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International Journal of Psychological Research

versão impressa ISSN 2011-2084

int.j.psychol.res. vol.6 no.1 Medellín jan./jun. 2013


DSM-5 Hype or Hope

Jorge Mauricio Cuartas Arias*,a,b, Carlos López Jaramillob

a Psychology faculty, University of San Buenaventura. Medellin, Colombia.
b Faculty of Medicine, Department of Psychiatry, University of Antioquia. Medellin, Colombia.
* Corresponding author. Faculty of Psychology, University of San Buenaventura. Medellín, Colombia. Tel. 57-4-5145600 Ext: 4245. Email:

After fourteen years of review, the expected update of the Diagnostic and Statistical Manual of Mental Disorders (DSM) has generated great controversy among psychiatrists and psychologists around the world. So far, it is known that the new version (DSM-5), officially presented for the first time in May 18 of this year as part of the annual meeting of the American Psychiatric Association (APA), will be available in Spanish language at the beginning of 2014. However, the reviews and comments for and against the new version suggest that there is no consensus in the scientific community to address mental illness. Beyond the instructive of categorical diagnosis that has prevailed in previous versions and a good part of the new text, the dimensional proposal is articulated with the use of clinical subtypes, severity levels and the inclusion of transverse symptoms, which allow to have a deterioration or vulnerability gradient (Regier, Kuhl, & Kupfer, 2013).

The new manual incorporates structural changes that eliminate multi-axial system and reorganizes the presentation of disease throughout the text (Regier et al., 2013). Although the manual constructed from empirical data and descriptive sophistries in its clinical components has not enough etiopathogenic reach of mental disorders and does not suggest a psychotherapeutic nor psychopharmacological line to address disorders, it provides a reference and a common language for professionals of mental health in favor of classifying the psychopathology and mental disorders (Sachdev, 2013).

Since this version it will not be necessary to wait for other two decades to make the changes recommended by researchers and concepts of experts because once the forceful data that supports such changes is found it will be possible to implement them immediately, which makes this manual a "living" instrument. From now on some possible clinical situations of interest, which could be considered as new disorders if they get support by investigations, are proposed. Nevertheless, the new manual has difficulties to refine the global criteria that could be the basis of the creation of specific constructs. Perhaps, that happens because of the lack of longitudinal and transcultural studies, which could be one of the most significant aspects at the moment of implement the new version. (Warren, 2013).

Maybe one of the strongest critiques about the DSM 5 is the lack of contemplation of the reaches in neuroscience and molecular biology to facilitate the categorization or dimension of the psychiatric disorder. However, the advances in neuroscience, pharmacogenetics and molecular genetics have not achieved to be forceful to delimit molecular channels circumscribed in specific pathologies. For instance, in June of 2013, it has been reported 1294 genes for Schizophrenia with studies of genetic association of Genome-wide association study (GWAS), of which the candidate gene of Neurexin 1 (NRXN1), a presynaptic protein related to the glutamatergic synapse and strongly associated with synaptogenesis, has 6 GWAS and 21 studies of genetic association. In a similar way, Autism has to date 574 candidate genes potentially associated, and the gene with more GWAS (3) is also NRXN1, which has 16 studies of genetic association (Yu et al., 2008). It is clear that these diseases are different, and the psychiatric nosology has evolved in a responsible way since the DSM I (1952) and the DSM II (1968), when Autism was a symptom of Schizophrenia. However, the molecular complexity to refine the etiopathogenesis does not allow yet to close the molecular "gap" that differentiate the molecular genetic of both disorders. Currently, biomedical sciences are enough advanced to define molecular channels that reveal patterns of susceptibility, but it is still necessary to analyze the epistatic processes in putative genes that could control the expression levels in the phenotype of interest and to progress regarding the mixing patterns and the genetic structure of populations (Cuartas et al., 2011).

For the time being the unexpected consequences that hang over the DSM 5 could be in the forensic reaches of the text and questioning the clinical and legal approaches of Pedophilia and the hypersexual disorder. With all this, and the impossibility of step back, it is observable the critical impact of DSM 5. Maybe some adjustments are going to be made during the first five years, which could facilitate the way to reach physiological and molecular basis of mental illness and to improve the diagnosis regarding the reconnaissance of the environmental variables that could delineate the final phenotype and its prognosis.


Cuartas Arias, J. M., Palacio Acosta, C. A., Valencia, J. G., Montoya, G. J., Arango Viana, J. C., Nieto, O. C...& Ruiz-Linares, A. (2011). Exploring epistasis in candidate genes for antisocial personality disorder. Psychiatric Genetics, 21(3), 115-24. doi: 10.1097/YPG.0b013e328343717.         [ Links ]

Regier, D. A., Kuhl, E. A. & Kupfer, D. J. (2013). The DSM-5: Classification and criteria changes. World psychiatry: official journal of the World Psychiatric Association, 12(2), 92-98. doi: 10.1002/wps.20050.         [ Links ]

Sachdev, P. S. (2013). Is DSM-5 defensible? The Australian and New Zealand journal of psychiatry, 47(1), 10-11. doi: 10.1177/0004867412468164.         [ Links ]

Warren, B. J. (2013). How culture is assessed in the DSM-5. Journal of psychosocial nursing and mental health services, 51(4), 40-45. doi: 10.3928/02793695-20130226-04.         [ Links ]

Yu, W., Gwinn, M. Clyne, M., Yesupriya, A. & Khoury, M. J. (2008). A navigator for human genome epidemiology. Nat Genet,40(2), 124-5. Retrieved from.         [ Links ]