gt;Two other investigational obesity drugs target the dopamine reward system  --  Contrave, which is a combination of bupropion and naltrexone, and Qnexa, which combines phentermine and topiramate.&lt;/p&gt;
&lt;p&gt;&quot;Some medications that have used similar dopamine modulation, until now, have failed,&quot; Wang said. &quot;These two companies are using the command of the modulation of the dopamine system with other neurological systems, such as the opiate or norepinephrine system. According to the trials, they&apos;ve been very effective.&quot;&lt;/p&gt;
&lt;p&gt;Wang called the new medications &quot;a bright light for the treatment of obesity.&quot;&lt;/p&gt;
&lt;p&gt;&lt;strong&gt;Kicking the Habit&lt;/strong&gt;&lt;/p&gt;
&lt;p&gt;Basically, the idea of medications that act on the dopamine system is &quot;to cool down those reward pathways,&quot; Levounis says. There are two strategies for doing so: an agonist strategy, or an antagonist strategy.&lt;/p&gt;
&lt;p&gt;The agonist strategy is &quot;feeding the beast, providing activity in the cell so that the cravings go down,&quot; Levounis said. Classic examples are nicotine patches, or methadone for opioid dependence.&lt;/p&gt;
&lt;p&gt;On the other hand, the antagonist strategy is to block the receptors. Naltrexone, for example, will block opioid receptors so that the drug addict won&apos;t feel anything if he or she attempts to get high.&lt;/p&gt;
&lt;p&gt;&quot;After a while, you say, &apos;This is not worth my time, my money, my trouble,&apos; so you stop using,&quot; Levounis explains.&lt;/p&gt;
&lt;p&gt;These have been the two main strategies in addiction pharmacotherapy, but there&apos;s now a &quot;third avenue&quot;  --  the partial agonist approach.&lt;/p&gt;
&lt;p&gt;The partial agonist is one molecule that blocks most receptors while still providing just a little bit of an &quot;oomph&quot; to calm cravings. That&apos;s how varenicline (Chantix) helps smokers quit, and how buprenorphine gets junkies off heroin or other opioids.&lt;/p&gt;
&lt;p&gt;But what about inhibitory control? What if medications could ramp up will power?&lt;/p&gt;
&lt;p&gt;&quot;It&apos;s an area of active research,&quot; Levounis says. &quot;There are some medications proposed, but nothing to write home about.&quot;&lt;/p&gt;
&lt;p&gt;He said treatment is typically twofold. For addicts, psychiatrists will try to &quot;cool down&quot; the reward pathways, often with medication. Then, they target the diminished frontal lobes.&lt;/p&gt;
&lt;p&gt;&quot;We try to beef up the frontal lobes as much as we can, and we do that with psychotherapy,&quot; Levounis said.&lt;/p&gt;
&lt;p&gt;Researchers agree that psychotherapy is key to regaining self-control, and it&apos;s the predominant treatment used in patients with addictive behaviors.&lt;/p&gt;
&lt;p&gt;Mark Smaller, PhD, a psychoanalyst in private practice in Chicago, said psychotherapy often reveals an underlying cause for an addiction or compulsive behavior. Usually, it&apos;s anxiety or depression.&lt;/p&gt;
&lt;p&gt;Acknowledging those problems may help change behaviors. Once they&apos;re realized, a patient can start working against them, with the help of the brain&apos;s own neuroplasticity. Essentially, neurons can disconnect and reconnect, or loosen their connections and tighten them, which often manifests in noticeable change.&lt;/p&gt;
&lt;p&gt;&quot;[Psychological] insights can actually begin to change brain chemistry and diffuse compulsions,&quot; he said. &quot;If you address those issues, you can have a positive impact on your life that can change the chemistry of your brain.&quot;&lt;/p&gt;
&lt;p&gt;Smaller said it &quot;creates a new psychological  --  if not neurological  --  structure that can help regulate behavior.&quot;&lt;/p&gt;
&lt;p&gt;Although research on neuroplasticity is relatively young, the concept of &quot;rewiring&quot; the brain is not new.&lt;/p&gt;
&lt;p&gt;In fact, too often, the electrician metaphor has been employed as an excuse for indulging, an explanation for a New Year&apos;s resolution deferred: &quot;I can&apos;t stop eating chocolate, I&apos;m just not wired that way.&quot;&lt;/p&gt;

&lt;hr&gt;
&lt;p&gt;&lt;img src=&quot;http://www.medpagetoday.com/upload/2009/10/30/16717.jpg&quot; mce_src=&quot;http://www.medpagetoday.com/upload/2009/10/30/16717.jpg&quot; alt=&quot;&quot;&gt;&lt;em&gt; is a collaboration between &lt;/em&gt;MedPage Today &lt;em&gt;and&lt;/em&gt; ABC News&lt;em&gt;.&lt;/p&gt;
    </recommendedItem>
    <recommendedItem id="20100101_19_299"
                     title="Teen Pregnancies, Births, and Abortions Increase"
                     score="0.004"
                     href="http://www.medpagetoday.com/OBGYN/Pregnancy/tb/18162?impressionId=1265819245048"
                     
      &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_235"
                     title="Congenital Anomalies Linked to Mom&apos;s Diabetes (CME/CE)"
                     score="-0.001"
                     href="http://www.medpagetoday.com/OBGYN/Pregnancy/tb/18065?impressionId=1265819245048"
                     
      &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;
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