Journal Digest

When people are depressed, they often say that everything looks dark and gloomy to them. And when they say that, they may mean it literally, a new study suggests.

It found that depressed people actually see less black and white contrast in objects than nondepressed people do.

It's possible to measure people's ability to perceive black and white contrasts with a technique called the pattern electroretinogram. Ludger Tebartz van Elst, M.D., a psychiatrist with Albert Ludwig University in Freiburg, Germany, and colleagues applied this technique to 40 subjects with major depression and to 40 healthy matched control subjects. Half of the depressed subjects were receiving antidepressants, and half were not.

They found that the depressed subjects were significantly poorer at perceiving black and white contrasts than control subjects were, and this held true regardless of antidepressant use. There was also a significant correlation between ability to see black and white contrasts and severity of depression, that is, subjects with the most severe symptoms were also the worst at distinguishing black and white contrasts.

Although these findings still need to be replicated, “this method could turn out to be a valuable tool for objectively measuring the subjective state of depression,” Tebartz van Elst said in an accompanying press release.

Results were published in the July 15 Biological Psychiatry.

A small fragment of RNA appears to protect rats against cocaine addiction and could theoretically protect humans, according to a study funded by the National Institute on Drug Abuse (NIDA) and published July 8 in Nature.

Researchers at the Scripps Research Institute in Jupiter, Fla., found that cocaine consumption increased levels of a specific microRNA sequence in the brains of rats, known to scientists as microRNA-212. As levels of the sequence increased, the rats exhibited a growing dislike for cocaine, ultimately controlling how much they consumed. In contrast, as levels of microRNA-212 decreased, the rats consumed more cocaine, and their behavior began to mirror that of humans who are cocaine abusers.

These findings suggest that microRNA-212 may play a pivotal role in regulating cocaine addiction. MicroRNA-212 is expressed in the dorsal striatum, a brain region that has been linked to drug abuse in humans.

The findings “offer promise for the development of a totally new class of anti-addiction medications,” Paul Kenny, Ph.D., an associate professor at the Scripps research facility and senior author of the study, said in a statement released by NIDA. “Because we are beginning to map out how this specific microRNA works, we may be able to develop new compounds to manipulate the levels of microRNA-212 therapeutically with exquisite specificity, opening the possibility of new treatments for drug addiction.”

The hormone oxytocin or some analog thereof might constitute a new type of antianxiety medication, various studies have suggested (Psychiatric News, November 21, 2008).

Now a small pilot study suggests that when oxytocin is given in conjunction with an antipsychotic medication, it might be able to reduce positive and negative symptoms in people with schizophrenia.

The study was headed by David Feifel, M.D., Ph.D., a professor of psychiatry at the University of California, San Diego. Results were published July 8 in Biological Psychiatry.

Nineteen subjects diagnosed with schizophrenia and with residual symptoms despite being on a stable dose of at least one antipsychotic participated in the study. Subjects were randomly assigned to receive three weeks of daily intranasal oxytocin, a week of washout, then three weeks of intranasal placebo, or three weeks of intranasal placebo, a week of washout, and three weeks of daily intranasal oxytocin. During the study, subjects were evaluated for positive and negative symptoms.

Fifteen of the 19 subjects completed the study. Their positive and negative symptoms were significantly lower after getting oxytocin than after getting a placebo, although the improvement in positive symptoms appeared statistically more robust.

There were no serious adverse effects reported during the study and no significant differences in rates of reported adverse effects between those taking the oxytocin and those taking placebo.

“The results support the hypothesis that oxytocin has antipsychotic properties and is well tolerated,” Feifel and colleagues said. “Higher doses and longer duration of treatment may produce larger benefits and should be evaluated in future studies.”

The study was funded by the Stanley Medical Research Institute.

David Kimbrough Oller, Ph.D., chair of the University of Memphis School of Audiology and Speech Language Pathology, and colleagues attached small battery-powered recorders to the clothing of more than 200 children aged 10 months to 4 years, some of whom had been diagnosed with autism or language delay and some of whom had not. During the next few days, the devices recorded what the children were saying, ultimately yielding some 1,500 all-day soundtracks.

Oller and his group then used automated software to analyze the soundtrack results. First the automated software separated sounds made by the children from sounds in the environment and other voices. Then the software classified and rated the children's utterances according to vocal-development theory and attempted to distinguish utterances in the autism/language-delay group from those in the normal-development group.

The researchers then assessed whether the automated software had accurately distinguished utterances made by the autism/language-delay group from the utterances made by the comparison group. It had, they reported July 19 in the Proceedings of the National Academy of Sciences. And “We compared many other configurations of groups as well—importantly autism versus typical development and language delay versus autism,” Oller told Psychiatric News. “All the comparisons showed very significant differentiation by the automated method.”

Thus the method could be used in the early detection of autism and speech and developmental disorders, Oller and his colleagues believe.

When youngsters have more than one anxiety disorder, the responsibility lies largely in the child's genes, a new study suggests. It was headed by Anna Ogliari, M.D., an assistant professor of developmental psychology at San Raffaele University in Milan, Italy, and published in the May Journal of Anxiety Disorders.

Ogliari and her colleagues used as their study sample 378 twin pairs aged 8 to 17 identified from the population-based Italian Twin Register. They evaluated the subjects for four common DSM-IV anxiety disorders—generalized anxiety disorder, panic disorder, social anxiety, and separation anxiety disorder—and then looked to see whether co-occurrence of these disorders in their subjects could be explained by genes or environment.

Genes were largely the culprits, they found. For example, 58 percent of the co-occurrence of general anxiety disorder and separation anxiety disorder could be explained by genes and 42 percent by environment, and 99 percent of the co-occurrence of social anxiety and panic disorder could be explained by genes and only 1 percent by environment.

“Our data suggest that genetic influences more than environmental factors (such as stressful life events outside the home or difficulties with peers) predispose to different anxiety disorders in children and adolescents,” Ogliari and her colleagues said.

The study was funded by the Italian Ministry of Health and the Italian Ministry of University and Research.

An abstract of “The Role of Genes and Environment in Shaping Co-occurrence of DSM-IV-Defined Anxiety Dimensions Among Italian Twins Aged 8-17” can be accessed at <www.sciencedirect.com/science/journal/08876185> by clicking on the May issue.