Journal Digest

Since only one-fifth of hoarders have been found to have obsessive-compulsive disorder (OCD), there is reason to think that hoarding may be due to something other than that illness.

And that something else may be inattention, David Tolin, Ph.D., director of the Anxiety Disorders Center at the Institute of Living in Hartford, Conn., believes, both on the basis of other researchers' findings and those of a new study that he conducted with Anna Villavicencio, Ph.D.

Tolin and Villavicencio wanted to clarify the relationship between the core features of hoarding, OCD symptoms, and symptoms of attention-deficit/hyperactivity disorder (ADHD). Their cohort included 39 subjects with hoarding disorder but not OCD, 26 with OCD but not hoarding disorder, and 36 controls with neither condition. All subjects had a diagnostic interview and completed self-report measures regarding the core features of hoarding, OCD symptoms, negative affect, and the inattentive and hyperactive/impulsive symptoms of ADHD.

The researchers then looked to see whether after controlling for negative affect, OCD symptoms or inattentive or hyperactive/impulsive symptoms significantly predicted any of the core features of hoarding.

The OCD symptoms and hyperactive/impulsive symptoms did not, but the inattention symptoms did. These results suggest that inattention—a problem of neurocognitive function—might be a central feature of hoarding disorder, the researchers concluded in their report, which was published in the February Behavior Research and Therapy.

But how might inattention lead to hoarding? By creating decision-making problems regarding what to discard, the researchers speculated, since other researchers have found that hoarders have trouble making decisions.

The study was funded by the National Institute of Mental Health.

It's been a decade since the human genome was sequenced. A look at some of the progress that has been made since then in identifying genes underlying human diseases was published in the February 10 Nature. The author was Eric Lander, Ph.D., director of the Broad Institute at the Massachusetts Institute of Technology and Harvard University.

For example, in 1990, the year that the Human Genome Project was launched, fewer than 100 Mendelian disease genes had been identified. Now 2,850 have been. As of 2000, only a dozen gene variants had been linked with common diseases. Now variants at more than 1,100 gene loci have been shown to affect more than 165 common diseases. Genetic variants at five different locations have been linked with macular degeneration. The results point "to a failure to inhibit specific inflammatory responses, spurring new therapeutic approaches," Lander wrote.

As for genes underlying psychiatric disorders, much less is known about them than about genes contributing to other types of illnesses. However, some progress has been made. Notably, genotyping studies have identified common variants in bipolar disorder and schizophrenia and deletions in autism and schizophrenia. Analyses suggest that these variants and deletions play a major role in bipolar disorder, schizophrenia, and autism. The challenge now is to determine how those variants and deletions contribute to the illnesses in question.

There is evidence that exercise can counter depression. There is also evidence that people with the "l" variant of the serotonin transporter gene are more protected against depression than are those with the "s" variant of the gene. Now a new study has found that exercise can counter depression in people with both gene variants, but especially in those with the "l" variant.

The study's lead researcher was Chad Rethorst, Ph.D., of the University of Texas Southwestern Medical Center. Results were published in the November 2010 Medicine & Science in Sports & Exercise.

A total of 171 college students participated in the study. They were genotyped for either the "s" variant or the "l" variant of the serotonin transporter gene, and they completed the Beck Depression Inventory. After that, they were allocated to a five-week exercise intervention or a no-treatment control group. At the end of this time, subjects again completed the Beck Depression Inventory.

Subjects in the exercise group experienced a significantly greater reduction in depressive symptoms than subjects in the control group. But in addition, those in the exercise group with at least one "l" copy of the serotonin transporter gene experienced a significantly greater reduction in depressive symptoms than did those in the exercise group who had two copies of the "s" variant of the gene.

The study was funded by the North American Society for the Psychology of Sport and Physical Activity and the state of Arizona.

A longitudinal study of about a thousand young adults in New Zealand found a highly significant link between duration of a cohabiting relationship and positive mental health.

The longer subjects cohabited, the less likely they were to be depressed, to experience suicidal ideation or make a suicide attempt, to abuse alcohol or be dependent on it, or to abuse illicit drugs or be dependent on them.

Couples who had cohabited for five years or longer had half the rates of such disorders compared with those who had not cohabited.

Moreover, it was the duration of cohabiting, rather than its legal status, that influenced mental health outcomes, they found. Also, the apparent protective mental health effect of cohabiting was similar for both men and women, although the protective effect against substance abuse was greater for women.

The study was headed by Sheree Gibb, Ph.D., of the University of Otago in Christchurch, New Zealand. Results were published in the January British Journal of Psychiatry. The study was funded by the Health Research Council of New Zealand and other groups.

There is ample evidence that cognitive-behavioral therapy (CBT) strategies, such as going to bed only when sleepy and getting up at the same time each day, can reduce chronic insomnia in older adults. But there are few clinicians available to teach such strategies, and the strategies generally take six to eight sessions to teach.

So Daniel Buysse, M.D., of the University of Pittsburgh's Sleep Medicine Institute, and his colleagues decided to design a briefer CBT intervention to correct chronic insomnia in older adults. It consists of only two teaching sessions plus two phone calls. They tested the intervention's efficacy in a randomized, controlled trial of 79 older subjects with chronic insomnia.

Half the subjects received the CBT intervention and the other half a control one (printed educational material about insomnia). Both interventions were delivered by a nurse practitioner with no prior experience in sleep medicine. Four weeks later, the outcomes of the subjects were evaluated. Fifty-five percent of subjects who had gotten CBT, but only 13 percent of the control group, were insomnia-free—a significant difference. Moreover, improvements were maintained at a six-month follow-up. Findings were published online January 24 in the Archives of Internal Medicine.

The study was funded by the National Institutes of Health and the University of Pittsburgh.