Strongest Warning Suggested for ADHD Drugs (Ritalin, Concerta, Methylin, Metadate, Adderall and Adderall XR) February 10, 2006 About 2.5 million children between age 4 and 17 take ADHD drugs, according to federal survey data cited by Dr. Andrew Mosholder, a medical officer in the Office of Drug Safety. The survey found 9.3 percent of 12-year-old boys and 3.7 percent of 11-year-old girls take the drugs, Mosholder said. WASHINGTON (AP) -- Ritalin and other stimulant drugs for attention deficit hyperactivity disorder should carry the strongest warning that they may be linked to an increased risk of death and injury, federal health advisers said Thursday. The Food and Drug Administration advisory panel voted in favor of the "black box" warning after hearing about the deaths of 25 people, including 19 children, who had taken the drugs. The vote was 8-7, with one abstention. One committee member, Dr. Curt Furberg, a professor of public health sciences at the Wake Forest University Baptist Medical Center, said it would be "inappropriate, unethical behavior" not to disclose that there was uncertainty about the safety of the drugs. (complete story) FDA: 25 Deaths While Taking ADHD Drugs February 8, 2006 WASHINGTON (AP) -- Twenty-five people died and 54 more suffered serious cardiovascular problems after taking drugs to treat attention deficit hyperactivity disorder between 1999 and 2003, the government says. Children accounted for 19 of the deaths and 26 of the cases of nonfatal cardiovascular problems, including heart attack, stroke, hypertension, palpitations and arrhythmia, according to a Food and Drug Administration report released Wednesday. The report's release came a day before an FDA panel was to discuss new ways of examining the potential cardiovascular risks of the drugs, which include amphetamines such as Adderall, and methylphenidates, sold as Ritalin, Concerta, Methylin and Metadate. Cardiovascular risks The few studies that have looked at longer-term use of ADHD drugs provide little information on those risks, the FDA said. The cardiovascular risks include heart attack, stroke, hypertension, palpitations and arrhythmia. In a letter sent Monday to acting FDA commissioner Dr. Andrew von Eschenbach, Grassley said in part, "I remain concerned that while both psychiatric and cardiovascular risk signals have cropped up across this class of drugs this past year, it appears that FDA is just now beginning to 'discuss approaches' for studying these risks." (complete story) Mercury and Autism: Accelerating Evidence? Neuroendocrinol Lett 2005; 26(5):439–446 Abstract: The causes of autism and neurodevelopmental disorders are unknown. Genetic and environmental risk factors seem to be involved. Because of an observed increase in autism in the last decades, which parallels cumulative mercury exposure, it was proposed that autism may be in part caused by mercury. We review the evidence for this proposal. Several epidemiological studies failed to find a correlation between mercury exposure through thimerosal, a preservative used in vaccines, and the risk of autism. Recently, it was found that autistic children had a higher mercury exposure during pregnancy due to maternal dental amalgam and thimerosal-containing immunoglobulin shots. It was hypothesized that children with autism have a decreased detoxification capacity due to genetic polymorphism. In vitro, mercury and thimerosal in levels found several days after vaccination inhibit methionine synthetase (MS) by 50%. Normal function of MS is crucial in biochemical steps necessary for brain development, attention and production of glutathione, an important antioxidative and detoxifying agent. Repetitive doses of thimerosal leads to neurobehavioral deteriorations in autoimmune susceptible mice, increased oxidative stress and decreased intracellular levels of glutathione in vitro. Subsequently, autistic children have significantly decreased level of reduced glutathione. Promising treatments of autism involve detoxification of mercury, and supplementation of deficient metabolites. (complete article) Getting the Lead Out A bold mandate from the European Union aims to make new electronics less toxic for everyone General Technology February 2006 By Billy Baker The life-cycle interval between innovation and obsolescence is notoriously short for many electronics, as indicated by the ever-growing mountain of discarded cellphones, computers, TVs, MP3 players and other equipment. The U.S. alone produces more than two million tons of e-waste a year, and 90 percent of it ends up in landfills, where it can potentially leach toxins into groundwater or emit carcinogens when burned. Tough legislation scheduled to take effect in Europe this July could help dramatically curb the problem. The Restriction of Hazardous Substances Directive, or RoHS, as the mandate is known, will force companies to eliminate nearly all of the hazardous substances-including lead, mercury, cadmium and two forms of flame retardant-found in new electronics manufactured or sold in the European Union. So what does all this mean for consumers? Most companies say their toxin-free products will look and act the same as their lead-laden counterparts. And despite the fact that the mandate will require RoHS compliance along the entire supply chain, at considerable cost to manufacturers (Intel has reportedly spent $100 million on the problem), companies insist that prices will remain unchanged. (complete story)

New Study of Neurofeedback for Treating ADHD February 2006 David Rabiner, Ph.D. Duke University A recently published study addresses random assignment, and also provides direct evidence of changes in brain activity for children receiving neurofeedback (Levesque, J., Beauregard, M., & Mensour, B. 2006. Effect of neurofeedback training on the neural substrates of selective attention in children with AD/HD: A functional magnetic resonance imaging study. Neuroscience Letters, 394, 216-221.) Results indicated clear improvements for children receiving neurofeedback treatment. Specifically, the authors reported the following: 1) For treated children, parent ratings of inattentive ADHD symptoms declined significantly - into the normal range - while those of control children remained clinically elevated. 2) For treated children, parent ratings of hyperactive/impulsive ADHD symptoms declined significantly - although not quite into the normal range - while those of control children showed a modest increase. 3) On the Digit Span test, scores for treated children increased significantly from time 1 to time 2; for control children, no significant increase was found. 4) On the Continuous Performance Test, scores for treated children increased significantly from time 1 to time 2; for control children, no significant increase was found. 5) On the Counting Stroop Task, treated children performed significantly better on both neutral and interference trials at time 2 compared to time 1; for control children, no increase in the accuracy of their performance was found. 6) FMRI results showed no difference in patterns of brain activation between treated and control children at time 1. At time 2, however, treated children showed a different pattern of brain activation during the interference trials, i.e., those that required more complex cognitive processing. The brain regions that were now activated were those believed to play important roles in selective attention and the suppression of inappropriate responses. This study provides important new evidence to support the use of neurofeedback as a treatment for ADHD. (complete report) Differential Anterior Prefrontal Activation during the Recognition Stage of a Spatial Working Memory Task Cerebral Cortex November 2005;15:1742--1749 doi:10.1093/cercor/bhi051 Neuroimaging studies commonly show widespread activations in the prefrontal cortex during various forms of working memory and long-term memory tasks. However, the anterior prefrontal cortex (aPFC, Brodmann area 10) has been mainly associated with retrieval in episodic memory, and its role in working memory is less clear. We conducted an event-related functional magnetic resonance imaging study to examine brain activations in relation to recognition in a spatial delayed-recognition task. Similar to the results from previous findings, several frontal areas were strongly activated during the recognition phase of the task, including the aPFC, the lateral PFC and the anterior cingulate cortex. Although the aPFC was more active during the recognition phase, it was also active during the delay phase of the spatial working memory task. In addition, the aPFC showed greater activity in response to negative probes (non-targets) than to positive probes (targets). While our analyses focused on examining signal changes in the aPFC, other prefrontal regions showed similar effects and none of the areas were more active in response to the positive probes than to the negative probes. Our findings support the conclusion that the aPFC is involved in working memory and particularly in processes that distinguish target and non-target stimuli during recognition. complete paper) Selective Serotonin-Reuptake Inhibitors and Risk of Persistent Pulmonary Hypertension of the Newborn New England Journal Volume 354:579-587 February 9, 2006 Number 6 Christina D. Chambers, Ph.D., M.P.H., Sonia Hernandez-Diaz, M.D., Dr.P.H., Linda J. Van Marter, M.D., M.P.H., Martha M. Werler, Sc.D., Carol Louik, Sc.D., Kenneth Lyons Jones, M.D., and Allen A. Mitchell, M.D. ABSTRACT Background Persistent pulmonary hypertension of the newborn (PPHN) is associated with substantial infant mortality and morbidity. A previous cohort study suggested a possible association between maternal use of the selective serotonin-reuptake inhibitor (SSRI) fluoxetine late in the third trimester of pregnancy and the risk of PPHN in the infant. We performed a case-control study to assess whether PPHN is associated with exposure to SSRIs during late pregnancy. Methods Between 1998 and 2003, we enrolled 377 women whose infants had PPHN and 836 matched control women and their infants. Maternal interviews were conducted by nurses, who were blinded to the study hypothesis, regarding medication use in pregnancy and potential confounders, including demographic variables and health history. Results Fourteen infants with PPHN had been exposed to an SSRI after the completion of the 20th week of gestation, as compared with six control infants (adjusted odds ratio, 6.1; 95 percent confidence interval, 2.2 to 16.8). In contrast, neither the use of SSRIs before the 20th week of gestation nor the use of non-SSRI antidepressant drugs at any time during pregnancy was associated with an increased risk of PPHN. Conclusions These data support an association between the maternal use of SSRIs in late pregnancy and PPHN in the offspring; further study of this association is warranted. These findings should be taken into account in decisions as to whether to continue the use of SSRIs during pregnancy.

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