<?xml version="1.0" encoding="utf-8"?>
<recommendedContent xmlns="http://api.mspoke.com">
    <recommendedItem id="20100101_19_443"
                     title="Evidence-Based Treatment Improves Older Stroke Victims&apos; Chances (CME/CE)"
                     score="0.012"
                     href="http://www.medpagetoday.com/Cardiology/Strokes/tb/18360?impressionId=1265776649207"
                     
      &lt;p&gt;Older stroke patients remain at higher risk for adverse outcomes than younger ones, but the gap has narrowed with wider implementation of evidence-based guidelines, researchers say.&lt;/p&gt;
&lt;p&gt;More than 10% of stroke patients over 80 died in the hospital, compared with 3% of those under age 50, Gregg C. Fonarow, MD, of the University of California Los Angeles, and colleagues reported online in &lt;em&gt;Circulation&lt;/em&gt;.&lt;/p&gt;
&lt;p&gt;But overall use of guideline-recommended therapies improved substantially in older patients from 2003 to 2009, particularly for patients over 90, they said.&lt;/p&gt;
&lt;p&gt;During that time, several hospitals and stroke centers have adopted &quot;Get with the Guidelines,&quot; an intervention to apply evidence-based guidelines to care. Adopters have seen &quot;substantial improvements ... in performance measures for ischemic stroke patients, including pharmacological and nonpharmacological management in each age group,&quot; the researchers wrote.&lt;/p&gt;
&lt;p&gt;Before launching the initiative in 2003, studies generally showed lower use of guideline-recommended therapy and worse outcomes in older stroke patients.&lt;/p&gt;
&lt;p&gt;To assess changes since initiative started, the researchers analyzed more than 502,036 ischemic stroke admissions to 1,256 hospitals participating in the guidelines program between 2003 and 2009. Mean patient age was 71, and 52.5% were women.&lt;/p&gt;
&lt;p&gt;They found that performance on most evidence-based measures was lower in older patients  --  those ages 80 and up  --  compared with younger patients.&lt;/p&gt;
&lt;p&gt;The largest differences were seen in the proportion of eligible patients who received intravenous tissue plasminogen activator (tPA) treatments (51.1% for older patients versus 61.6% for those under 50, &lt;em&gt;P&lt;/em&gt;&amp;lt;0.001).&lt;/p&gt;
&lt;p&gt;Providers were also less likely to treat older stroke patients with lipid-lowering therapies than younger patients (54.2% versus 71.7%, &lt;em&gt;P&lt;/em&gt;&amp;lt;0.001).&lt;/p&gt;
&lt;p&gt;The smallest differences involved antithrombotic therapy within 48 hours of admission and at discharge.&lt;/p&gt;
&lt;p&gt;In terms of outcomes, older patients had a significantly higher inhospital mortality rate (10.3% versus 3%), and they were less likely to be discharged home. Rather, they were more likely to be discharged to a skilled nursing facility (42.1% versus 5.3%, &lt;em&gt;P&lt;/em&gt;&amp;lt;0.001) or hospice (12% versus 0.5%, &lt;em&gt;P&lt;/em&gt;&amp;lt;0.001).&lt;/p&gt;
&lt;p&gt;With each 10-year age increase, patients with ischemic stroke were 31% less likely to be discharged home and 27% more likely to die in the hospital.&lt;/p&gt;
&lt;p&gt;But the researchers said that, generally, the use of guideline-recommended therapies improved substantially in older patients from 2003 to 2009.&lt;/p&gt;
&lt;p&gt;In those ages 90 and older, use of intravenous tPA increased threefold, from 20.4% in 2003 to 62.4% in 2009. And use of lipid lowering therapy increased from 15.6% in 2003 to 71.7%.&lt;/p&gt;
&lt;p&gt;The researchers wrote that by 2009, &quot;many of the age-related differences in care had narrowed or were eliminated.&quot;&lt;/p&gt;
&lt;p&gt;They cautioned, however, that there could be residual confounding by unmeasured factors. For example, physicians may be uncertain about risks versus benefits in treating older patients who are under-represented in RCTs.&lt;/p&gt;
&lt;p&gt;The authors noted that their study was limited by its reliance on the accuracy and completeness of medical records.&lt;/p&gt;
&lt;p&gt;Also, they noted, the &quot;Get with the Guidelines&quot; program tends to attract larger teaching hospitals, which already have a &quot;strong interest in stroke care and quality improvement,&quot; and thus the findings may not be generalizable.&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 &quot;Get with the Guidelines&quot; program is supported by the American Heart Association and the American Stroke Association, as well as grants from Pfizer and the Merck-Schering Plough Partnership.&lt;/p&gt;&lt;p&gt;Fonarow reported relationships with Pfizer, Merck/Schering Plough, BMS/Sanofi.&lt;/p&gt;&lt;p&gt;Co-authors reported relationships with Boehringer Ingelheim, Ferrer, CoAxia, Talecris, Concentric Medical, and Cygnis.&lt;/p&gt;&lt;/div&gt;&lt;div style=&quot;clear:both;&quot;&gt;&lt;/div&gt;
    </recommendedItem>
    <recommendedItem id="20100101_19_463"
                     title="AAPM: Online Program Helps Manage Pain (CME/CE)"
                     score="0.012"
                     href="http://www.medpagetoday.com/MeetingCoverage/AAPM/tb/18393?impressionId=1265776649207"
                     
      &lt;p&gt;SAN ANTONIO  --  A personalized, online self-management program helped patients with pain syndromes improve coping skills and reduce stress and depression in two studies reported here.&lt;/p&gt;
&lt;p&gt;Patients randomized to the self-management program demonstrated significant improvement in multiple social, emotional, and behavioral outcomes after six months (&lt;em&gt;P&lt;/em&gt;&amp;lt;0.05 to &lt;em&gt;P&lt;/em&gt;&amp;lt;0.01). Improvement in some parameters occurred within one month. A control group that was not exposed to the program showed no significant improvement.&lt;/p&gt;
&lt;p&gt;&quot;Our goal is to help people communicate better with providers, understand better how they can use social support, understand the comorbid conditions, like anxiety and depression, and develop cognitive skills to help get them through their pain episodes,&quot; said Emil Chiauzzi, PhD, of Inflexxion, the Newton, Mass. company that developed the program.&lt;/p&gt;
&lt;p&gt;Although the studies involved patients with migraine or low-back pain, programs are being developed for other types of pain condition, including several forms of neuropathic pain.&lt;/p&gt;
&lt;p&gt;The online program, demonstrated at &lt;a href=&quot;http://www.painACTION.com&quot; mce_href=&quot;http://www.painACTION.com&quot; target=&quot;_blank&quot;&gt;www.painACTION.com&lt;/a&gt;, employs patient-specific information to generate individualized self-management strategies.&lt;/p&gt;
&lt;p&gt;Patient responses to assessments are analyzed by a &quot;recommendation engine,&quot; which produces content recommendations designed to address each patient&apos;s informational and self-management needs.&lt;/p&gt;
&lt;p&gt;Elements on the Web site include multimedia education units, a pain inventory, interactive tools that provide information based on patient-provider communication, and medication risk management.&lt;/p&gt;
&lt;p&gt;&quot;The content on the Web site is focused on teaching people practical skills to manage the behavioral side of pain,&quot; Jonas Bromberg, PsyD, also of Inflexxion, said in an interview.&lt;/p&gt;
&lt;p&gt;Bromberg presented results of a randomized study involving 210 patients, all of whom met International Headache Society diagnostic criteria for migraine, with or without aura.&lt;/p&gt;
&lt;p&gt;Patients assigned to the online program completed at least eight 30-minute session during the first month of the study and at least five more 30-minute sessions during the five-month follow-up period. Patients in the control group continued to receive usual care without exposure to the Web site.&lt;/p&gt;
&lt;p&gt;Participants assigned to the online program had a minimum set of requirements for each session, which were provided at log-in. Follow-up assessments occurred at one, three, and six months.&lt;/p&gt;
&lt;p&gt;The two groups were balanced with respect to sex and headache frequency and severity, the researchers said.&lt;/p&gt;
&lt;p&gt;Bromberg reported that patients assigned to the self-management program demonstrated significant improvement in: &lt;ul&gt; &lt;li&gt;Headache self-efficacy (&lt;em&gt;P&lt;/em&gt;&amp;lt;0.01 compared with baseline)&lt;/li&gt; &lt;li&gt;Use of relaxation (&lt;em&gt;P&lt;/em&gt;&amp;lt;0.05 to &lt;em&gt;P&lt;/em&gt;&amp;lt;0.01)&lt;/li&gt; &lt;li&gt;Use of social support (&lt;em&gt;P&lt;/em&gt;&amp;lt;0.01)&lt;/li&gt; &lt;li&gt;Pain catastrophizing (&lt;em&gt;P&lt;/em&gt;&amp;lt;0.01)&lt;/li&gt; &lt;li&gt;Depression (&lt;em&gt;P&lt;/em&gt;&amp;lt;0.05 to &lt;em&gt;P&lt;/em&gt;&amp;lt;0.01)&lt;/li&gt; &lt;li&gt;Stress (&lt;em&gt;P&lt;/em&gt;&amp;lt;0.01)&lt;/li&gt; &lt;/ul&gt;&lt;/p&gt;
&lt;p&gt;Chiauzzi presented results from a randomized study of 209 patients with low-back pain. The design was similar to that of the migraine study, except results were analyzed for between-group differences.&lt;/p&gt;
&lt;p&gt;The results showed significant improvement in the study group versus control group with respect to: &lt;ul&gt; &lt;li&gt;Stress (&lt;em&gt;P&lt;/em&gt;&amp;lt;0.01)&lt;/li&gt; &lt;li&gt;Coping (&lt;em&gt;P&lt;/em&gt;&amp;lt;0.01)&lt;/li&gt; &lt;li&gt;Social supports (&lt;em&gt;P&lt;/em&gt;&amp;lt;0.05)&lt;/li&gt; &lt;/ul&gt;&lt;/p&gt;
&lt;p&gt;The data showed significant effects of both treatment (&lt;em&gt;P&lt;/em&gt;&amp;lt;0.01) and time (&lt;em&gt;P&lt;/em&gt;&amp;lt;0.01) favoring the Web site versus control. Chiauzzi said patients assigned to the Web site had greater mean improvement at posttest, three months, and six months.&lt;/p&gt;
&lt;p&gt;Qualitative analysis suggested that Web site participants had clinically meaningful improvement in depression, anxiety, and stress.&lt;/p&gt;
&lt;p&gt;Additionally, patients in the self-management program reported a 12.3% decrease in pain from baseline, versus 7% in the control group.&lt;/p&gt;
&lt;p&gt;Access to the Web site did not improve physical functioning.&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 studies were funded by the National Institutes of Health.&lt;/p&gt;&lt;p&gt;Chiauzzi and Bromberg are employees of Inflexxion, developer of the online program.&lt;/p&gt;&lt;/div&gt;&lt;div style=&quot;clear:both;&quot;&gt;&lt;/div&gt;
    </recommendedItem>
    <recommendedItem id="20100101_19_346"
                     title="Daytime Sleepiness More Common in Young (CME/CE)"
                     score="0.008"
                     href="http://www.medpagetoday.com/PrimaryCare/SleepDisorders/tb/18221?impressionId=1265776649207"
                     
      &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_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=1265776649207"
                     
      &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_323"
                     title="Peptide Predicts Heart Failure in Older Patients (CME/CE)"
                     score="0.005"
                     href="http://www.medpagetoday.com/Cardiology/CHF/tb/18193?impressionId=1265776649207"
                     
      &lt;p&gt;Serial measurement of a natriuretic peptide predicted the risk of heart failure and cardiovascular death in older patients who were initially free of heart failure, data from a longitudinal cohort study showed.&lt;/p&gt;
&lt;p&gt;An increase of more than 25% in levels of N-terminal pro-B type natriuretic peptide (NT-proBNP) doubled the risk of heart failure and cardiovascular death. In contrast, a more than 25% decrease in NT-proBNP was associated with a greater than 40% reduction in the risk of both end points.&lt;/p&gt;
&lt;p&gt;&quot;NT-proBNP levels frequently change over time, and these fluctuations reflect dynamic changes in cardiovascular risk,&quot; Christopher R. deFilippi, MD, of the University of Maryland in Baltimore, and co-authors concluded in an article in the Feb. 2 issue of the &lt;em&gt;Journal of the American College of Cardiology&lt;/em&gt;.&lt;/p&gt;
&lt;p&gt;&quot;This change in [NT-proBNP] level reflects a significant change in patient risk independent of cardiovascular risk factors, ejection fraction, or medication use,&quot; they added. &quot;Ultimately, NT-proBNP levels may guide further diagnostic testing or potential preventive measures to reduce the risk of developing heart failure or dying of cardiovascular disease.&quot;&lt;/p&gt;
&lt;p&gt;About 80% of cardiovascular deaths occur in older adults. Assessing cardiovascular risk in older patients is challenging because traditional cardiovascular risk factors are less predictive in older versus middle-age populations, the authors wrote.&lt;/p&gt;
&lt;p&gt;Subclinical cardiovascular disease is common among older adults and increases the risk of cardiovascular events, including heart failure. Repeated measures of traditional markers of cardiovascular disease in patients with subclinical disease are associated with increased risk compared with patients who remain free of identifiable disease, the authors continued.&lt;/p&gt;
&lt;p&gt;Levels of BNP and NT-proBNP are associated with long-term cardiovascular outcomes in the general population. However, the peptides&apos; ability to provide additional prognostic information beyond that of traditional risk factors remained controversial.&lt;/p&gt;
&lt;p&gt;To examine the prognostic value of NT-proBNP in an older population, deFilippi and colleagues analyzed data on 3,000 participants in the Cardiovascular Health Study. The authors hypothesized that NT-proBNP levels in an ambulatory population of older patients would independently predict new-onset heart failure and cardiovascular death.&lt;/p&gt;
&lt;p&gt;&quot;Furthermore, we anticipated that serial measurements of NT-proBNP, as a possible surrogate for change in subclinical disease status, identify a dynamic change in long-term risk of incident heart failure and cardiovascular mortality,&quot; the authors wrote.&lt;/p&gt;
&lt;p&gt;Stored serum samples obtained at enrollment and two to three years later were used to measure NT-proBNP levels. Median follow-up for the cohort was 11.9 years.&lt;/p&gt;
&lt;p&gt;After separating the study group into quintiles of NT-proBNP levels, investigators found that patients with the highest baseline levels of the peptide (&amp;gt;267.7 pg/mL) had a threefold greater risk of new-onset heart failure (HR 3.05, 95% CI 2.46 to 3.78) and cardiovascular death (HR 3.02, 95% CI 2.36 to 3.86) compared with patients in the lowest NT-proBNP quintile (&amp;lt;47.5 pg/mL).&lt;/p&gt;
&lt;p&gt;The researchers identified 190 pg/mL as the NT-proBNP threshold for increased risk. Among study participants with baseline levels less than 190 pg/mL, an increase greater than 25% to a level above 190 pg/mL had a twofold increased risk of heart failure (HR 2.13, 95% CI 1.68 to 2.71) and cardiovascular death (HR 1.91, 95% CI 1.43 to 2.53) compared with participants whose NT-proBNP levels remained below 190 pg/mL.&lt;/p&gt;
&lt;p&gt;Among study participants with elevated baseline NT-proBNP levels, an increase greater than 25% also doubled the risk of heart failure (HR 2.06, 95% CI 1.56 to 2.72) and cardiovascular disease (HR 1.88, 95% CI 1.37 to 2.57).&lt;/p&gt;
&lt;p&gt;A decrease greater than 25% from baseline significantly reduced the risk of heart failure (HR 0.58, 95% CI 0.36 to 0.93) and cardiovascular death (HR 0.57, 95% CI 0.32 to 1.01) compared with participants whose baseline levels remained elevated.&lt;/p&gt;
&lt;p&gt;The investigators noted limitations of the study including the fact that a quarter of the participants did not have a follow-up blood sample and those who did were younger and had fewer cardiac risk factors.&lt;/p&gt;
&lt;p&gt;In addition, the length of follow-up could not account for differences in treatment over time, and the accuracy of NT-proBNP levels in samples as much as 20 years old cannot be assured.&lt;/p&gt;
&lt;p&gt;The study is noteworthy for highlighting the concept of dynamic risk assessment based on serial measurement of NT-proBNP, Richard W. Troughton, MB ChB, PhD, Matthew G. Daly, MB ChB, and Christopher M. Frampton, PhD, of the University of Otago in Christchurch, New Zealand, wrote in an editorial.&lt;/p&gt;
&lt;p&gt;&quot;The findings confirm a modest improvement in risk stratification by including a single measurement of NT-proBNP levels,&quot; they wrote &quot;The investigators take this a step further by showing that serial NT-proBNP measurement at a later time provides a further modest improvement in risk stratification.&quot;&lt;/p&gt;
&lt;p&gt;&quot;Whether the improvement in risk stratification achieved by performing serial NT-proBNP testing crosses a threshold of definite clinical value needs further evaluation, with particular consideration of the cost-effectiveness of such a strategy,&quot; they added.&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 National Institutes of Health, University of Pittsburgh, and Roche Diagnostics.&lt;/p&gt;&lt;p&gt;DeFilippi disclosed relationships with Siemens, Roche Diagnostics, BG Medicine, and Critical Diagnostics. Co-author Robert H. Christenson disclosed relationships with Roche Diagnostics, Siemens Healthcare Diagnostics, and Response Biomedical. Co-author Stephen L. Seliger disclosed a relationship with Roche.&lt;/p&gt;&lt;/div&gt;&lt;div style=&quot;clear:both;&quot;&gt;&lt;/div&gt;
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