By Hema Zbogar
Winter 2005-06, Vol 9 No 2
Concurrent anxiety disorder, a poor initial response to antidepressants and current suicide risk increase the risk of developing treatment-resistant depression (TRD), according to researchers at the University Clinic of Brussels in Belgium. TRD is defined as an inadequate response to at least two consecutive antidepressants from different classes, given at presumably adequate doses. Researchers initiated a large European study involving seven centres and 996 individuals with major unipolar depression. Participants had received at least one antidepressant treatment at adequate doses during their last depressive episode. Each participant was evaluated using the Mini-International Neuropsychiatric Interview. Participants also answered a questionnaire about their demographic, psychosocial, psychiatric and somatic characteristics. The researchers then developed a checklist of previous treatments that included drug class, duration of treatment, dose and adherence, as well as the exact sequence of antidepressants that participants had received, in case they had participated in multiple trials. The last depressive episode was defined as resistant if the participant had not responded to at least two consecutive antidepressant trials. According to this definition, 356 participants (36%) were treatment-resistant; 346 (35%) were responsive and the remaining 294 (30%) had issues that put them at risk of developing TRD. A two-step logistic regression analysis found that comorbid anxiety disorder, a poor response to the initial antidepressant treatment, a depression with features of melancholia and current suicidal risk predicted development of TRD. The authors stress the urgency of identifying the risks of TRD because as many as 50 per cent of people with depression do not respond to first-line treatment.
European Neuropsychopharmacology, October 2005, v. 15 (suppl. 3):S326. Pierre Oswald et al., Erasme Hospital, University Clinic of Brussels, Belgium.
Children with attention-deficit hyperactivity disorder (ADHD) are more likely to become smokers, and those with more ADHD symptoms are at higher risk, according to researchers at Duke University Medical Center. Although ADHD has already been associated with increased risk of smoking, this is the first time to examine a non-clinical sample to determine the extent to which the number of symptoms, independent of full diagnosis, confers risk of smoking. Researchers studied 15,197 participants from the national Longitudinal Study of Adolescent Health. They examined the relationship between self-reported ADHD symptoms and the lifetime likelihood of being a regular smoker, defined by having smoked at least one cigarette a day for 30 days. For individuals reporting regular smoking, the researchers also examined the extent to which ADHD symptoms predicted age at onset of regular smoking and number of cigarettes smoked. Controlling for demographic and conduct disorder symptoms, each reported inattention or hyperactivity/impulsivity symptom significantly increased the likelihood of regular smoking. For those reporting lifetime regular smoking, reported symptoms decreased the estimated age at onset and increased the number of cigarettes smoked. The researchers caution that their findings do not mean that diagnosis of ADHD as a child leads a person to become a smoker, particularly since the study only looked at self-reported symptoms and not a clinical diagnosis. However, they recommend that children with a high number of ADHD symptoms get additional or specialized education about the hazards of smoking. The researchers call for more research to understand exactly what the relationship is between ADHD symptoms and smoking risk.
Archives of General Psychiatry, October 2005, v. 62: 1142–1147. Scott H. Kollins et al., Duke University Medical Center, Durham, North Carolina.
Adolescent girls with eating disorders may be at risk of developing anxiety disorders, and vice versa, according to a study out of the University of Iowa. Researchers examined the simultaneous occurrence of eating disorders and mood disorders among 672 female twins, age 16–18, from the Minnesota Twin Family Study. Participants completed structured interviews that determined the presence of anorexia or bulimia, and assessed mood, anxiety and substance use. Eating disorders were highly likely to co-exist with major depression, anxiety disorders and nicotine dependence. Within a group of 14 identical twin pairs who did not both have an eating disorder, the risk for anxiety disorders was increased among the non-eating-disordered co-twins. Among 52 identical twin pairs of whom only one had an anxiety disorder, those without anxiety disorders had an increased risk for eating disorders. The researchers speculate that eating disorders and anxiety disorders share familial risk factors. They call for further studies to determine whether genetic or environmental factors, or both, explain shared transmission.
International Journal of Eating Disorders, September 2005, v. 38: 99–105. Pamela K. Keel et al., Department of Psychology, University of Iowa, Iowa City.
A family history of alcohol dependence has little to do with the age at which a child takes his or her first alcoholic drink, according to researchers at the University of Iowa Hospitals and Clinics. Using data collected through the ongoing Collaborative Study on the Genetics of Alcoholism, researchers examined two groups of children aged 7–17: those from families with a high occurrence of alcohol dependence and those from families with no such history. They looked at four factors that may affect age at first drink: child characteristics, family demographics, family psychopathology and child behaviour problems. It was found that child and environmental factors were stronger predictors of age at first drink than family history. Three variables explained 45 per cent of the variance: Age at interview accounted for 38 per cent, conduct scale score accounted for 6.2 per cent and the number of alcohol-dependent adult siblings accounted for 0.5 per cent. No family history measures of alcohol dependence or antisocial personality disorder were predictive. The researchers conclude that although there may be genetic components operating on drinking behaviour, these seem to only be related to level of risk and ultimately must interact with the environment. They suggest that preventive efforts may need to focus on aspects of the child, the family and the home environment.
Alcoholism: Clinical and Experimental Research, October 2005, v. 162: 1941–1947. Margareth I. Helgeland et al., Sogn Centre for Child and Adolescent Psychiatry, Oslo, Norway.
The greater the time between onset of psychosis and its treatment, the greater the severity of negative symptoms, according to researchers at the University of North Carolina School of Medicine. Researchers conducted a literature search and 43 publications met their selection criteria. The duration of treatment ranged from the end of the first hospitalization to 15 years. Shorter duration of untreated psychosis was associated with greater response to antipsychotic treatment, as measured by severity of global psychopathology, positive symptoms, negative symptoms and functional outcomes. At the time of treatment initiation, duration of initially untreated psychosis was associated with severity of negative symptoms, but not with the severity of positive symptoms, general psychopathology or neurocognitive function. The authors point out that currently there is a delay of more than one year between the time symptoms first emerge and the person first receives treatment. They conclude that early treatment may improve long-term prognosis by limiting progression of the illness and preserving the client’s ability to respond to antipsychotics.
American Journal of Psychiatry, October 2005, v. 162: 1785–1804. Diana O. Perkins et al., Department of Psychiatry, University of North Carolina School of Medicine, Chapel Hill, North Carolina.
Researchers at McLean Hospital in Boston have identified an area of the brain that appears to play a key role in why cocaine and other stimulants are highly addictive. Researchers found that the cerebellar vermis, which is involved in other psychiatric illnesses, appears to play a role in drug addiction. The study involved reviewing published data on the vermis that had not been analyzed for the vermis’ involvement in addiction. In the original 1998 study, researchers used functional magnetic resonance imaging (fMRI) to scan the brains of 10 individuals addicted to crack-cocaine as they viewed a video of people lighting up a crack pipe. Compared to a control group of non-users, users reported an increased desire for cocaine following this cue and had increased activity in several brain areas, including the anterior cingulate cortex. The new analysis shows activation in the vermis in cocaine users while they viewed the cocaine-use video. As part of the investigation, researchers also reanalyzed data from an unrelated study which found distribution of a drug that targets the dopamine transporter, the protein that seems to be blocked by such stimulants as cocaine, through the use of positron emission tomography (PET). The new data show, in non-drug using participants, that the vermis may contain dopamine transporters and thus may be a target for cocaine and other stimulants, thereby increasing dopamine in the brain. The researchers suggest that if the vermis plays a key role in the brain’s dopamine system, this could explain its role in addiction, as well as in other brain disorders, such as Parkinson’s disease, which is characterized by a shortage of dopamine.
Neuropsychopharmacology, October 12, 2005 online, doi:10.1038/sj.npp.1300937. Carl M. Anderson et al., Brain Imaging Center, McLean Hospital, Harvard Medical School, Belmont, Massachusetts.
Psychological stress caused by parental loss, abuse or neglect during infancy may result in memory loss and cognitive decline in middle age, according to researchers at the University of California, Irvine School of Medicine. The study, conducted on rats, may be the first to show that early emotional stress initiates a slow deterioration of brain-cell communication in adulthood. These cell-signalling deficits occur in the hippocampus, a brain region involved in learning, storage and recall of learned memories. Researchers limited nesting material in cages where baby rats lived with their mothers. This lack of material resulted in emotional stress for the mothers and their offspring. Evidence of this stress seemed to disappear by the time the baby rats became young adults. However, by middle age, the rats began to show problems in their ability to remember the location of objects they had seen before and to recognize objects they had encountered the previous day. These memory deficits worsened as the rats grew older, compared with rats that had not been subjected to stress during their first week of life. The stress-induced rats had normal electrical activity in their brain cells when they were young adults, but brain cell activity was faulty by middle age. The changes in brain-cell activity were consistent with the rats’ behavioural changes. The authors suggest that the study may lead to the development of more effective ways to prevent cognitive impairment later in life.
Journal of Neuroscience, October 2005, v. 25: 9328–9338. Kristen L. Brunson et al., Department of Anatomy/Neurobiology, University of California, Irvine.