Previously Hovatta's team have explored the genetic background of anxiety in experimental models. The current study follows up on these findings in humans using data collected as part of national Health 2000 Survey consisting of 321 individuals who had been diagnosed with anxiety disorder and 653 healthy controls. Hovatta says it was interesting that different genes showed evidence for association to specific types of anxiety disorders, such as panic disorder, social phobias or generalised anxiety disorder. The results will be published in Biological Psychiatry in October.

"Environmental factors, such as stressful life events, may trigger an anxiety disorder more easily in people who have a genetic predisposition to the illness," Iiris Hovatta says. The focus in the team's further studies will be to understand the molecular and cellular processes that link these genes to the regulation of anxiety behaviour.

Furthermore, the team's international collaborators in Spain and the United States are trying to replicate these findings in their anxiety disorder datasets to see whether the genes identified by Finnish scientists predispose to anxiety disorders in other populations as well. Only by replicating the results firm conclusions can be drawn about the role of these genes in the predisposition to anxiety in more general.

A closer understanding of the genetics and neurobiology of anxiety disorders is expected to help improve treatment of the illness using both drugs and therapy-based approaches. For the time being, no targeted drugs are available for the treatment of anxiety disorders. Some patients with anxiety disorders do benefit from the currently used medication, but about half of the patients do not.

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"These changes in gene expression correlated with changes in the tissue that included greater cell proliferation, marked inflammation, and increased apoptosis," Stoner says.

In the animals fed berry powder, however, a fifth of the carcinogen affected genes - exactly 462 of them - showed near-normal levels of activity, when compared with controls. Most of these genes are associated with cell proliferation and death, cell attachment and movement, the growth of new blood vessels and other processes that contribute to cancer development. The tissue also appeared more normal and healthy.

Lastly, of the 462 genes restored to normal by the berries, 53 of them were also returned to normal by a second chemoprevention agent tested during a companion study.

"Because both berries and the second agent maintain near-normal levels of expression of these 53 genes, we believe their early deregulation may be especially important in the development of esophageal cancer," Stoner says.

"What's emerging from studies in cancer chemoprevention is that using single compounds alone is not enough," Stoner says. "And berries are not enough. We never get 100 percent tumor inhibition with berries. So we need to think about another food that we can add to them that will boost the chemopreventive activities of berries alone."

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