Improvement in indices of cellular protection after psychological treatment for social anxiety disorder

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.

Progress of clinical evaluation for vascular aging in humans

“…There is an increasing number of studies demonstrating that telomeres shortened during the aging of human both in cell culture and in normal tissues in vivo. [ 44 , 45 , 46 , 47 ] In human, meta-analyses have supported a strong relation between short telomeres and mortality risk of ASCVD, particularly at younger ages. [ 48 ] Telomerase is a reverse transcriptase that adds new DNA onto the telomeres.…”

Enriching CBT by Neuroscience: Novel Avenues to Achieve Personalized Treatments

“…In addition to macro-level MRI and PET assessments of the brain, neuroscience also provides tools to investigate therapy-induced effects on cells, proteins, and enzymes, e.g., inflammatory cytokines, markers of oxidative stress (Chen et al, 2011), and telomere biology (Månsson et al, 2019). These studies broadly support the notion that CBT not only can ameliorate psychiatric symptoms but also reduce the expression of inflammatory cytokines and improve cellular protection.…”

Moment-to-moment brain signal variability reliably predicts psychiatric treatment outcome

“…Two patients had previously used beta blockers in social situations, but agreed not to use them during the study period. For further study and sample details, see Månsson et al, 2019 (17). See also Table S1 for a detailed summary of demographic and clinical status, and comorbid mental illness.…”