<?xml version="1.0" encoding="utf-8"?>
<recommendedContent xmlns="http://api.mspoke.com">
    <recommendedItem id="20100101_19_3225"
                     title="Cigarettes Won&apos;t Help Teens&apos; Depression (CME/CE)"
                     score="0.014"
                     href="http://www.medpagetoday.com/PrimaryCare/Smoking/tb/21978?impressionId=1283458822686"
                     
      &lt;p&gt;Even though some teens use cigarettes to self-medicate, smoking may only increase their depressive symptoms, researchers say.&lt;/p&gt;
&lt;p&gt;After adjustment, smokers who reported psychobiological benefits from smoking were at higher risk of developing elevated depressive symptoms than never-smokers (HR 1.9, 95% CI 1.3 to 2.8), Michael Chaiton, MD, of the University of Toronto, and colleagues reported online in &lt;em&gt;Addictive Behaviors&lt;/em&gt;.&lt;/p&gt;
&lt;p&gt;&quot;The perceived positive benefits may be the result of alleviation of symptoms of withdrawal and craving resulting from abstinence,&quot; they wrote.&lt;/p&gt;
&lt;p&gt;Self-medication has been one of the main hypotheses to explain the association between depression and smoking in teens.&lt;/p&gt;
&lt;p&gt;But it isn&apos;t well-known whether using cigarettes to improve mood or functioning is associated with changes in depressive symptoms.&lt;/p&gt;
&lt;p&gt;So the researchers assessed data from the Nicotine Dependence in Teens study, which followed 1,293 patients ages 12 to 13 at enrollment.&lt;/p&gt;
&lt;p&gt;They singled out a subsample of 662 teens who reported self-medication scores and broke them into never-smokers, smokers who had self-medicated, and smokers who didn&apos;t self-medicate.&lt;/p&gt;
&lt;p&gt;Those who smoked at least 25 cigarettes per week had consistently higher self-medication scores than those who smoked less.&lt;/p&gt;
&lt;p&gt;The researchers found that those who reported more psychobiological improvement through smoking had higher depressive symptom scores, as well as greater variation in scores over time. However, they also experienced significant deceleration of the observed increase in depressive symptom scores over time, compared with both never smokers and non-self-medicating smokers.&lt;/p&gt;
&lt;p&gt;That means self-medication scores may help identify a subgroup of smokers who are susceptible to depression, the researchers said.&lt;/p&gt;
&lt;p&gt;After adjustment for age, sex, and initial level of depressive symptoms, smokers with higher self-medication scores had a higher risk of onset of elevated depressive symptoms than never-smokers (HR 2.4, 95% CI 1.7 to 3.3).&lt;/p&gt;
&lt;p&gt;This effect persisted after further controlling for academic achievement, alcohol use, and perception of friends smoking (HR 1.9, 95% CI 1.3 to 2.8).&lt;/p&gt;
&lt;p&gt;While smokers with low self-medication scores had a marginally higher risk of developing elevated depressive symptoms, the association wasn&apos;t significant after adjustment.&lt;/p&gt;
&lt;p&gt;The researchers concluded that smoking appears to be ineffective at reducing depressive symptoms, and any perceived positive benefits may be the result of alleviation of symptoms of withdrawal and craving resulting from abstinence.&lt;/p&gt;
&lt;p&gt;The study was limited by self-report, repeated measurements which could increase errors and overestimate depression symptoms, and only five years of follow-up, so long-term effects could not be assessed. Also, the researchers noted, trends in self-medicating among adults may be different than among adolescents.&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 Canadian Cancer Society.&lt;/p&gt;&lt;p&gt;Chaiton was supported by a CIHR doctoral research award.&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_3027"
                     title="BP Should Pay Mental Health Claims, Groups Say"
                     score="0.002"
                     href="http://www.medpagetoday.com/PublicHealthPolicy/EnvironmentalHealth/tb/21689?impressionId=1283458822686"
                     
      &lt;p&gt;Mental health groups, including the American Psychiatric Association (APA), are crying foul over comments from the independent administrator overseeing claims related to BP&apos;s massive oil spill in the Gulf of Mexico.&lt;/p&gt;
&lt;p&gt;Kenneth Feinberg told a House of Representatives committee last month that it was &quot;highly unlikely&quot; that claims emphasizing mental health problems, rather than physical injuries or illnesses, would be paid out of the $20 billion BP has set aside to compensate damages resulting from the spill.&lt;/p&gt;
&lt;p&gt;&quot;If you start compensating purely mental anguish without a physical injury  --  anxiety, stress  --  we&apos;ll be getting millions of claims from people watching television,&quot; Feinberg testified. &quot;You have to draw the line somewhere.&quot;&lt;/p&gt;
&lt;p&gt;Feinberg is a Washington, D.C., attorney who previously led distribution of nearly $7 billion in compensation to victims of the 9/11 terrorist attacks and their families.&lt;/p&gt;
&lt;p&gt;In response, the APA issued a statement calling on Feinberg to rethink his position.&lt;/p&gt;
&lt;p&gt;&quot;Mental illnesses brought on by difficult situations surrounding the BP oil spill may be less visible than other injuries, but they are real,&quot; the group&apos;s president, Carol A. Bernstein, MD, said in the statement.&lt;/p&gt;
&lt;p&gt;&quot;An entire way of life has been destroyed, and this is causing anxiety, depression, post-traumatic stress disorder, substance use disorders, thoughts of suicide, and other problems,&quot; according to Bernstein.&lt;/p&gt;
&lt;p&gt;Local health officials in the Gulf region have warned that they expect a wave of mental health problems affecting residents whose lives and livelihoods have been disrupted.&lt;/p&gt;
&lt;p&gt;The state of Louisiana has requested $10 million from the BP relief fund to cover emergency mental health services. &quot;Our teams of counselors imbedded [sic] in the impacted communities are now warning us of an emerging behavioral health crisis,&quot; wrote the state&apos;s health secretary, Alan Levine, in a letter sent to BP in late June, when oil was still gushing from the broken underwater well.&lt;/p&gt;
&lt;p&gt;&quot;Our Louisiana Spirit crisis counseling teams have already engaged and counseled almost 2,000 individuals in the affected areas, and are reporting palpable increases in anxiety, depression, stress, grief, excessive drinking, earlier drinking, and suicide ideation,&quot; he added.&lt;/p&gt;
&lt;p&gt;Bernstein said Feinberg should put mental health claims on the same footing as those asserting physical illnesses and injuries resulting from the Gulf oil spill.&lt;/p&gt;
&lt;p&gt;Another group critical of Feinberg was the National Alliance on Mental Health. Its executive director said in a letter that Feinberg&apos;s position is &quot;incompatible with modern scientific knowledge of mental illness and the impact of traumatic events.&quot;&lt;/p&gt;

    </recommendedItem>
    <recommendedItem id="20100101_19_2899"
                     title="Epilepsy Drugs&apos; Link to Suicide Not Seen in All Patients (CME/CE)"
                     score="-0.006"
                     href="http://www.medpagetoday.com/Neurology/Seizures/tb/21525?impressionId=1283458822686"
                     
      &lt;p&gt;Using antiepileptics was not associated with an increased likelihood of attempting  --  or completing  --  suicide in patients with epilepsy, researchers found.&lt;/p&gt;
&lt;p&gt;However, the class of medications was associated with greater odds of attempted or completed suicide in patients with depression and those taking the drugs for indications other than epilepsy, depression, and bipolar disorder, according to Alejandro Arana, MD, of Risk MR Pharmacovigilance Services in Zaragoza, Spain, and colleagues.&lt;/p&gt;
&lt;p&gt;The odds ratios for those two groups of patients were 1.65 (95% CI 1.24 to 2.19) and 2.57 (95% CI 1.78 to 3.71), respectively, the researchers reported in the Aug. 5 issue of the &lt;em&gt;New England Journal of Medicine&lt;/em&gt;.&lt;/p&gt;
&lt;p&gt;Those findings are not entirely consistent with the results of a 2008 &lt;a href=&quot;http://www.medpagetoday.com/ProductAlert/Prescriptions/8184&quot; mce_href=&quot;http://www.medpagetoday.com/ProductAlert/Prescriptions/8184&quot; target=&quot;_blank&quot;&gt;FDA meta-analysis&lt;/a&gt; that found an increased risk of suicidal behavior or ideation with the use of 11 antiepileptics.&lt;/p&gt;
&lt;p&gt;That led the agency to require a &lt;a href=&quot;http://www.medpagetoday.com/ProductAlert/Prescriptions/12191&quot; mce_href=&quot;http://www.medpagetoday.com/ProductAlert/Prescriptions/12191&quot; target=&quot;_blank&quot;&gt;class-wide warning&lt;/a&gt; of suicidality for antiepileptics used for any indication later that year.&lt;/p&gt;
&lt;p&gt;Arana and his colleagues noted that the FDA&apos;s meta-analysis included the harder endpoints of attempted and completed suicide, as well as the softer endpoint of suicidal ideation, which might explain the discrepancy with the current analysis.&lt;/p&gt;
&lt;p&gt;The current study also had a longer follow-up period, they noted.&lt;/p&gt;
&lt;p&gt;Arana&apos;s group analyzed data on antiepileptic use collected as part of clinical practice from the U.K.&apos;s Health Improvement Network. Patients with a history of attempted or completed suicide  --  either personally or in the family  --  were excluded, leaving 5,130,795 patients.&lt;/p&gt;
&lt;p&gt;The researchers focused on the 10 drugs from the FDA&apos;s meta-analysis that were available in the U.K.  --  carbamazepine, gabapentin (Neurontin), lamotrigine (Lamictal), levetiracetam (Keppra), oxcarbazepine (Trileptal), pregabalin (Lyrica), tiagabine (Gabitril), topiramate (Topamax), valproate (Depacon), and zonisamide (Zonegran). Felbamate (Felbatol) was not marketed in the U.K.&lt;/p&gt;
&lt;p&gt;Through a mean follow-up of 6.2 years, 8,212 patients attempted suicide, and 464 were successful.&lt;/p&gt;
&lt;p&gt;Compared with the rate of attempted or successful suicide in patients who did not have epilepsy, depression, or bipolar disorder and did not use antiepileptics (15.1 per 100,000 person-years), rates were elevated for patients with one of the three conditions, regardless of antiepileptic use.&lt;/p&gt;
&lt;p&gt;The rate ranged from 38.2 per 100,000 person-years for patients with epilepsy who were not taking an antiepileptic to 441.3 for patients with bipolar disorder who were taking an antiepileptic.&lt;/p&gt;
&lt;p&gt;&quot;The underlying illness was more strongly associated with suicide-related events than was the use or nonuse of antiepileptic drugs,&quot; the researchers noted.&lt;/p&gt;
&lt;p&gt;However, in analyses adjusted for age, duration of illness, previous medication use, history of mental disorders, alcohol abuse, and chronic disease score, use of antiepileptics conferred additional risk of suicide in patients with depression and those taking the drugs for indications other than epilepsy, depression, and bipolar disorder.&lt;/p&gt;
&lt;p&gt;In regard to the greater chances of suicide in patients with depression, the researchers noted, &quot;Although a causal role of antiepileptic drugs is possible, it is also possible that the use of antiepileptic drugs in these patients is a marker of severe depression or the presence of another condition that may be associated with an increased risk of suicide-related events.&quot;&lt;/p&gt;
&lt;p&gt;There was actually a slightly decreased likelihood of suicide with antiepileptic use among patients with epilepsy (OR 0.59, 95% CI 0.35 to 0.98).&lt;/p&gt;
&lt;p&gt;There was no significant relationship between antiepileptic use and suicide in patients with bipolar disorder (OR 1.13, 95% CI 0.35 to 3.61) or those with both epilepsy and depression (OR 1.24, 95% CI 0.56 to 2.72).&lt;/p&gt;
&lt;p&gt;The study was limited, Arana and his colleagues wrote, in that researchers have shown that suicide is under-reported in the database used, some of the results may be partially attributable to confounding by indication, and exclusions may mean that the results are not generalizable to a high-risk population.&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 Sepracor, which is developing the antiepileptic eslicarbazepine acetate (Stedesa) for partial-onset seizures and bipolar disorder. Risk MR Pharmacovigilance Services SL collaborated with Risk MR.&lt;/p&gt;&lt;p&gt;Arana&apos;s employer received fees from Risk MR for his participation in review activities such as data monitoring boards, statistical analysis, and endpoint committees and for writing and reviewing the manuscript. Arana was previously employed by Pfizer and Novartis. He reported that his employer has received money from UCB Pharma and Novartis for consulting and grants from Novartis.&lt;/p&gt;&lt;/div&gt;&lt;div style=&quot;clear:both;&quot;&gt;&lt;/div&gt;
    </recommendedItem>
    <recommendedItem id="20100101_19_2890"
                     title="Expectation Drives Placebo Response in Parkinson&apos;s (CME/CE)"
                     score="-0.006"
                     href="http://www.medpagetoday.com/Neurology/ParkinsonsDisease/tb/21514?impressionId=1283458822686"
                     
      &lt;p&gt;Patients with Parkinson&apos;s disease who strongly expect a therapeutic benefit are likely to exhibit significant dopamine release when given a placebo, a small randomized study found.&lt;/p&gt;
&lt;p&gt;Significant dopamine release (&lt;em&gt;P&lt;/em&gt;=0.03) was seen among patients told they had a 75% chance of receiving active levodopa, unlike those told their chances of being given the active drug were 25, 50 or 100%, according to Sarah C. Lidstone, PhD, of the Pacific Parkinson&apos;s Research Centre in Vancouver, and colleagues.&lt;/p&gt;
&lt;p&gt;&quot;The promise of symptom improvement that is elicited by a placebo is a powerful modulator of brain neurochemistry,&quot; the researchers wrote in the August &lt;em&gt;Archives of General Psychiatry.&lt;/em&gt;&lt;/p&gt;
&lt;p&gt;Previous studies have suggested that administration of a placebo can activate reward circuitry in the brain, resulting in the release of dopamine in the ventral striatum.&lt;/p&gt;
&lt;p&gt;Lidstone and colleagues sought to explore if the magnitude of dopamine release following administration of a placebo in patients with Parkinson&apos;s disease would reflect the reward expectation of midbrain dopamine neurons, and to what extent this dopamine activity could be modified by patients&apos; degree of expectation of clinical benefit.&lt;/p&gt;
&lt;p&gt;&quot;If the placebo effect is indeed analogous to the expectation of reward, we would predict that dopamine release could be modified by probability alone, by the expected magnitude of the clinical benefit associated with active medication, or by the product of these two variables, the expected reward value,&quot; they explained.&lt;/p&gt;
&lt;p&gt;They enrolled 30 patients with mild-to-moderate Parkinson&apos;s disease, all of whom underwent three raclopride positron emission tomographic (PET) scans, the first of which took place 12 to 18 hours after withdrawal of antiparkinson medication.&lt;/p&gt;
&lt;p&gt;The second scan took place one hour after oral administration of immediate-release levodopa/carbidopa (250/25 mg). The following day the patients were randomized into four groups and told of the probability (25%, 50%, 75%, 100%) of their next dose being active drug or placebo.&lt;/p&gt;
&lt;p&gt;All patients actually were given placebo, after signing a consent form explaining that the study involved the use of some deception that would be explained later.&lt;/p&gt;
&lt;p&gt;The third scan was done an hour after the placebo administration, revealing significant differences in raclopride binding between the groups.&lt;/p&gt;
&lt;p&gt;Significant dopamine release was present in the putamen area of the dorsal striatum (&lt;em&gt;P&lt;/em&gt;=0.002) as well as in the ventral striatum (&lt;em&gt;P&lt;/em&gt;&amp;lt;0.001) only when the probability of levodopa treatment was 75%.&lt;/p&gt;
&lt;p&gt;Previous dopaminergic response to levodopa in the second scan modulated dopamine release in the dorsal striatum, but the expectation of clinical improvement was also required to drive dopamine release in the ventral striatum in the third scan, the investigators found.&lt;/p&gt;
&lt;p&gt;They then performed an analysis of covariance, in which they added the expected reward value as a covariate, but found no additional effect on placebo-induced dopamine release beyond what was associated with probability.&lt;/p&gt;
&lt;p&gt;To verify that the degree of placebo-related dopamine release related to the expectation of benefit, not the actual or perceived benefit, the investigators also added objective and subjective changes in motor function to the analysis, and found no effect in either the putamen or the ventral striatum.&lt;/p&gt;
&lt;p&gt;This confirmed that it was the expectation of benefit, rather than the perception or experience of benefit, that modulated dopamine release.&lt;/p&gt;
&lt;p&gt;In explaining why patients did not respond if the expectation of receiving active drug was 50 or 100%, the authors stated that patients with Parkinson&apos;s disease may not be able to distinguish between 50% and lower probabilities of receiving the drug and also may utilize past experience with a drug rather than reward expectation if they are certain to receive active drug.&lt;/p&gt;
&lt;p&gt;The study was the first to demonstrate that verbal instructions to a patient can directly modulate dopamine release, and the findings may have important implications for the design of clinical trials, according to the authors.&lt;/p&gt;
&lt;p&gt;&quot;We have shown that both the probability of receiving active treatment  --  which varies in clinical trials depending on the study design and the information provided to the patient  --  as well as the treatment history of the patient influence dopamine system activity and consequently clinical outcome,&quot; they wrote.&lt;/p&gt;
&lt;div style=&quot;float:left;border-style:solid;border-width:1px;border-color:#8dabbc;font-family:arial;font-size:12px;background-color:#DBE9F2;padding:5px;&quot;&gt;&lt;p&gt;The study was funded by the Michael Smith Foundation for Health Research, the Canadian Instiitutes for Health Research, and a TRIUMF Life Sciences Grant. One author also was supported by the Canada Research Chairs Program.&lt;/p&gt;&lt;p&gt;No other financial disclosures were reported.&lt;/p&gt;&lt;/div&gt;&lt;div style=&quot;clear:both;&quot;&gt;&lt;/div&gt;
    </recommendedItem>
    <recommendedItem id="20100101_19_2865"
                     title="Social Rejection Linked to Inflammation (CME/CE)"
                     score="-0.006"
                     href="http://www.medpagetoday.com/Psychiatry/AnxietyStress/tb/21484?impressionId=1283458822686"
                     
      &lt;p&gt;Social rejection may be bad for your health  --  at least that&apos;s the implication of a small study linking rejection to increases in inflammatory markers associated with disorders such as asthma, arthritis, cardiovascular disease, and depression.&lt;/p&gt;
&lt;p&gt;The study, conducted in the lab among 124 healthy adults, found a test of social rejection triggered increases in oral levels of two inflammatory markers, Shelley Taylor, PhD, and colleagues at the University of California Los Angeles reported.&lt;/p&gt;
&lt;p&gt;Further testing in 31 of those participants found that one of the two inflammatory markers was associated with greater activity in brain regions linked to processing rejection-related distress, Taylor and colleagues wrote online in the &lt;em&gt;Proceedings of the National Academy of Sciences&lt;/em&gt;.&lt;/p&gt;
&lt;p&gt;While the study was small, the findings start to pin down the neural pathways that are involved in reactions to acute social stress and may help explain the &quot;considerable variability&quot; in susceptibility to disorders with an inflammatory component, the researchers argued.&lt;/p&gt;
&lt;p&gt;Taylor and colleagues conducted a two-part experiment  --  a standard stress test involving speaking and calculating under pressure in public and a functional magnetic resonance imaging study of brain regions active when participants were socially rejected.&lt;/p&gt;
&lt;p&gt;In the first, 124 healthy adult volunteers took the Trier Social Stress test, which involves composing and delivering an impromptu speech to a panel of nonresponsive judges. Then they were asked to perform difficult mental arithmetic  --  counting backward from 2,935 by 7s and by 13s  --  while being urged to go faster by an &quot;apparently exasperated experimenter,&quot; Taylor and colleagues wrote.&lt;/p&gt;
&lt;p&gt;Before and after the test, the researchers collected oral fluids, which were tested for levels of a soluble receptor for tumor necrosis factor-&amp;#945; (sTNF&amp;#945;RII) and interleukin-6 (IL-6), both known to be markers of inflammatory activity.&lt;/p&gt;
&lt;p&gt;As expected, Taylor and colleagues wrote, levels of both markers increased significantly, at&lt;em&gt; P&lt;/em&gt;&amp;lt;0.005 for sTNF&amp;#945;RII and &lt;em&gt;P&lt;/em&gt;&amp;lt;0.05 for IL-6, and the increases were positively and significantly correlated (at r=0.53 and &lt;em&gt;P&lt;/em&gt;&amp;lt;0.001).&lt;/p&gt;
&lt;p&gt;The volunteers were asked to complete a second experiment  --  playing a computer game called Cyberball while undergoing fMRI scanning. All told, 31 participants were eligible and took part.&lt;/p&gt;
&lt;p&gt;In the game, participants had to throw a virtual ball back and forth to two other &quot;players&quot; but did not know that the other players were actually computer-generated. In one game, the ball was shared equally, but in the other, the volunteer got a few passes at the beginning and then was ignored for the rest of the 60-throw game.&lt;/p&gt;
&lt;p&gt;The researchers correlated levels of the two markers, as measured after the previous stress test, with activity in regions of the brain previously linked with rejection-related stress  --  the dorsal anterior cingulate cortex (dACC) and the anterior insula.&lt;/p&gt;
&lt;p&gt;As expected, Taylor and colleagues wrote, those who had high levels of sTNF&amp;#945;RII on the stress test had significantly elevated activity in both regions during the game in which they were excluded, as compared with the game in which they were included. The differences were significant at &lt;em&gt;P&lt;/em&gt;&amp;lt;0.005 for the dACC and &lt;em&gt;P&lt;/em&gt;&amp;lt;0.05 for both the right and left anterior insula.&lt;/p&gt;
&lt;p&gt;On the other hand, the researchers reported, IL-6 was only weakly correlated with one region  --  the right anterior insula.&lt;/p&gt;
&lt;p&gt;&quot;Considered together,&quot; they argued, &quot;these data demonstrate that neural responses to social rejection are associated with potentiated inflammatory responses to an episode of acute social stress.&quot;&lt;/p&gt;
&lt;p&gt;Taylor and colleagues cautioned that the observed associations were correlational, so that causality can&apos;t be determined. As well, they said, more research is needed to see if neural responses to social rejection are uniquely related to differences in inflammatory responses or if they are part of a more general system that can be activated by several types of negative events.&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 NIH and a Society in Science: Branco Weiss Fellowship.&lt;/p&gt;&lt;p&gt;The authors declared they had no conflicts.&lt;/p&gt;&lt;/div&gt;&lt;div style=&quot;clear:both;&quot;&gt;&lt;/div&gt;
    </recommendedItem>
</recommendedContent>
