<?xml version="1.0" encoding="utf-8"?>
<recommendedContent xmlns="http://api.mspoke.com">
    <recommendedItem id="20100101_19_412"
                     title="Depression During Pregnancy Linked to Kids&apos; Behavior Problems (CME/CE)"
                     score="0.013"
                     href="http://www.medpagetoday.com/Psychiatry/Depression/tb/18321?impressionId=1265744182716"
                     
      &lt;p&gt;Children born to mothers who were depressed during pregnancy were more than twice as likely to display antisocial behavior by age 16 as children whose mothers had not been depressed, researchers found.&lt;/p&gt;
&lt;p&gt;Of 120 mothers from South London who were followed from pregnancy through their children&apos;s teen years, 31% had depression during pregnancy, according to Dale Hay, PhD, of Cardiff University in Wales, and colleagues.&lt;/p&gt;
&lt;p&gt;Children born to these women were significantly more likely to display antisocial behavior (OR 2.46, 95% CI 1.10 to 5.48) and commit violent acts (OR 4.36, 95% CI 1.54 to 12.41) before age 16, the researchers reported in the January/February issue of &lt;em&gt;Child Development&lt;/em&gt;.&lt;/p&gt;
&lt;p&gt;The associations were magnified in women who also had a history of behavior problems when they were children.&lt;/p&gt;
&lt;p&gt;&quot;A focus on mothers&apos; history of conduct problems and depression during pregnancy, as opposed to broader measures of the social environment, would hold promise for more targeted early interventions to prevent the development of serious antisocial behavior,&quot; Hay&apos;s group wrote.&lt;/p&gt;
&lt;p&gt;Previous studies have linked mothers&apos; mental health problems in pregnancy with disruptive behaviors in their children, but it&apos;s unclear what explains the relationship, according to the researchers.&lt;/p&gt;
&lt;p&gt;To explore the issue, they turned to the South London Child Development Study, which prospectively followed 120 pregnant women and their children into the teenage years.&lt;/p&gt;
&lt;p&gt;All families came from a relatively disadvantaged urban area. These families were more likely to belong to the working class and to be from ethnic minority groups than the general U.K. population.&lt;/p&gt;
&lt;p&gt;One-third of the children had been arrested or diagnosed with a conduct disorder by age 16. Of these 88.9% had been arrested and 45% had committed violent acts, including theft from a person, violent disorder, fighting, carrying a weapon, and assault.&lt;/p&gt;
&lt;p&gt;The association between maternal depression during pregnancy and risk of antisocial behavior remained relatively constant in analyses controlling for family environment, a child&apos;s exposure to maternal depression after birth, mothers&apos; substance use during pregnancy, and parental antisocial behavior.&lt;/p&gt;
&lt;p&gt;None of the factors fully explained the relationship. Neither did the arrest history of the biological father.&lt;/p&gt;
&lt;p&gt;But, the researchers wrote in the paper, &quot;it would be unwise to conclude that paternal risk factors are unimportant, given that we did not have more detailed information about the father&apos;s own history of conduct disorders.&quot;&lt;/p&gt;
&lt;p&gt;They explored several potential mechanisms for the link between maternal depression and a child&apos;s behavior problems: &lt;ul&gt; &lt;li&gt;Direct effects on the fetus from biological correlates of the mothers&apos; depressive symptoms&lt;/li&gt; &lt;li&gt;Depression in pregnancy as a sign of environmental adversity&lt;/li&gt; &lt;li&gt;Re-exposure to maternal depression after birth&lt;/li&gt; &lt;li&gt;Indirect effects of depression on the developing fetus driven by mothers&apos; smoking, drinking, and drug taking during pregnancy &lt;/li&gt; &lt;li&gt;A genetic explanation whereby women who experience depression in pregnancy may also have a greater genetic risk for antisocial behavior, which they pass on to their offspring &lt;/li&gt; &lt;/ul&gt;&lt;/p&gt;
&lt;p&gt;Hay and her colleagues noted that these explanations are not necessarily mutually exclusive.&lt;/p&gt;
&lt;p&gt;They also acknowledged some limitations of the study, including the lack of information about fetal growth and neuroendocrine measures on the mother and child and the relatively small sample size.&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 SLCDS has been funded by U.K. project grants from the Medical Research Council, by the Psychiatric Research Trust, and by the South West G.P. Trust. The current analysis was partially supported by an Economic and Social Research Council studentship to one of Hay&apos;s co-authors and by a Medical Research Council U.K. Program Grant.&lt;/p&gt;&lt;p&gt;The authors did not report any 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_395"
                     title="Evidence-Based Care Cuts ADHD Symptoms, Not Impairment (CME/CE)"
                     score="0.012"
                     href="http://www.medpagetoday.com/Pediatrics/ADHD-ADD/tb/18292?impressionId=1265744182716"
                     
      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_405"
                     title="Difficult Childhood Lingers in the Mind (CME/CE)"
                     score="0.011"
                     href="http://www.medpagetoday.com/Psychiatry/GeneralPsychiatry/tb/18312?impressionId=1265744182716"
                     
      &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_372"
                     title="Low Serotonin Eyed as Mechanism for SIDS (CME/CE)"
                     score="0.01"
                     href="http://www.medpagetoday.com/Neurology/GeneralNeurology/tb/18262?impressionId=1265744182716"
                     
      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_341"
                     title="Doctor&apos;s Orders: Brain&apos;s Wiring Makes Change Hard"
                     score="0.009"
                     href="http://www.medpagetoday.com/Psychiatry/Addictions/tb/18207?impressionId=1265744182716"
                     
      &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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