NM  Vol.3 No.1 , March 2012
Differential Relationships among Facets of Alexithymia and BDNF- and Dopamine-Related Polymorphisms
Abstract: Alexithymia refers to a cluster of emotion-related deficits such as difficulty attending to and identifying one’s feelings. Although not a diagnosable psychiatric condition, alexithymia is considered a personality risk factor for multiple pathologies, including somatoform, substance use, eating, and mood disorders. Evidence suggests heritability, but few studies have examined the influence of specific genes on alexithymic traits. Candidate genes explored thus far include those involved in modulation of brain-derived neurotrophic factor (BDNF) and dopamine, two neurotransmitters whose functions have been implicated in human emotion processing. This study investigated the relationship between the C270T polymorphism of the BDNF gene, facets of alexithymia, and possible interactions with the COMT, DAT1, and ANKK1 genes in a sample of 130 healthy adults. Given the multidimensionality of the alexithymia construct and its overlap with the related constructs of emotional intelligence and mood awareness, we used principal components analysis to derive Clarity of Emotion and Attention to Emotion as specific facets of alexithymia. Results showed that the C270T C/C genotype group had lower Clarity of Emotion scores relative to the C/T genotype group, even after covarying for COMT, DAT1, and ANKK1 genotypes. Dopamine-related genes had no association with alexithymia dimensions, nor did they interact with the C270T polymorphism to predict Clarity of Emotion. Although the molecular mechanisms by which this polymorphism influences BDNF are unknown, this study suggests a role for BDNF in modulating aspects of alexithymia. We discuss these results in the context of BDNF’s trophic effects in the nervous system.
Cite this paper: N. S. Koven and L. H. Carr, "Differential Relationships among Facets of Alexithymia and BDNF- and Dopamine-Related Polymorphisms," Neuroscience and Medicine, Vol. 3 No. 1, 2012, pp. 7-13. doi: 10.4236/nm.2012.31002.

[1]   G. B. Taylor, M. Bagby and J. D. Parker, “Disorders of Affect Regulation: Alexithymia in medical and Psychiatric Illness,” Cambridge University Press, New York City, 1997. doi:10.1017/CBO9780511526831

[2]   J. L. King and B. Mal-linckrodt, “Family Environment and Alexithymia in Clients and Non-Clients,” Psychotherapy Research, Vol. 10, No. 1, 2000, pp. 78-86. doi:10.1080/713663595

[3]   S. Koponen, T. Taiminen, K. Honkalampi, M. Joukamaa, H. Vinnamaki, T. Kurki, et al., “Alexithymia after Traumatic Brain Injury: Its Relation to Magnetic Resonance Imaging,” Psychosomatic Medicine, Vol. 67, No. 5, 2005, pp. 807-812. doi:10.1097/01.psy.0000181278.92249.e5

[4]   S. B. Zeitlin, R. J. McNally and K. L. Cassiday, “Alexithymia in Victims of Sexual Assault: An Effect of Re- peated Traumatization?” American Journal of Psychiatry, Vol. 150, No. 4, 1993, pp. 661-663.

[5]   J. K. Salminen, S. Saarij?rvi, E. ??rel?, T. Toikka and J. Kauhanen, “Prevalence of Alexithymia and Its Association with Sociodemographic Variables in the General Population of Finland,” Journal of Psychosomatic Research, Vol. 46, No. 1, 1998, pp. 75-82. doi:10.1016/S0022-3999(98)00053-1

[6]   M. M. J?rgensen, R. Zachariae, A. Skytthe and K. Kyvik, “Genetic and Environmental Factors in Alexithymia: A Population-Based Study of 8,785 Danish Twin Pairs,” Psychotherapy and Psychosomatics, Vol. 76, No. 6, 2007, pp. 369-375. doi:10.1159/000107565

[7]   E. M. Valera and H. Berenbaum, “A Twin Study of Alexithymia,” Psychotherapy and Psychosomatics, Vol. 70, No. 5, 2001, pp. 239-246. doi:10.1159/000056261

[8]   H. M. Abdolmaleky, C. L. Smith, J. R. Zhou and S. Thiagalingam, “Epigenetic Alterations of the Dopaminergic System in Major Psychiatric Disorders,” Methods in Molecular Biology, Vol. 448, 2008, pp. 187-212. doi:10.1007/978-1-59745-205-2_9

[9]   N. T. Walter, C. Mon-tag, S. A. Markett and M. Reuter, “Interaction Effect of Functional Variants of the BDNF and DRD2/ANKK1 Gene Is Associated with Alexithymia in Healthy Human Subjects,” Psychosomatic Medicine, Vol. 73, No. 1, 2011, pp. 23-28. doi:10.1097/PSY.0b013e31820037c1

[10]   B. J. Ham, M. S. Lee, Y. M. Lee, M. K. Kim, M. J. Choi, K. S. Oh, et al., “As-sociation between the Catechol-O-Methyltransferase Val108/158Met Polymorphism and Alexithymia,” Neuropsychobiology, Vol. 52, No. 3, 2005, pp. 151-154. doi:10.1159/000087846

[11]   S. Hermes, J. Hennig, M. Stingl, F. Leichsenring and F. Leweke, “No Association between Catechol-O-Methyltransferase val158met Polymorphism and Alexithymia,” Zeitschrift fur Psychosomatische Medizin und Psychotherapie, Vol. 57, No. 1, 2011, pp. 51-61.

[12]   T. Poh-jalainen, J. O. Rinne, K. N?gren, P. Lehikoinen, K. Anttila, E. K. Syv?lathi et al., “The A1 Allele of the Human D2 Dopamine Receptor Gene Predicts Low D2 Receptor Availability in Healthy Volunteers,” Molecular Psychiatry, Vol. 3, No. 3, 1998, pp. 256-260. doi:10.1038/

[13]   H. Gündel, A. Lopez-Sala, A. O. Ceballos-Baumann, J. Deus, N. Cardoner, B. Marten-Mittag, C. Soriano-Mas, et al., “Alexithymia Correlates with Size of the Right Anterior Cingulate,” Psychosomatic Medicine, Vol. 66, No. 1, 2004, pp. 132-140. doi:10.1097/01.PSY.0000097348.45087.96

[14]   H. Karlsson, P. N??t?nen and H. Stenman, “Cortical Activation in Alexi-thymia as a Response to Emotional Stimuli,” British Journal of Psychiatry, Vol. 192, 2008, pp. 32-38. doi:10.1192/bjp.bp.106.034728

[15]   N. S. Koven, R. M. Roth, M. A. Garlinghouse, L. A. Flashman and A. J. Saykin, “Regional Gray Matter Correlates of Perceived Emotional Intelligence,” Social, Cognitive, and Affective Neuroscience, Vol. 6, No. 5, 2010, pp. 582-590. doi:10.1093/scan/nsq084

[16]   C. Montag, B. Weber, E. Jentgens, C. Elger and M. Reuter, “An Epistasis Effect of Functional Variants on the BDNF and DRD2 Genes Modulates Grey Matter Volume of the Anterior Cingulate Cortex in Healthy Humans,” Neuropsychologia, Vol. 48, No. 4, 2010, pp. 1016-1021. doi:10.1016/j.neuropsychologia.2009.11.027

[17]   H. Kunugi, A. Ueki, M. Otsuka, K. Isse, H. Hirasawa and K. Kato, “A Novel Polymorphism of the Brain-Derived Neurotrophic Factor (BDNF) Gene Associated with Late-Onset Alzheimer’s Disease,” Molecular Psychiatry, Vol. 6, No. 1, 2001, pp. 83-86. doi:10.1038/

[18]   A. Parsian, R. Sinha, B. Racette, J. H. Zhao and J. S. Perlmutter, “Association of a Variation in the Promoter Region of the Brain-Derived Neurotrophic Factor Gene with Familiar Parkinson’s Disease,” Parkinsonism and Related Disorders, Vol. 10, No. 4, 2004, pp. 213-219. doi:10.1016/j.parkreldis.2003.12.003

[19]   A. Szczepankiewicz, M. Skibińska, J. Hauser, A. Leszc-zyńska-Rodziewicz, M. Dmitrzak-Weglarz, P. M. Czerski, et al., “Association Study of the Brain-Derived Neurotrophic Factor (BDNF) Gene C-270T Polymorphism with Bipolar Affective Disorder,” Archives of Psychiatry and Psychotherapy, Vol. 8, 2006, pp. 31-39.

[20]   G. Szekeres, A. Juhász, A. Rimanóczy, S. Kéri and Z. Janka, “The C270T Polymorphism of the Brain-Derived Neurotrophic Factor Gene Is Associated with Schizo- phrenia,” Schizophrenia Research, Vol. 65, No. 1, 2003, pp. 15-18. doi:10.1016/S0920-9964(02)00505-4

[21]   M. Nakatome, K. Honda, Z. Tun, Y. Kato, S. Harihara, K. Omoto, et al., “Genetic Polymorphism of the 3’ VNTR Region of the Human Dopaminergic Function Gene DAT1 (Human Dopamine Transporter Gene) in the Mongolian Population,” Human Biology, Vol. 68, No. 4, 1996, pp. 509-515.

[22]   A. M. Kang, M. A. Palmatier and K. K. Kidd, “Global Variation of a 40-bp VNTR in the 3’ Untranslated Region of the Dopamine Transporter Gene (SLC6A3),” Biological Psychiatry, Vol. 46, No. 2, 1999, pp. 151-160. doi:10.1016/S0006-3223(99)00101-8

[23]   J. Mill, P. Asherson, C. Browes, U. D’Souza and I. Craig, “Expression of the Dopamine Transporter Gene Is Regulated by the 3’ UTR VNTR: Evidence from Brain and Lymphocytes Using Quantitative RT-PCR,” American Journal of Medical Genetics, Vol. 114, No. 8, 2002, pp. 975-979. doi:10.1002/ajmg.b.10948

[24]   A. Diamond, “Consequences of Variations in Genes that Affect Dopamine in Prefrontal Cortex,” Cerebral Cortex, Vol. 17, No. 1, 2007, pp. 161-170. doi:10.1093/cercor/bhm082

[25]   E. Coffey, H. Berenbaum and J. G. Kerns, “The Dimensions of Emotional Intelligence, Alexithymia, and Mood Awareness: Associations with Personality and Performance on an Emotional Stroop Task,” Cognition and Emotion, Vol. 17, No. 4, 2003, pp. 671-679. doi:10.1080/02699930302304

[26]   N. S. Koven and W. Tho-mas, “Mapping Facets of Alexi- thymia to Executive Dysfunction in Daily Life,” Personality and Individual Differences, Vol. 49, No. 1, 2010, pp. 24-28. doi:10.1016/j.paid.2010.02.034

[27]   R. Becerra, A. Amos and S. Jongenelis, “Organic Alexi- thymia: A Study of Acquired Emotional Blindness,” Brain Injury, Vol. 16, No. 7, 2002, pp. 633-45. doi:10.1080/02699050110119817

[28]   D. V. Sheehan, Y. Lecrubier, K. Harnett-Sheehan, P. Amorim, J. Janavs, E. Weiller, et al., “The Mini International Neuropsychiatric Interview (M.I.N.I.): The Development and Validation of a Structured Diagnostic Psychiatric Interview for DSM-IV and ICD-10,” Journal of Clinical Psychiatry, Vol. 59, No. 20, 1998, pp. 22-23.

[29]   P. Salovey, J. D. Mayer, S. L. Goldman, C. Turvey and T. P. Palfai, “Emotional Attention, Clarity, and Repair: Ex-ploring Emotional Intelligence Using the Trait meta- Mood Scale,” In: J. W. Pennebaker, Ed., Emotion, Disclosure, and Health, American Psychological Association, Washington DC, 1995, pp. 125-154. doi:10.1037/10182-006

[30]   A. Swinkles and T. A. Giuliano, “The Measurement and Conceptualization of Mood Awareness: Monitoring and Labeling One’s Mood States,” Personality and Social Psychology Bulletin, Vol. 21, No. 9, 1995, pp. 934-950.

[31]   R. M. Bagby, G. J. Taylor and J. D. A. Parker, “The Twenty-Item Toronto Alexithymia Scale: II. Convergent, Discriminant, and Concurrent Validity,” Journal of Psychoso-matic Research, Vol. 38, No. 1, 1994, pp. 33-40. doi:10.1016/0022-3999(94)90006-X

[32]   C. G. Kooiman, P. Spinhoven and R. W. Trijsburg, “The Assessment of Alexithymia: A Critical Review of the Literature and a Psychometric Study of the Toronto Alexithymia Scale-20,” Journal of Psychosomatic Research, Vol. 53, No. 6, 2002, pp. 1083-1090. doi:10.1016/S0022-3999(02)00348-3

[33]   M. B. Harris, “Correlates and Characteristics of Boredom Proneness and Boredom,” Journal of Applied Social Psychology, Vol. 3, No. 3, 2000, pp. 576-598. doi:10.1111/j.1559-1816.2000.tb02497.x

[34]   M. Garcia-Garcia, F. Barceló, I. C. Clemente and C. Escera, “The Role of the Dopamine Transporter DAT1 Genotype on the Neural Correlates of Cognitive Flexibility,” European Journal of Neuroscience, Vol. 31, No. 4, 2010, pp. 754-760. doi:10.1111/j.1460-9568.2010.07102.x

[35]   B. G. Tabachnick and L. S. Fidell, “Using Multivariate Statistics” 5th Edition, Pearson Education, Boston, 2007.

[36]   J. P. Stevens, “Applied Multivariate Statistics for the Social Sciences,” 4th Edition, Lawrence Erlbaum Associates, Mahwah, 2002.

[37]   E. Guadagnoli and W. F. Velicer, “Relation of Sample Size to the Stability of Component Patterns,” Psychological Bulletin, Vol. 103, No. 2, 1988, pp. 265-275. doi:10.1037/0033-2909.103.2.265

[38]   R. D. Anderson and H. Rubin, “Statistical Inference in Factor Analysis,” Proceedings of the 3rd Berkeley Symposium of Mathematical Statistics and Probability, Vol. 5, 1956, pp. 111-150.

[39]   H. A. Wishart, R. M. Roth, A. J. Saykin, H. Rhodes, G. J. Tsongalis, K. A. Pattin, et al., “COMT Val158Met Genotype and Individual Differences in Executive Function in Healthy Adults,” Journal of the International Neuropsychological Society, Vol. 17, No. 1, 2011, pp. 174-180. doi:10.1017/S1355617710001402

[40]   K. J. Rothman, “No Adjustments Are Needed for Multiple Comparisons,” Epidemi-ology, Vol. 1, No. 1, 1990, pp. 43-46. doi:10.1097/00001648-199001000-00010

[41]   K. G. Bath and F. S. Lee, “Variant BDNF (Val66Met) Impact on Brain Struc-ture and Function,” Cognitive, Affective, and Behavioral Neuroscience, Vol. 6, No. 1, 2006, pp. 79-85. doi:10.3758/CABN.6.1.79