<?xml version="1.0" encoding="utf-8"?>
<recommendedContent xmlns="http://api.mspoke.com">
    <recommendedItem id="20100101_19_395"
                     title="Evidence-Based Care Cuts ADHD Symptoms, Not Impairment (CME/CE)"
                     score="0.011"
                     href="http://www.medpagetoday.com/Pediatrics/ADHD-ADD/tb/18292?impressionId=1265743530712"
                     
      Adhering to guidelines when treating children with attention deficit hyperactivity disorder (ADHD) relieved symptoms but had no effect on kids&apos; performance in school or in their relationships with others, researchers found.&lt;br&gt;
&lt;br&gt;Although parents and teachers noted significant improvements in symptoms among ADHD kids (&lt;em&gt;P&lt;/em&gt;&amp;lt;0.001) in a special treatment program, there weren&apos;t similar outcomes for functional impairment, Jeffery N. Epstein, PhD, of the Center for ADHD at Cincinnati Children&apos;s Hospital in Ohio, reported in the February &lt;em&gt;Archives of Pediatrics and Adolescent Medicine&lt;/em&gt;.&lt;br&gt;
&lt;br&gt;&quot;This finding highlights the need for physicians to work with or refer patients to educational and mental healthcare specialists who can work with children to develop skills to address targeted areas of deficit,&quot; the researchers wrote.&lt;/p&gt;
&lt;p&gt;University-associated trials have shown stimulants are effective against ADHD, but these findings may not be translated into community practices  --  a potential public health concern, the researchers suggested.&lt;/p&gt;
&lt;p&gt;Guidelines for proper treatment exist, but they can be difficult to put into practice because of time, effort, and reimbursement concerns.&lt;/p&gt;
&lt;p&gt;So the researchers decided to test the efficacy of a quality improvement intervention called ADHD Collaborative, designed to enhance physician adherence to evidence-based, ADHD treatment guidelines.&lt;/p&gt;
&lt;p&gt;They conducted a case series involving 785 children ages 7 to 11, who were treated by 158 physicians at rural, suburban, and urban practices.&lt;/p&gt;
&lt;p&gt;The researchers found that, based on teacher and parent ratings, children showed vast improvements in ADHD symptoms (&lt;em&gt;P&lt;/em&gt;&amp;lt;0.001).&lt;/p&gt;
&lt;p&gt;&quot;Improvement of ADHD symptoms occurred mainly in the first three months of treatment and remained improved and relatively stable thereafter,&quot; the researchers wrote. &quot;These results suggest that community-based physicians can achieve gains in ADHD symptom improvement comparable with carefully controlled, university-based clinical trials.&quot;&lt;/p&gt;
&lt;p&gt;However, there were no significant improvements in functional impairment as measured by parents and teachers.&lt;/p&gt;
&lt;p&gt;The proportion of functionally impaired children didn&apos;t change after treatment for any outcomes except teachers&apos; ratings of writing and assignment completion (&lt;em&gt;P&lt;/em&gt;=0.03 and &lt;em&gt;P&lt;/em&gt;=0.04, respectively).&lt;/p&gt;
&lt;p&gt;&quot;Effective treatment likely requires a multimodal strategy that includes a focus on teaching children [organizational and learning] skills,&quot; they wrote, adding that collaboration with other mental health or educational services &quot;appears to be warranted.&quot;&lt;/p&gt;
&lt;p&gt;Researchers said the study was limited because it didn&apos;t have a control group. Thus, it couldn&apos;t determine whether a similar pattern of treatment response would have been observed without physician training.&lt;/p&gt;
&lt;p&gt;The lack of a control group also made it impossible to account for any potential placebo effects.&lt;/p&gt;
&lt;p&gt;Finally, the authors didn&apos;t collect data on medication adherence.&lt;/p&gt;
&lt;p&gt;Still, they concluded that &quot;large improvements in symptoms can be achieved in primary care settings when physicians provide evidence-based ADHD care using medication.&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 study was supported by the Cincinnati Children&apos;s Hospital Medical Center Patient Innovation Fund.&lt;/p&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_372"
                     title="Low Serotonin Eyed as Mechanism for SIDS (CME/CE)"
                     score="0.01"
                     href="http://www.medpagetoday.com/Neurology/GeneralNeurology/tb/18262?impressionId=1265743530712"
                     
      Low brainstem levels of serotonin and the enzyme that makes it could underlie sudden infant death syndrome (SIDS), researchers suggested.&lt;br&gt;
&lt;br&gt;In an autopsy study, SIDS cases showed 26% lower serotonin levels in two major components of the medulla&apos;s serotonin system  --  the raph&amp;#233; obscurus (&lt;em&gt;P&lt;/em&gt;=0.05) and paragigantocellularis lateralis (&lt;em&gt;P&lt;/em&gt;=0.04)  --  compared with age-adjusted controls who died from known causes.&lt;br&gt;
&lt;br&gt;These brainstem circuits control breathing, blood pressure, and heart rate during sleep, Hannah C. Kinney, MD, of Children&apos;s Hospital Boston, and colleagues reported in the Feb. 3 issue of the &lt;em&gt;Journal of the American Medical Association&lt;/em&gt;.&lt;br&gt;
&lt;br&gt;A baby with an abnormality in control of these systems might not be able to respond to a life-threatening challenge like asphyxia by rousing from sleep or turning its head the researchers explained.&lt;p&gt;&lt;/p&gt;
&lt;p&gt;SIDS occurs in the &quot;critical first year of life, when homeostatic systems are still maturing,&quot; they noted.&lt;/p&gt;
&lt;p&gt;Mary McClain, RN, MS, of Boston University Medical Center, who counsels families that have lost a baby to SIDS, commented that these findings help establish the biological basis for urging parents to place their babies on their backs to sleep.&lt;/p&gt;
&lt;p&gt;The researchers obtained tissue samples from autopsies of 41 children who died from SIDS, seven who died acutely from known causes (including a car accident, drowning, pneumonia, and unsuspected congenital heart disease), and five who died in the hospital with chronic conditions causing hypoxia-ischemia.&lt;/p&gt;
&lt;p&gt;SIDS cases had mean serotonin levels of 31.4 pmol/mg of protein in the paragigantocellularis lateralis, compared with 40.0 pmol/mg among the controls who died acutely (&lt;em&gt;P&lt;/em&gt;=0.04).&lt;/p&gt;
&lt;p&gt;Levels averaged 55.4 versus 75.5 pmol/mg of protein, respectively, in the raph&amp;#233; obscurus (&lt;em&gt;P&lt;/em&gt;=0.05).&lt;/p&gt;
&lt;p&gt;These abnormalities in the medulla did not appear to involve the catecholamine system. Catecholamine levels were similar between SIDS cases and controls.&lt;/p&gt;
&lt;p&gt;Nor was there evidence for excessive degradation of dopamine or neurotransmitter turnover in SIDS cases, supporting the idea that the key abnormality is reduced synthesis of serotonin, the researchers said.&lt;/p&gt;
&lt;p&gt;Another marker of serotonin function  --  tryptophan hydroxylase (TPH2), the key enzyme involved in synthesis of serotonin  --  also supported this conclusion, with 22% lower levels in the raph&amp;#233; obscurus in SIDS than in controls (&lt;em&gt;P&lt;/em&gt;=0.03).&lt;/p&gt;
&lt;p&gt;Serotonin receptor binding was 29% to 55% lower in three medullary nuclei that receive serotonin projections, notable for a decrease in binding with older age in SIDS cases, but not controls, the researchers noted.&lt;/p&gt;
&lt;p&gt;Given similar findings in three previous investigations, this &quot;may reflect a progressive decrease with age in those infants with the &apos;SIDS abnormality,&apos;&quot; they wrote. Or it&apos;s possible that those with a &quot;stronger abnormality take longer to outgrow the risk period for SIDS and continue to die at older ages,&quot; Kinney&apos;s group wrote.&lt;/p&gt;
&lt;p&gt;Likewise, serotonin receptor binding in infants who died from SIDS was significantly lower in those without known risk factors for SIDS, such as &lt;a href=&quot;http://www.medpagetoday.com/Pediatrics/GeneralPediatrics/17365&quot; mce_href=&quot;http://www.medpagetoday.com/Pediatrics/GeneralPediatrics/17365&quot; target=&quot;_blank&quot;&gt;sleeping face down&lt;/a&gt;, &quot;suggesting that additional risk factors are necessary to precipitate death when the medullary serotonin system is less compromised,&quot; they added.&lt;/p&gt;
&lt;p&gt;Although repetitive apnea and agonal &lt;a href=&quot;http://www.medpagetoday.com/Pulmonology/SleepDisorders/2817&quot; mce_href=&quot;http://www.medpagetoday.com/Pulmonology/SleepDisorders/2817&quot; target=&quot;_blank&quot;&gt;impaired gasping&lt;/a&gt; before death have been reported in some SIDS cases, chronic impaired oxygenation in the hospitalized children in the study produced a very different serotonin pattern than that seen in SIDS.&lt;/p&gt;
&lt;p&gt;Children who died with chronic hypoxia conditions had 55% higher serotonin levels in the raph&amp;#233; obscurus (&lt;em&gt;P&lt;/em&gt;=0.02) and 126% higher levels in the paragigantocellularis lateralis (&lt;em&gt;P&lt;/em&gt;=0.002) than the SIDS cases.&lt;/p&gt;
&lt;p&gt;They also had 640% higher dopamine levels in the raph&amp;#233; obscurus than the SIDS cases (&lt;em&gt;P&lt;/em&gt;=0.006).&lt;/p&gt;
&lt;p&gt;This suggested &quot;that the primary mechanisms underlying serotonin abnormalities in SIDS are not mediated by chronic hypoxia-ischemia,&quot; Kinney&apos;s group wrote.&lt;/p&gt;
&lt;p&gt;The researchers cautioned that their neurotransmitter measurements may have been off somewhat due to prolonged postmortem intervals.&lt;/p&gt;
&lt;p&gt;They also warned that the study was limited by inability to perform these measurements at the synapse in postmortem tissues and by the small sample of controls.&lt;/p&gt;
&lt;div style=&quot;float:left;border-style:solid;border-width:1px;border-color:#8dabbc;font-family:arial;font-size:12px;background-color:#DBE9F2;padding:5px;&quot;&gt;&lt;p&gt;The study was supported by the First Candle/SIDS Alliance, CJ Martin Overseas Fellowship (National Health and Medical Research Council of Australia), CJ Murphy Foundation for Solving the Puzzle of SIDS, CJ Foundation for SIDS, National Institute of Child Health and Development, and the Developmental Disabilities Research Center at Children&apos;s Hospital Boston.&lt;/p&gt;&lt;p&gt;The researchers reported no conflicts of interest.&lt;/p&gt;&lt;p&gt;McClain provided no information on 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_368"
                     title="Lancet Retracts 1998 MMR-Autism Paper"
                     score="0.01"
                     href="http://www.medpagetoday.com/Pediatrics/Vaccines/tb/18255?impressionId=1265743530712"
                     
      &lt;p&gt;Editors of &lt;em&gt;The Lancet&lt;/em&gt; have retracted the 1998 study that first suggested autism might be caused by the MMR vaccine, less than a week after an official rebuke to the paper&apos;s lead author, Andrew Wakefield, MBBS, and two co-authors.&lt;/p&gt;
&lt;p&gt;In a brief note posted on the journal&apos;s Web site, &lt;em&gt;Lancet&lt;/em&gt; editors wrote, &quot;It has become clear that several elements of the 1998 paper by Wakefield et al. are incorrect, contrary to the findings of an earlier investigation.... Therefore, we fully retract this paper from the published record.&quot;&lt;/p&gt;
&lt;p&gt;Evidence presented in a Jan. 28 hearing before the U.K. General Medical Council&apos;s Fitness to Practise Panel persuaded the journal that the paper had misrepresented how the study was conducted.&lt;/p&gt;
&lt;p&gt;&lt;span class=&quot;msgBody&quot;&gt;The council, which has no direct American equivalent, is an independent, nationwide regulatory body that registers doctors and enforces standards of medical practice in the U.K.&lt;/span&gt;&lt;/p&gt;
&lt;p&gt;Hospital records and other sources contradicted findings of a 2004 investigation by Wakefield&apos;s institution, the Royal Free and University College, that the study had been properly vetted by an institutional review board.&lt;/p&gt;
&lt;p&gt;&quot;The claims in the original paper that children were &apos;consecutively referred&apos; and that investigations were &apos;approved&apos; by the local ethics committee have been proven to be false,&quot; according to the &lt;em&gt;Lancet&lt;/em&gt; editors.&lt;/p&gt;
&lt;p&gt;The editor of Britain&apos;s other leading medical journal, &lt;em&gt;BMJ&lt;/em&gt;, congratulated &lt;em&gt;The Lancet&lt;/em&gt; for its action.&lt;/p&gt;
&lt;p&gt;&quot;This will help to restore faith in this globally important vaccine and in the integrity of the scientific literature,&quot; according to a statement from Fiona Godlee, MB, BChir, BSc.&lt;/p&gt;
&lt;p&gt;In the 1998 paper, Wakefield and colleagues reported on findings in 12 children who, they said, had developed intestinal inflammation and autistic symptoms following MMR vaccination. They suggested that the inflammation released gut proteins into the circulation that eventually migrated to the brain, causing permanent damage reflected in autism symptoms.&lt;/p&gt;
&lt;p&gt;The report and the ensuing mass-media publicity sparked consternation among parents and the medical community. Vaccination rates in Britain and the U.S. dropped sharply, and measles rates spiked in consequence.&lt;/p&gt;
&lt;p&gt;Although subsequent population-based research and other studies have failed to confirm a causal link between MMR vaccines and autism, a vocal group of parents of autistic children continues to insist that it is real. They call Wakefield a hero.&lt;/p&gt;
&lt;p&gt;However, a nearly decade-long investigation by a British journalist, Brian Deer, uncovered discrepancies between the &lt;em&gt;Lancet&lt;/em&gt; paper and hospital records and other sources. (See &lt;a href=&quot;http://www.medpagetoday.com/Pediatrics/Autism/12850&quot; mce_href=&quot;http://www.medpagetoday.com/Pediatrics/Autism/12850&quot; target=&quot;_blank&quot;&gt;Father of Vaccine-Autism Link Said to Have Fudged Data&lt;/a&gt;)&lt;/p&gt;
&lt;p&gt;Whereas the &lt;em&gt;Lancet&lt;/em&gt; paper indicated that, in most cases, symptoms developed within days of vaccination, the records indicated that this was true only for one child, according to Deer&apos;s account in the &lt;em&gt;Times of London&lt;/em&gt;.&lt;/p&gt;
&lt;p&gt;The patients&apos; records also indicated that five of the children had psychosocial problems before vaccination, said the &lt;em&gt;Times&lt;/em&gt;, but the &lt;em&gt;Lancet&lt;/em&gt; paper described them as &quot;developmentally normal.&quot;&lt;/p&gt;
&lt;p&gt;In addition, the &lt;em&gt;Lancet&lt;/em&gt; paper described abnormal intestinal pathology results in the children, but the hospital pathology reports showed no findings of inflammation, the &lt;em&gt;Times&lt;/em&gt; report said.&lt;/p&gt;
&lt;p&gt;At last week&apos;s hearing, the U.K.&apos;s General Medical Council panel heard evidence that Wakefield had taken blood samples from children attending his son&apos;s birthday party and performed spinal taps on other children in a hospital without due regard for their safety.&lt;/p&gt;
&lt;p&gt;The panel found Wakefield guilty of more than 30 charges that he had acted unethically in conducting the study. He could be stripped of his license to practice in Britain, but no ruling has been made yet.&lt;/p&gt;
&lt;p&gt;Two of Wakefield&apos;s 12 co-authors on the 1998 paper, John Walker-Smith, MD, and Simon Murch, PhD, were also found to have committed ethical violations. The other 10 co-authors had previously repudiated the paper&apos;s findings and were not charged.&lt;/p&gt;
&lt;p&gt;Wakefield was in London while the hearing took place but did not attend. Afterward, he told reporters he was innocent of wrongdoing and would continue his research.&lt;/p&gt;
&lt;p&gt;Wakefield is now based at Thoughtful House, a private autism research and treatment facility in Austin, Texas. After the panel&apos;s ruling, it issued a statement expressing disappointment and calling the charges &quot;unfounded and unfair.&quot;&lt;/p&gt;

    </recommendedItem>
    <recommendedItem id="20100101_19_343"
                     title="U.S. Marshals Seize Unapproved Ozone Generators"
                     score="0.009"
                     href="http://www.medpagetoday.com/PublicHealthPolicy/EnvironmentalHealth/tb/18228?impressionId=1265743530712"
                     
      &lt;p&gt;WASHINGTON  --  U.S. Marshals have seized 77 unapproved ozone generators, valued at almost $76,000 from a California device manufacturer, the FDA announced.&lt;/p&gt;
&lt;p&gt;The devices were advertised as treatments for various conditions, including cancer, AIDS, hepatitis, herpes, and other diseases, but lacked approval or efficacy data to support the claims made on their behalf, an FDA release said.&lt;/p&gt;
&lt;p&gt;The raid came after the company, Applied Ozone Systems (AOS) of Auburn, Calif., failed to respond to a voluntary recall request last December, the agency said.&lt;/p&gt;
&lt;p&gt;The FDA raised concerns that patients using AOS-IM and AOS-IMD devices will consider it an appropriate treatment for an affliction and delay or stop FDA-approved and proven medical treatments. Patients using the devices may risk infection from contamination of the applicator or catheter, the release said.&lt;/p&gt;
&lt;p&gt;The FDA recommended that healthcare professionals and consumers cease use of the devices.&lt;/p&gt;
&lt;p&gt;The agency said it obtained an inspection warrant for the company&apos;s manufacturing facilities after the owner refused to admit FDA inspectors. It said the inspection revealed several breaches of the FDA&apos;s good manufacturing practice requirements for medical devices, which had never been approved in the first place.&lt;/p&gt;
&lt;p&gt;Ozone is an unstable allotrope of oxygen with three atoms, instead of the normal two. Ozone generators produce ozone from oxygen and have consumer and industrial applications, but ozone itself is harmful to the respiratory system, even at relatively low concentrations.&lt;/p&gt;
&lt;p&gt;Instructions with the Applied Ozone Systems devices suggest blowing ozoned air into the rectal and vaginal areas.&lt;/p&gt;
&lt;p&gt;Friday&apos;s seizure was part of a joint effort of the FDA and the California Department of Public Health to remove or prevent unapproved or unsafe medical devices from entering the market.&lt;/p&gt;
&lt;p&gt;A statement on the company&apos;s Web site said the two ozone generator models, which sold for $750 and $1,200 respectively, were no longer available by order of the FDA and California authorities.&lt;/p&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=1265743530712"
                     
      &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;

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