网范文：“The cultural epigenetics of psychopathology” 我们扩展认知范式，基于渐近极限定理，通过基因表达的表观遗传流行病学和信息理论，来探讨精神疾患成因。在这篇医学心理范文中,我们认识到文化在人类生物学的基本影响,另一个平行遗产机制,和更熟悉的遗传和表观遗传相互影响。我们通过一个模型，通过文化充当催化剂,并与个人本体之间变得错综复杂,这本身就是文化驱动的社会互动。
嵌入文化，英语论文网站，作为人类精神发展的重要组成部分及其障碍,将可能是生物精神病学的重点。目前我们工作在精神病学上，英语论文题目，有着基因和环境的交互影响,以避免主观主义的作用，可能会创建特定的文化,,事实上,传统的文化和表观遗传系统可能提供复杂疾病。下面的范文进行详述。
Abstract
We extend a cognitive paradigm for gene expression based on the asymptotic limit theorems of information theory to the epigenetic epidemiology of mental disorders. In particular, we recognize the fundamental role culture plays in human biology, another heritage mechanism parallel to, and interacting with, the more familiar genetic and epigenetic systems. We do this via a model through which culture acts as another tunable epigenetic catalyst that both directs developmental trajectories, and becomes convoluted with individual ontology, via a mutually-interacting crosstalk mediated by a social interaction that is itself culturally driven.
We call for the incorporation of embedding culture as an essential component of the epigenetic regulation of human mental development and its dysfunctions, bringing what is perhaps the central reality of human biology into the center of biological psychiatry. Current US work on gene-environment interactions in psychiatry must be extended to a model of gene-cultureenvironment interaction to avoid becoming victim of an extreme American individualism that threatens to create paradigms particular to that culture and that are, indeed, peculiar in the context of the world’s cultures. The cultural and epigenetic systems of heritage may well provide the ‘missing’ heritability of complex diseases now under so much intense discussion.
Key Words: biological psychiatry; cognitive paradigm; gene expression; holonomy; homotopy; information source; mental disorder; spontaneous symmetry breaking; topology
Introduction
Mental disorders and culture Human mental disorders are not well understood. Official classifications as the Diagnostic and Statistical Manual of Mental Disorders - fourth edition, (DSMIV, 1994), the standard descriptive nosology in the US, have even been characterized as ‘prescientific’ by P. Gilbert (2017) and others. Johnson-Laird et al. (2017) claim that current knowledge about psychological illnesses is comparable to the medical understanding of epidemics in the early 19th century. Physicians realized then that cholera, for example, was a specific disease, which killed about a third of the people whom it infected. What they disagreed about was the cause, the pathology, and the communication of the disease.
Similarly, according to Johnson-Laird et al., most medical professionals these days realize that psychological illnesses occur (cf. DSMIV), but they disagree about their cause and pathology. Notwithstanding DSMIV, Johnson-Laird et al. doubt whether any satisfactory a priori definition of psychological illness can exist because it is a matter for theory to elucidate. Atmanspacher (2017) argues that formal theory of high level cognitive process is itself at a point similar to that of physics 400 years ago, in that the basic entities, and the relations between them, have yet to be delineated. More generally, simple arguments from genetic determinism regarding mental disorders fail, in part because of a draconian population bottleneck that, early in our species’ history, resulted in an overall genetic diversity less than that observed within and between contemporary chimpanzee subgroups.
Manolio et al. (2017) describe this conundrum more generally in terms of ‘finding the missing heritability of complex diseases’. They observe, for example, that at least 40 loci have been associated with human height, a classic complex trait with an estimated heritability of about 80 %, yet they explain only about 5 % of phenotype variance despite studies of tens of thousands of people.
This result, they find, is typical across a broad range of supposedly heritable diseases, and call for extending beyond current genome-wide assoication approaches to illuminate the genetics of complex diseases and enhance its potential to enable effective disease prevention or treatment. Arguments from psychosocial stress fare better (e.g., Brown et al., 1973; Dohrenwend and Dohrenwend, 1974; Eaton, 1978), particularly for depression (e.g., Risch et al., 2017), but are affected by the apparently complex and contingent developmental paths determining the onset of schizophrenia, dementias, psychoses, and so forth, some of which may be triggered in utero by exposure to infection, low birthweight, or other functional teratogens. P. Gilbert suggests an extended evolutionary perspective, in which evolved mechanisms like the ‘flight-or-fight’ response are inappropriately excited or suppressed, resulting in such conditions as anxiety or post traumatic stress disorders. Nesse (2017) suggests that depression may represent the dysfunction of an evolutionary adaptation which down-regulates foraging activity in the face of unattainable goals.
Kleinman and Good, however, (1985, p. 492) outline something of the cross cultural subtleties affecting the study of depression that seem to argue against any simple evolutionary or genetic interpretation. They state that, when culture is treated as a constant, as is common when studies are conducted in our own society, it is relatively easy to view depression as a biological disorder, triggered by social stressors in the presence of ineffective support, and reflected in a set of symptoms or complaints that map back onto the biological substrate of the disorder.
However, they continue, when culture is treated as a significant variable, for example, when the researcher seriously confronts the world of meaning and experience of members of non-Western societies, many of our assumptions about the nature of emotions and illness are cast in sharp relief. Dramatic differences are found across cultures in the social organization, personal experience, and consequences of such emotions as sadness, grief, and anger, of behaviors such as withdrawal or aggression, and of psychological characteristics such as passivity and helplessness or the resort to altered states of consciousness.
They are organized differently as psychological realities, communicated in a wide range of idioms, related to quite varied local contexts of power relations, and are interpreted, evaluated, and responded to as fundamentally different meaningful realities. Depressive illness and dysphoria are thus not only interpreted differently in non-Western societies and across cultures; they are constituted as fundamentally different forms of social reality. Since publication of that landmark study, a number of comprehensive overviews have been published that support its conclusions, for example Bebbington (1993), Jenkins, Kleniman and Good (1990), Journal of Clinical Psychiatry (Supplement 13), and Manson (1995).
As Marsella (2017) writes, it is now clear that cultural variations exist in the areas of meaning, perceived causes, onset patterns, epidemiology, symptom expression, course, and outcome, variations having important implications for understanding clinical activities including conceptualization, assessment, and therapy. Kleinman and Cohen (1997) argue forcefully that several myths have become central to psychiatry. The first is that the forms of mental illness everywhere display similar degrees of prevalence.
The second is an excessive adherence to a principle known as the pathogenic/pathoplastic dichotomy, which holds that biology is responsible for the underlying structure of a malaise, whereas cultural beliefs shape the specific ways in which a person experiences it. The third myth maintains that various unusual culture-specific disorders whose biological bases are uncertain occur only in exotic places outside the West. In an effort to base psychiatry in ‘hard’ science and thus raise its status to that of other medical disciplines, psychiatrists have narrowly focused on the biological underpinnings of mental disorders while discounting the importance of such ‘soft’ variables as culture and socioeconomic status.
Heine (2017) describes an explicit cultural psychology that views the person as containing a set of biological potentials interacting with particular situational contexts that constrain and afford the expression of various constellations of traits and patterns of behavior. He says that, unlike much of personality psychology, cultural psychology focuses on the constraints and affordances inherent to the cultural environment that give shape to those biological potentials. Human nature, from this perspective, is seen as emerging from participation in cultural worlds, and of adapting oneself to the imperatives of cultural directives, meaning that our nature is ultimately that of a cultural being.
Heine describes how cultural psychology does not view culture as a super- ficial wrapping of the self, or as a framework within which selves interact, but as something that is intrinsic to the self, so that without culture there is no self, only a biological entity deprived of its potential. Individual selves, from Heine’s perspective, are inextricably grounded in a configuration of consensual understandings and behavioral customs particular to a given cultural and historical context, so that understanding the self requires an understanding of the culture that sustains it. Heine argues, then, that the process of becoming a self is contingent on individuals interacting with, and seizing meanings from, the cultural environment.
Heine warns that the extreme nature of American individualism means that a psychology based on late 20th century American research not only stands the risk of developing models that are particular to that culture, but of developing an understanding of the self that is peculiar in the context of the world’s cultures. Indeed, as Norenzayan and Heine (2017) point out, for the better part of a hundred years, a considerable controversy has raged within anthropology regarding the degree to which psychological and other human universals do, in fact, actually exist independent of the particularities of culture. Arnett (2017), in a provocatively titled The Neglected 95 %, similarly argues that US psychological research focuses too narrowly on Americans, who comprise less than 5 percent of the world’s population, and on perhaps another 7 percent in Western countries.
He asserts that the majority of the world’s population lives in under vastly different conditions, underlying doubts of how representative American psychological research can be, and finds the narrowness of American research to be a consequence of a focus on a philosophy of science that emphasizes fundamental processes and ignores or strips away cultural context. Henrich et al. (2017), in a wide-ranging review, extend the considerations of Norenzayan and Heine, finding that Western, educated, industrialized and democratic (WEIRD) subjects, across domains of visual perception, fairness, categorization, spatial cognition, memory, moral reasoning, and self-concepts, constitute frequent outliers compared with the rest of the species.
They conclude that addressing questions of human psychology will require tapping broader subject pools. As Durham (1991) and Richerson and Boyd (2017) explore at some length, humans are endowed with two distinct but interacting heritage systems: genes and culture. Durham (1991), for example, writes that genes and culture constitute two distinct but interacting systems of information inheritance within human populations and information of both kinds has influence, actual or potential, over behaviors, which creates a real and unambiguous symmetry between genes and phenotypes on the one hand, and culture and phenotypes on the other.
Genes and culture, in his view, are best represented as two parallel lines or tracks of hereditary influence on phenotypes. Both genes and culture can be envisioned as generalized languages in that they have recognizable ‘grammar’ and ‘syntax’, in the sense of Wallace (2017) and Wallace and Wallace (2017, 2017). More recent work has identified epigenetic heritage mechanisms involving such processes as environmentally-induced gene methylation, that can have strong influence across several generations (e.g., Jablonka and Lamb, 1995, 1998; Jabolonka, 2017), and are the subject of intense current research. There are, it seems, two powerful heritage mechanisms in addition to the genetic where one may perhaps find the ‘missing heritability of complex diseases’ that Manolio et al. seek. Here, however, we are particularly interested in the phenotypes of madness, and in their relations to genes, culture, and environment.()
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