Abstract
Telomere attrition is a hallmark of cellular aging and shorter telomeres have been reported in mood and anxiety disorders. Telomere shortening is counteracted by the enzyme telomerase and cellular protection is also provided by the antioxidant enzyme glutathione peroxidase (GPx). Here, telomerase, GPx, and telomeres were investigated in 46 social anxiety disorder (SAD) patients in a within-subject design with repeated measures before and after cognitive behavioral therapy. Treatment outcome was assessed by the Liebowitz Social Anxiety Scale (self-report), administered three times before treatment to control for time and regression artifacts, and posttreatment. Venipunctures were performed twice before treatment, separated by 9 weeks, and once posttreatment. Telomerase activity and telomere length were measured in peripheral blood mononuclear cells and GPx activity in plasma. All patients contributed with complete data. Results showed that social anxiety symptom severity was significantly reduced from pretreatment to posttreatment (Cohen’s d = 1.46). There were no significant alterations in telomeres or cellular protection markers before treatment onset. Telomere length and telomerase activity did not change significantly after treatment, but an increase in telomerase over treatment was associated with reduced social anxiety. Also, lower pretreatment telomerase activity predicted subsequent symptom improvement. GPx activity increased significantly during treatment, and increases were significantly associated with symptom improvement. The relationships between symptom improvement and putative protective enzymes remained significant also after controlling for body mass index, sex, duration of SAD, smoking, concurrent psychotropic medication, and the proportion of lymphocytes to monocytes. Thus, indices of cellular protection may be involved in the therapeutic mechanisms of psychological treatment for anxiety.
Highlights
Psychiatric disorders have been linked to increased risks of somatic illnesses and even premature death[1], the underlying mechanisms are not clear
A large withingroup treatment effect (Cohen’s d = 1.46) was observed on the primary social anxiety measure, indicating substantial symptom improvement that exceeded effects reported in our previous randomized controlled trials (RCTs) on internet-delivered cognitive behavioral therapy (CBT) for social anxiety disorder (SAD), e.g., refs. 47,48,58
We found that putatively enhanced cellular protection, as indexed by increases in activity of the telomere-preserving enzyme telomerase and antioxidant enzyme glutathione peroxidase (GPx), paralleled social anxiety reduction
Summary
Psychiatric disorders have been linked to increased risks of somatic illnesses and even premature death[1], the underlying mechanisms are not clear. A large study including >1200 participants found that anxiety-disordered patients, relative to healthy controls, exhibit shorter mean leukocyte telomere length[11]. This is in alignment with other studies on disorders of the anxiety and affective spectrum[12,13], Månsson et al Translational Psychiatry (2019)9:340 including depression and posttraumatic stress disorder— for a review see Darrow et al.[14]. A small-scale study showed that antidepressant response to a selective serotonin reuptake inhibitor (SSRI) was associated with lower pretreatment telomerase and a greater increase in telomerase activity over the course of treatment[18]. Markers of oxidative stress have been related to treatment outcome[19], e.g., increased oxidative stress is associated with poorer response to antidepressants[20]
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