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<recommendedContent xmlns="http://api.mspoke.com">
    <recommendedItem id="20100101_19_355"
                     title="Obesity Delays Puberty in Boys (CME/CE)"
                     score="0.011"
                     href="http://www.medpagetoday.com/Pediatrics/Obesity/tb/18235?impressionId=1265786539095"
                     
      &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="0.01"
                     href="http://www.medpagetoday.com/Psychiatry/Addictions/tb/18207?impressionId=1265786539095"
                     
      &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_322"
                     title="Switch to Low-Fat Milk in Schools Shows Benefit"
                     score="0.007"
                     href="http://www.medpagetoday.com/PrimaryCare/DietNutrition/tb/18192?impressionId=1265786539095"
                     
      &lt;p&gt;When New York City public schools made the switch from whole milk to skim or low-fat milk, students cut their annual fat and total calorie consumption, department researchers found.&lt;/p&gt;
&lt;p&gt;Milk-drinking students consumed 5,960 fewer calories and 619 fewer grams of fat per year after they made the switch, Philip M. Alberti, PhD, of the New York Department of Health and Mental Hygiene, and colleagues reported in the Jan. 29 issue of CDC&apos;s &lt;em&gt;Morbidity &amp;amp; Mortality Weekly Report&lt;/em&gt;.&lt;/p&gt;
&lt;p&gt;At 3,500 calories per pound, the reduction would be the equivalent of 1.7 pounds of body weight over the course of a year.&lt;/p&gt;
&lt;p&gt;&quot;The switch to lower-fat milk likely has improved the overall nutritional environment of NYC public schoolchildren,&quot; Alberti and colleagues wrote.&lt;/p&gt;
&lt;p&gt;On the other hand, most of the low-fat milk consumed was chocolate milk, which has a substantially higher sugar content than unflavored milk, the researchers found.&lt;/p&gt;
&lt;p&gt;In 2005, the New York City Department of Education began reviewing its food policies and determined that replacing whole milk with fat-free or low-fat milk could decrease students&apos; fat and calorie intake.&lt;/p&gt;
&lt;p&gt;At subsequent board meetings, milk industry advocates suggested that without whole milk or chocolate- or strawberry-flavored milk, student milk consumption would decline, thus decreasing calcium and vitamin intake.&lt;/p&gt;
&lt;p&gt;Nonetheless, the Department of Education began phasing out whole milk in 2005, and limited flavored milk to fat-free chocolate milk.&lt;/p&gt;
&lt;p&gt;The researchers didn&apos;t have data on student consumption of milk, so they analyzed system-wide school milk purchases.&lt;/p&gt;
&lt;p&gt;They found that per-student school milk purchases dropped 8% between 2004 and 2006, but then gradually began to increase. By 2009, purchases had risen 1.3% from five years prior: from 112 per student in 2004 to 114 in 2009.&lt;/p&gt;
&lt;p&gt;Fat-free milk accounted for 42% of all purchases in 2009, compared with less than 7% in 2004.&lt;/p&gt;
&lt;p&gt;In 2004, students purchased more than 18 billion calories and 520 million grams of fat in the form of milk. That fell to less than 14 billion calories and 98 million grams of fat in 2009, representing a 25% and 81% decrease, respectively.&lt;/p&gt;
&lt;p&gt;Over that five-year time period, the researchers calculated that if calorie and fat savings were distributed among all students  --  including those who don&apos;t drink milk  --  they would consume 3,484 fewer calories and 382 fewer grams of fat each year.&lt;/p&gt;
&lt;p&gt;If the data were limited to students who do drink milk during the school day  --  62% of students in 2004 and 63% in 2009  --  the savings increased to 5,960 calories and 619 fat grams per year.&lt;/p&gt;
&lt;p&gt;Alberti and colleagues wrote that the data show the milk policy change reduced fat and calorie intake while still providing protein, calcium, and vitamins A and D.&lt;/p&gt;
&lt;p&gt;&quot;Other school systems can use these results to guide changes to their own school food policies,&quot; they said.&lt;/p&gt;
&lt;p&gt;They noted, however, that the majority of low-fat milk consumed  --  60% of all milk purchases  --  was chocolate milk, a concern because sweetened milk has more calories than reduced-fat white milk and contains twice as much sugar.&lt;/p&gt;
&lt;p&gt;But limiting its availability would &quot;further reduce milk consumption,&quot; they wrote.&lt;/p&gt;
&lt;p&gt;The authors noted that the study was limited because there were no data to evaluate the magnitude of the correlation between milk purchasing and milk consumption. Also, no data were collected on students&apos; diets, so the researchers could not assess the policy&apos;s larger effects on diet.&lt;/p&gt;

    </recommendedItem>
    <recommendedItem id="20100101_19_265"
                     title="How Many Calories in that Happy Meal? (CME/CE)"
                     score="0.003"
                     href="http://www.medpagetoday.com/PrimaryCare/DietNutrition/tb/18099?impressionId=1265786539095"
                     
      Putting nutrition labels on fast food may lead parents to pick lower-calorie meals for their children, researchers say.&lt;br&gt;
&lt;br&gt;In a small waiting room study, parents ordered about 20% fewer calories for their kids when they chose from a menu with nutrition information on it, Pooja Tandon, MD, of the University of Washington, and colleagues reported online in &lt;em&gt;Pediatrics&lt;/em&gt;.&lt;br&gt;
&lt;br&gt;&quot;One hundred calories over time and at a population level is actually a significant amount in terms of being able to avert weight gain,&quot; Tandon told &lt;em&gt;MedPage Today&lt;/em&gt;.&lt;br&gt;
&lt;br&gt;Many fast-food restaurants don&apos;t provide nutrition information at the point of purchase. In a recent study, just about half  --  54%  --  of the largest chains made some nutritional information available on site. The majority  --  86%  --  provided it only through their Web sites, leaving consumers clueless while ordering.&lt;br&gt;
&lt;br&gt;Labels have long been advocated as a means of lowering calorie consumption. So to determine whether nutrition labeling specifically on fast-food menus would lead to lower-calorie choices for children, the researchers conducted a randomized, controlled experiment in a primary care pediatric clinic in Seattle.&lt;p&gt;&lt;/p&gt;
&lt;p&gt;Parents of children ages 3 to 6 were given a McDonald&apos;s menu, and then asked to pick out meals anonymously&lt;strong&gt; &lt;/strong&gt;for themselves and their child.&lt;/p&gt;
&lt;p&gt;The menus were identical, with one exception: those given to parents in the intervention group included nutrition information, while the menus given to parents in the control group had none. The menus did include prices for both groups.&lt;/p&gt;
&lt;p&gt;A total of 99 parents participated between October 2008 and January 2009. Some 62% reported eating fast food one to four times over the previous month, mostly because it was quick, cheap, or fun.&lt;/p&gt;
&lt;p&gt;The researchers found that parents who were given nutritional information ordered an average of 102 fewer calories for their kids than did controls (567.1 cal versus 671.5 cal, &lt;em&gt;P&lt;/em&gt;=0.04).&lt;/p&gt;
&lt;p&gt;On average, the nutrition-labeled menu reduced total calories ordered by 20%, the researchers wrote.&lt;/p&gt;
&lt;p&gt;The difference remained significant after adjustment for gender, race, education, BMI, fast-food frequency, and child&apos;s BMI z-score (&lt;em&gt;P&lt;/em&gt;=0.004).&lt;/p&gt;
&lt;p&gt;&quot;We know that fast food consumption is rising alongside alarming rates of child obesity in this country,&quot; Tandon said. &quot;These results make me optimistic that if parents are given nutritional information at the point of ordering  --  and not on a Web site or tray liner  --  they will have the tools to make healthier, lower-calorie choices for their children.&quot;&lt;/p&gt;
&lt;p&gt;Research has suggested that even small changes in behavior that affect energy balance by about 100 calories per day could avert weight gain in most adults.&lt;/p&gt;
&lt;p&gt;Interestingly, Tandon said, there were no differences between the groups when it came to parents&apos; choices for themselves. Both ordered about the same number of calories.&lt;/p&gt;
&lt;p&gt;&quot;I&apos;m not sure exactly what&apos;s going on with this group of parents, but this is a trend we&apos;ve seen,&quot; Tandon said. &quot;I would hypothesize that there are some other factors at play when people are choosing for themselves and their children in terms of wanting children to eat healthier than they might for themselves.&quot;&lt;/p&gt;
&lt;p&gt;There was also a positive correlation between how many calories the parent ordered and how many calories he or she ordered for the child (&lt;em&gt;P&lt;/em&gt;=0.02).&lt;/p&gt;
&lt;p&gt;&quot;We do know that if a child has one or two parents who are overweight, that increases their chance of being overweight, so [obesity] probably is a combination of genetic and environmental factors,&quot; Tandon said.&lt;/p&gt;
&lt;p&gt;Tandon noted that a growing number of local and state governments have adopted restaurant menu labeling regulations, and legislation for federal labeling standards has been introduced in both the House and the Senate.&lt;/p&gt;
&lt;p&gt;&quot;At a time when menu labeling is being discussed throughout country at the national level, I think these results support the&lt;strong&gt; &lt;/strong&gt;idea that an informed parent will be able to make smarter healthier choices for their child,&quot; she added.&lt;/p&gt;
&lt;p&gt;The study was limited because it was not conducted in a real restaurant setting. Food choices are made within social and environmental contexts, Tandon said, and the results of a mock menu survey in a clinic may not fully represent that reality. A randomized experiment in a real restaurant setting would be an ideal follow-up.&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_235"
                     title="Congenital Anomalies Linked to Mom&apos;s Diabetes (CME/CE)"
                     score="-0"
                     href="http://www.medpagetoday.com/OBGYN/Pregnancy/tb/18065?impressionId=1265786539095"
                     
      &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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