<?xml version="1.0" encoding="utf-8"?>
<recommendedContent xmlns="http://api.mspoke.com">
    <recommendedItem id="20100101_19_405"
                     title="Difficult Childhood Lingers in the Mind (CME/CE)"
                     score="0.01"
                     href="http://www.medpagetoday.com/Psychiatry/GeneralPsychiatry/tb/18312?impressionId=1265752022750"
                     
      &lt;p&gt;Adversities faced in childhood have effects on mental health far into the future, researchers affirmed.&lt;/p&gt;
&lt;p&gt;Mental illness in adulthood was increasingly likely the more traumas faced in childhood, Ronald C. Kessler, PhD, of Harvard, and colleagues reported in the February issue of the &lt;em&gt;Archives of General Psychiatry&lt;/em&gt;.&lt;/p&gt;
&lt;p&gt;Childhood difficulties potentially explained 32.4% of all the psychiatric disorders examined, they said, based on analyses of the National Comorbidity Survey Replication.&lt;/p&gt;
&lt;p&gt;Adversities relating to family dysfunction  --  substance-abusing parents, sexual or physical abuse in the home, neglect, etc.  --  appeared to have the strongest link to onset and persistence of psychiatric disorders, they reported.&lt;/p&gt;
&lt;p&gt;These findings match folk wisdom and decades of research into the negative effects of child maltreatment, commented John McGrath, MD, PhD, of the Queensland Centre for Mental Health Research in Wacol, Australia, and colleagues in an accompanying editorial.&lt;/p&gt;
&lt;p&gt;But the lack of specificity between certain exposures to particular mental health outcomes  --  such as the death of one&apos;s mother leading to depression  --  was notable, the editorialists said.&lt;/p&gt;
&lt;p&gt;&quot;Thus, childhood trauma upsets the orderly psychological and biological cascades of development, leaving the affected individual at increased risk of a wide range of adverse mental health outcomes,&quot; they wrote.&lt;/p&gt;
&lt;p&gt;Rather than continue to rehash the epidemiology, it&apos;s time to focus on prevention and intervention, McGrath&apos;s group emphasized.&lt;/p&gt;
&lt;p&gt;&quot;It is unrealistic to think that we could protect all children from all adversities, but can we identify factors that bolster resilience and focus our efforts on the most vulnerable subgroups?&quot; they asked.&lt;/p&gt;
&lt;p&gt;The researchers examined joint associations of 12 retrospectively reported childhood adversities with lifetime incidence of disorders meeting Diagnostic and Statistical Manual of Mental Disorders (DSM-IV) criteria in the National Comorbidity Survey Replication I, a cross-sectional survey of a nationally-representative sample of adults in 9,282 American households.&lt;/p&gt;
&lt;p&gt;Among the respondents, 53.4% reported at least one childhood adversity, most commonly parental divorce (17.5%), family violence (14.0%), family economic problems (10.6%), and parental mental illness (10.3%).&lt;/p&gt;
&lt;p&gt;These adversities were all individually and significantly linked to first onset of psychiatric disorders with odds ratios of 1.5 to 1.9 for dysfunctional family factors (physical abuse, sexual abuse, neglect, parental mental illness, parental substance abuse, parental criminality, or family violence) and 1.0 to 1.5 for other factors like life-threatening childhood physical illness, extreme poverty, parental divorce, or loss of or separation from parents.&lt;/p&gt;
&lt;p&gt;Despite some apparent but not significantly meaningful variation in type of adversity with type of psychiatric disorder, the researchers said they could rule out that all types were the same for future mental health risk (&lt;em&gt;P&lt;/em&gt;&amp;lt;0.001).&lt;/p&gt;
&lt;p&gt;Problems tended to cluster, though. Among people who faced one adversity in childhood, 51.2% to 95.1% faced others as well, depending on the adversity.&lt;/p&gt;
&lt;p&gt;Risk of mental illness rose with number of issues faced in childhood from an odds ratio of 1.3 for one up to 3.4 for six and 3.2 for seven or more adversities.&lt;/p&gt;
&lt;p&gt;&quot;This subadditive pattern has important implications for intervention because it means that prevention or amelioration of only a single childhood adversity in youths exposed to many childhood adversities is unlikely to have important preventive effects,&quot; the researchers wrote.&lt;/p&gt;
&lt;p&gt;Overall, childhood adversities were projected to account for 44.6% of childhood-onset disorders, 32.0% of adolescent-onset disorders, and 28.6% of adult-onset disorders.&lt;/p&gt;
&lt;p&gt;The researchers also looked at persistence through the second part of the National Comorbidity Survey Replication which went beyond just core diagnostic assessment in 5,692 respondents.&lt;/p&gt;
&lt;p&gt;In a complex multivariate interactive analysis, childhood adversity from dysfunctional family factors appeared significantly linked to persistence in a given year (&lt;em&gt;P&lt;/em&gt;&amp;lt;0.001) whereas the number of factors was not significant.&lt;/p&gt;
&lt;p&gt;These significant factors were parental mental illness, physical abuse, sexual abuse, and neglect, but they carried modest effects individually with odds ratios of 1.2.&lt;/p&gt;
&lt;p&gt;But in one simulation, not being exposed to childhood trauma would only increase the time since the most recent episode of psychiatric illness by 1.6%, suggesting &quot;quite modest&quot; substantive importance in determining persistence.&lt;/p&gt;
&lt;p&gt;&quot;These results indirectly suggest that the public health implications of childhood adversities are greater for primary than for secondary prevention because the associations of childhood adversities with disorder onset are much stronger than the associations with persistence,&quot; Kessler&apos;s group wrote.&lt;/p&gt;
&lt;p&gt;The researchers cautioned that recall bias may have limited their study such that the results could be considered an &quot;upper bound&quot; for the real association and that the study could not prove causality.&lt;/p&gt;
&lt;div style=&quot;float:left;border-style:solid;border-width:1px;border-color:#8dabbc;font-family:arial;font-size:12px;background-color:#DBE9F2;padding:5px;&quot;&gt;&lt;p&gt;The National Comorbidity Survey Replication is supported by a grant from the National Institute of Mental Health with supplemental support from the National Institute on Drug Abuse, the Substance Abuse and Mental Health Services Administration, a grant from the Robert Wood Johnson Foundation, and the John W. Alden Trust.&lt;/p&gt;&lt;p&gt;The analyses were supported by a grant from the NIMH; the John D. and Catherine T. MacArthur Foundation; the Pfizer Foundation; grants from the U.S. Public Health Service; an award from the Fogarty International Center; the Pan American Health Organization; Eli Lilly; Ortho-McNeil Pharmaceutical; GlaxoSmithKline; and Bristol-Myers Squibb.&lt;/p&gt;&lt;p&gt;Kessler reported financial conflicts of interest with GlaxoSmithKline, Kaiser Permanente, Pfizer, sanofi-aventis, Shire Pharmaceuticals, Wyeth-Ayerst, Eli Lilly, Bristol-Myers Squibb, Johnson &amp;amp; Johnson Pharmaceuticals, and Ortho-McNeil Pharmaceutical.&lt;/p&gt;&lt;p&gt;The editorialists reported no conflicts of interest.&lt;/p&gt;&lt;/div&gt;&lt;div style=&quot;clear:both;&quot;&gt;&lt;/div&gt;
    </recommendedItem>
    <recommendedItem id="20100101_19_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=1265752022750"
                     
      &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_346"
                     title="Daytime Sleepiness More Common in Young (CME/CE)"
                     score="0.007"
                     href="http://www.medpagetoday.com/PrimaryCare/SleepDisorders/tb/18221?impressionId=1265752022750"
                     
      &lt;p&gt;Compared with 20-somethings and seniors, middle-age adults are less likely to suffer daytime sleepiness when they don&apos;t get a good night&apos;s sleep, according to a small study.&lt;/p&gt;
&lt;p&gt;When three groups of healthy adults  --  young (20 to 30 years old), middle-age (40 to 55) and older (66 to 83)  --  were studied over four nights, slow wave sleep decreased and the number of nocturnal awakenings progressively increased with age, wrote Derk-Jan Dijk, PhD, of the Surrey Sleep Center at the University of Surrey in Guildford, England, and colleagues in the Feb. 1 issue of &lt;em&gt;Sleep.&lt;/em&gt;&lt;/p&gt;

&lt;p&gt;As the likelihood for eight hours of uninterrupted deep sleep decreased with age, there was no increase in the likelihood of daytime sleepiness, which led Dijk and colleagues to conclude that as people age there may be a change in the &quot;sleep (duration and depth) required to maintain alertness.&quot;&lt;/p&gt;
&lt;p&gt;Based on that observation, the authors wrote that it could be argued that &quot;an eight-hour episode rich in [slow wave sleep] is insufficient for young adults but that an eight-hour sleep episode with less [slow wave sleep] is sufficient for older adults.&quot;&lt;/p&gt;
&lt;p&gt;As a result, middle-age and older adults are less likely to build up &quot;sleep debt&quot; during the daylight hours, so they manage with less time in deep sleep at night, less homeostatic sleep pressure.&lt;/p&gt;
&lt;p&gt;The authors hypothesized that this apparent need for less sleep may be a factor in age-related insomnia.&lt;/p&gt;
&lt;p&gt;If older adults are unaware of the need for less sleep, &quot;their self-selected time in bed, which provides an input to the sleep homeostat, may become maladaptive and lead to reduced sleep consolidation and associated complaints.&quot;&lt;/p&gt;
&lt;p&gt;Dijk and colleagues recruited 44 young adults, 35 middle-age adults, and 31 older adults for their study. All were healthy at baseline and all were initially assessed for an eight-hour nocturnal sleep episode.&lt;/p&gt;
&lt;p&gt;They were then randomized to two nights of either selective short wave sleep interruption by acoustic stimuli or sleep without disruption, followed by one night of recovery sleep.&lt;/p&gt;
&lt;p&gt;Two standardized measurement tools, the Multiple Sleep Latency Test (MSLT) and the Karolinska Sleepiness Scale (KSS), were used to assess objective and subjective sleep propensity.&lt;/p&gt;
&lt;p&gt;&quot;Total sleep time per eight hour time in bed decreased significantly and progressively across the age groups such that older adults slept approximately 20 minutes less than middle-aged, who slept 23 minutes less than young adults,&quot; they wrote.&lt;/p&gt;
&lt;p&gt;The reduction in total sleep time &quot;was primarily related to an increase in the number of awakenings and the duration of wakefulness after sleep onset, rather than an increase in latency to sleep onset.&quot;&lt;/p&gt;
&lt;p&gt;As a result, sleep efficiency decreased significantly from 92.1% for the youngest group, to 82% for the older group (effect of age, &lt;em&gt;P&amp;lt;&lt;/em&gt;0.0001).&lt;/p&gt;
&lt;p&gt;The subjective sleep propensity tests revealed that &quot;young people were significantly sleepier than the middle-age people, who were the least sleepy of the three groups.&quot; Daytime sleepiness for the oldest group &quot;fell in between the other two groups [and] was not significantly different from either.&quot;&lt;/p&gt;
&lt;p&gt;All three groups, regardless of age, demonstrated increased daytime sleepiness following a night of experimental disruption of slow wave sleep, but when the participants had an uninterrupted eight hours of deep sleep, it was only the youngest group that was drowsy during the daytime hours.&lt;/p&gt;
&lt;p&gt;The authors noted that although there was less daytime sleepiness among middle-age and older adults in this study, sleep propensity was not measured during the evening hours, so it was possible that the age-related difference might diminish at twilight.&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 sponsored by H. Lundbeck A/S.&lt;/p&gt;&lt;p&gt;Dijk reported receiving research support from the Air Force Office of Scientific Research, the Biotechnology and Biological Sciences Research Council, GlaxoSmithKline, H. Lundbeck A/S, Merck, Pfizer, Philips Lighting, sanofi-aventis, and Takeda.&lt;/p&gt;&lt;/div&gt;&lt;div style=&quot;clear:both;&quot;&gt;&lt;/div&gt;
    </recommendedItem>
    <recommendedItem id="20100101_19_261"
                     title="Scrubbing Away Germs Can Backfire on Backsides (CME/CE)"
                     score="0.001"
                     href="http://www.medpagetoday.com/Pediatrics/GeneralPediatrics/tb/18121?impressionId=1265752022750"
                     
      Rashes from toilet seats are once again afflicting American children, and the rare condition is often misdiagnosed, which may delay proper treatment.&lt;br&gt;
&lt;br&gt;That&apos;s the conclusion from a report based of five-cases of toilet-seat contact dermatitis investigated by researchers at Johns Hopkins University School of Medicine and reported in the Jan. 25 issue of &lt;em&gt;Pediatrics&lt;/em&gt;.&lt;br&gt;
&lt;br&gt;While toilet-seat dermatitis is commonly thought to result from allergies to wooden seats, the report concludes that another source is plastic toilet seats cleaned with harsh detergents.&lt;/p&gt;
&lt;p&gt;&quot;This case series and previous reports have documented that toilet-seat dermatitis is much more common than previously recognized in the U.S. and around the world,&quot; Bernard A. Cohen, MD, and colleagues wrote.&lt;/p&gt;
&lt;p&gt;&quot;Furthermore, the incidence of this condition is rising in North America because of a resurgent popularity of exotic-wood toilet seats and frequent use of detergents that contain highly irritant/sensitizing compounds such as quaternary ammonium compounds, phenol, formaldehyde, etc. in public restrooms.&quot;&lt;/p&gt;
&lt;p&gt;Of the cases analyzed by the authors, two occurred in the U.S. and the other three occurred in India.&lt;/p&gt;
&lt;p&gt;Both U.S. cases were girls, a 6-year-old who had a rash for over two years before it was correctly diagnosed and a 10-year-old whose rash lasted for a year. In both cases, the rashes seemed to worsen during the school year when the girls were using school restrooms. The younger girl&apos;s dermatitis twice became infected with methicillin-resistant &lt;em&gt;Staphylococcus aureus &lt;/em&gt;and required treatment with antibiotics.&lt;/p&gt;
&lt;p&gt;After doctors determined the rashes were the result of contact with toilet seats and instructed the girls to use toilet-seat covers and apply moisturizers and topical steroids to the affected areas, the eruptions cleared up within a few weeks.&lt;/p&gt;
&lt;p&gt;The cases in India included a 14-month old boy and two girls, 12 and 10.&lt;/p&gt;
&lt;p&gt;The boy and the 12-year-old girl were both initially misdiagnosed with ringworm and unsuccessfully treated with clotrimazole cream. The other girl was unsuccessfully treated with ayurvedic and homeopathic topical medications before doctors diagnosed toilet-seat dermatitis. Two of the children were instructed to use soaps that only exacerbated the problem.&lt;/p&gt;
&lt;p&gt;In all three cases, the rashes cleared up with some combination of topical steroids, using toilet-seat covers, replacing the household toilet seat, and limiting time on the toilet.&lt;/p&gt;
&lt;p&gt;The authors distinguished between two types of toilet-seat dermatitis: allergic contact dermatitis, the better described form of the condition, in which a patient develops allergy to wooden toilet seats, and irritant contact dermatitis, in which the rashes result from contact with harsh detergents used on plastic toilet seats.&lt;/p&gt;
&lt;p&gt;They noted that detergents used in public restrooms and in hospitals are potentially more irritating to the skin than those used at home and that alkaline detergents are more likely to cause skin irritation than acidic detergents, because they perturb the body&apos;s natural acidic environment.&lt;/p&gt;
&lt;p&gt;Toilet-seat dermatitis was first identified as an external skin rash in 1927. Exposure to wooden toilet seats and associated varnish, lacquers, and paints led to sensitization and development of an allergic contact dermatitis.&lt;/p&gt;
&lt;p&gt;The condition nearly disappeared in the U.S. in 1980s and 1990s, after public facilities and homeowners in the U.S. changed from wooden to plastic toilet seats and sanitary seat covers became readily available.&lt;/p&gt;
&lt;p&gt;However, in recent years the number of cases has grown as a result of homeowners installing toilet seats made of exotic woods and the increased use of harsh toilet seat detergents.&lt;/p&gt;
&lt;p&gt;Most reports have focused on adults with rashes, but little previous attention has focused on the condition in children. &quot;In this case series we describe toilet-seat contact dermatitis in children and underscore a typical history and physical findings that we hope will aid clinicians in recognizing this disease,&quot; the authors wrote.&lt;/p&gt;
&lt;p&gt;&quot;It is important to underscore that regular use of toilet-seat covers is the key to success in treatment,&quot; the authors wrote. &quot;Such seat covers can be purchased at any major retailer such as Walmart or online.&lt;/p&gt;
&lt;p&gt;As an alternative, newspaper cutouts could be used to provide barrier protection. Although it is possible to develop an allergy to toilet-seat covers, none have been reported thus far in the literature.&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 reported no sources of funding or 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_235"
                     title="Congenital Anomalies Linked to Mom&apos;s Diabetes (CME/CE)"
                     score="-0.003"
                     href="http://www.medpagetoday.com/OBGYN/Pregnancy/tb/18065?impressionId=1265752022750"
                     
      &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>