Estoy leyendo un libro de difusión científica titulado "Por qué somos como somos" del conocido conductor del programa Redes para la Ciencia (RTVE), Eduardo Punset. Allí me encontré con información sobre algo que yo había pensado antes, pero no lo había articulado por falta de fundamento científico de mi parte, así que me sorprendió encontrarlo en este libro sencillo de leer pero con gran seriedad intelectual.
Escribe Punset: "...sin duda la herencia, lo que llamamos predisposición genética, existe. Y no sólo para las cualidades más o menos positivas, también para la enfermedad. Es interesante desde el punto de vista analítico el hecho de que existan familias con graves enfermedades mentales en las que encontramos a la vez el genio y la esquizofrenia, en ocasiones en el mismo individuo. Dos recientes premios Nobel son esquizofrénicos. [...]
Las investigaciones que se están llevando a cabo sobre estos temas desde el punto de vista evolucionista son apasionantes y algunas nos acercan a hipótesis sorprendentes. Por ejemplo, según afirma Tobias, es posible que en su origen (que puede remontarse 150,000 años) el gen de la esquizofrenia haya sido decisivo en cuestiones que nada tienen que ver con el comportamiento psicótico, sino con el genio, la capacidad de liderazgo, la música o la religiosidad. Asunto este de la religiosidad que fue determinante en los primeros tiempos de evolución de la cultura. Hoy día, sin embargo, la ciencia apuesta con mayor facilidad por desvincular las enfermedades mentales como la depresión o la esquizofrenia del genio para considerarlas, simplemente, enfermedades mentales." Texto completo AQUÍ
Su cita de Philip Tobias es de un programa en Redes para la Ciencia, con otro paleoantropólogo llamado Ralph Holloway.
Por experiencia propia, sobre la vinculación entre "enfermedades" mentales y religión sí me atreví a escribir algo AQUÍ mismo.
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Is schizophrenia the price that Homo sapiens pays for language?
Timothy J. Crow*
Prince of Wales Centre, University Department of Psychiatry, Warneford Hospital, Oxford, OX3 7JX, UK
Received 7 March 1997; accepted 17 July 1997. Available online 13 February 1998.
Abstract
The dichotomy between schizophrenia and manic-depressive illness is, as E. Kraepelin suspected, flawed; no unequivocal separation can be achieved. There are no categories of psychosis, but only continua of variation. However, the definition of nuclear symptoms by K. Schneider reveals the fundamental characteristics of the core syndrome—it is independent of the environment and constant in incidence across populations that have been separated for thousands of years. The associated genetic variation must be as old as Homo sapiens and represent a component of diversity that crosses the population as a whole. The fecundity disadvantage that accompanies the syndrome requires a balance in a substantial and universal advantage; this advantage, it is proposed, is the speciation characteristic of language; language and psychosis have a common evolutionary origin. Language, it is suggested, originated in a critical change on the sex chromosomes (the ‘speciation event’—the genetic change that defined the species) occurring in East Africa between 100 and 250 thousand years ago that allowed the two hemispheres to develop with a degree of independence. Language can be understood as bi-hemispheric with one component function—a linear output sequence—confined to the dominant hemisphere—and a second—parallel distributed sampling occurring mainly in the non-dominant hemisphere. This mechanism provides an account of the generativity of language. The significance of nuclear symptoms is that these reflect a breakdown of bi-hemispheric coordination of language, perhaps specifically of the process of ‘indexicalisation’ (the distinction between ‘I’ and ‘you’) of self- versus other-generated references. Nuclear symptoms can be described as ‘language at the end of its tether’; the phenomena and population characteristics of the nuclear syndrome of schizophrenia thus yield clues to the origin of the species.
Keywords: Nuclear; Schizophrenia; Speciation; Language; Dominance
Molecular Psychiatry 14, 1072-1082 (December 2009)
The role of genetic variation in the causation of mental illness: an evolution-informed frameworkGenetic variation in the causation of mental illness
R Uher
Abstract
The apparently large genetic contribution to the aetiology of mental illness presents a formidable puzzle. Unlike common physical disorders, mental illness usually has an onset early in the reproductive age and is associated with substantial reproductive disadvantage. Therefore, genetic variants associated with vulnerability to mental illness should be under strong negative selection pressure and be eliminated from the genetic pool through natural selection. Still, mental disorders are common and twin studies indicate a strong genetic contribution to their aetiology. Several theories have been advanced to explain the paradox of high heritability and reproductive disadvantage associated with the same common phenotype, but none provides a satisfactory explanation for all types of mental illness. At the same time, identification of the molecular substrate underlying the large genetic contribution to the aetiology of mental illness is proving more difficult than expected. The quest for genetic variants associated with vulnerability to mental illness is predicated upon the common disease/common variant (CDCV) hypothesis. On the basis of a summary of evidence, it is concluded that the CDCV hypothesis is untenable for most types of mental illness. An alternative evolution-informed framework is proposed, which suggests that gene–environment interactions and rare genetic variants constitute most of the genetic contribution to mental illness. Common mental illness with mild reproductive disadvantage is likely to have a large contribution from interactions between common genetic variants and environmental exposures. Severe mental illness that confers strong reproductive disadvantage is likely to have a large and pleiotropic contribution from rare variants of recent origin. This framework points to a need for a paradigm change in genetic research to enable major progress in elucidating the aetiology of mental illness.
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