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

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          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.

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          Most cited references47

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          Oxidative stress shortens telomeres.

          Telomeres in most human cells shorten with each round of DNA replication, because they lack the enzyme telomerase. This is not, however, the only determinant of the rate of loss of telomeric DNA. Oxidative damage is repaired less well in telomeric DNA than elsewhere in the chromosome, and oxidative stress accelerates telomere loss, whereas antioxidants decelerate it. I suggest here that oxidative stress is an important modulator of telomere loss and that telomere-driven replicative senescence is primarily a stress response. This might have evolved to block the growth of cells that have been exposed to a high risk of mutation.
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            Identification of a specific telomere terminal transferase activity in Tetrahymena extracts.

            We have found a novel activity in Tetrahymena cell free extracts that adds tandem TTGGGG repeats onto synthetic telomere primers. The single-stranded DNA oligonucleotides (TTGGGG)4 and TGTGTGGGTGTGTGGGTGTGTGGG, consisting of the Tetrahymena and yeast telomeric sequences respectively, each functioned as primers for elongation, while (CCCCAA)4 and two nontelomeric sequence DNA oligomers did not. Efficient synthesis of the TTGGGG repeats depended only on addition of micromolar concentrations of oligomer primer, dGTP, and dTTP to the extract. The activity was sensitive to heat and proteinase K treatment. The repeat addition was independent of both endogenous Tetrahymena DNA and the endogenous alpha-type DNA polymerase; and a greater elongation activity was present during macronuclear development, when a large number of telomeres are formed and replicated, than during vegetative cell growth. We propose that the novel telomere terminal transferase is involved in the addition of telomeric repeats necessary for the replication of chromosome ends in eukaryotes.
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              Advantages and limitations of Internet-based interventions for common mental disorders.

              Several Internet interventions have been developed and tested for common mental disorders, and the evidence to date shows that these treatments often result in similar outcomes as in face-to-face psychotherapy and that they are cost-effective. In this paper, we first review the pros and cons of how participants in Internet treatment trials have been recruited. We then comment on the assessment procedures often involved in Internet interventions and conclude that, while online questionnaires yield robust results, diagnoses cannot be determined without any contact with the patient. We then review the role of the therapist and conclude that, although treatments including guidance seem to lead to better outcomes than unguided treatments, this guidance can be mainly practical and supportive rather than explicitly therapeutic in orientation. Then we briefly describe the advantages and disadvantages of treatments for mood and anxiety disorders and comment on ways to handle comorbidity often associated with these disorders. Finally we discuss challenges when disseminating Internet interventions. In conclusion, there is now a large body of evidence suggesting that Internet interventions work. Several research questions remain open, including how Internet interventions can be blended with traditional forms of care. Copyright © 2014 World Psychiatric Association.
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                Author and article information

                Contributors
                +46 (0) 70 580 3267 , kristoffer.mansson@ki.se
                Journal
                Transl Psychiatry
                Transl Psychiatry
                Translational Psychiatry
                Nature Publishing Group UK (London )
                2158-3188
                19 December 2019
                19 December 2019
                2019
                : 9
                : 340
                Affiliations
                [1 ]ISNI 0000 0004 1937 0626, GRID grid.4714.6, Centre for Psychiatry Research, Department of Clinical Neuroscience, , Karolinska Institutet, ; Stockholm, Sweden
                [2 ]ISNI 0000 0004 1936 9377, GRID grid.10548.38, Department of Psychology, , Stockholm University, ; Stockholm, Sweden
                [3 ]ISNI 0000 0004 1936 9457, GRID grid.8993.b, Department of Psychology, , Uppsala University, ; Uppsala, Sweden
                [4 ]ISNI 0000 0001 0930 2361, GRID grid.4514.4, Department of Clinical Sciences Lund, Psychiatry, , , Lund University, ; Lund, Sweden
                [5 ]ISNI 0000 0004 1937 0626, GRID grid.4714.6, Department of Molecular Medicine and Surgery, , Karolinska Institutet, ; Stockholm, Sweden
                [6 ]ISNI 0000 0000 9241 5705, GRID grid.24381.3c, Center for Molecular Medicine, , Karolinska University Hospital, ; Stockholm, Sweden
                [7 ]ISNI 0000 0004 1937 0626, GRID grid.4714.6, Centre for Psychiatry Research, Department of Clinical Neuroscience, , Karolinska Institutet, & Stockholm Health Care Services, Region Stockholm, ; Stockholm, Sweden
                [8 ]ISNI 0000 0004 1937 0626, GRID grid.4714.6, Department of Clinical Neuroscience, , Karolinska Institutet, ; Stockholm, Sweden
                [9 ]ISNI 0000 0004 1936 9377, GRID grid.10548.38, Stress Research Institute, , Stockholm University, ; Stockholm, Sweden
                [10 ]ISNI 0000 0001 2162 9922, GRID grid.5640.7, Department of Behavioural Sciences and Learning, , Linköping University, ; Linköping, Sweden
                [11 ]ISNI 0000 0001 1034 3451, GRID grid.12650.30, Centre for Demographic and Ageing Research, , Umeå University, ; Umeå, Sweden
                [12 ]ISNI 0000 0004 0646 7373, GRID grid.4973.9, Center for Magnetic Resonance (DRCMR), Centre for Functional and Diagnostic Imaging and Research, , Copenhagen University Hospital, ; Hvidovre, Denmark
                [13 ]ISNI 0000 0001 2297 6811, GRID grid.266102.1, Department of Psychiatry, , University of California, ; San Francisco, CA USA
                Author information
                http://orcid.org/0000-0002-5963-6295
                http://orcid.org/0000-0002-5681-9416
                http://orcid.org/0000-0002-5681-4906
                http://orcid.org/0000-0001-5273-0150
                http://orcid.org/0000-0002-4458-6475
                http://orcid.org/0000-0003-4987-2718
                Article
                668
                10.1038/s41398-019-0668-2
                6920472
                31852887
                f03ee764-a576-46ff-b336-ca258b4e80eb
                © The Author(s) 2019

                Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

                History
                : 7 January 2019
                : 11 November 2019
                : 22 November 2019
                Funding
                Funded by: Dr Lindqvist gratefully acknowledges support from the Swedish Research Council (2015-00387), Marie Sklodowska Curie Actions, Cofund (Project INCA 600398), the Swedish Society of Medicine, the Söderström-Königska Foundation, the Sjöbring Foundation, OM Persson Foundation and the province of Scania (Sweden) state grants (ALF).
                Funded by: Dr Lavebratt gratefully acknowledges support from the Swedish Research Council (2014-10171), the Swedish Brain Foundation, the regional agreement (ALF) on medical training and clinical research between Stockholm County Council and Karolinska Institutet and the Ekhaga Foundation.
                Funded by: Dr Furmark gratefully acknowledges support by research grants from the Swedish Brain Foundation (FO2016-0106 and FO2018-0255), the Swedish Research Council (2016-0228), Riksbankens Jubileumsfond – the Swedish Foundation for Humanities and Social Sciences (2017-0639:1).
                Categories
                Article
                Custom metadata
                © The Author(s) 2019

                Clinical Psychology & Psychiatry
                human behaviour,personalized medicine
                Clinical Psychology & Psychiatry
                human behaviour, personalized medicine

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