Leigh - Genes, memes, culture, and mental illness: toward an integrative model
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Genes, memes, culture, and mental illness: toward an integrative model: summary, description and annotation
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Memes are bits of information that are replicated and passed on across individuals and generations. Memes arose when the human brain acquired the capacity to imitate others and supplement the genes as a means of providing information to the developing individual. Memes, unlike genes, have evolved rapidly in the course of human history and form the building blocks of culture. Unlike genes, memes can be stored outside of the organism in the form of written language, recordings, and in the digital form that can be replicated and transmitted without intervening human brain, like computer viruses.;Genes and mental illness -- How does stress work? the role of memes in epigenesis -- Culture and mental illness -- Genetic-memetic model of mental illness-migration and natural disasters as illustrations -- What do we inherit from our parents and ancestors? -- Genes -- Evolution -- Learning, imitation, and memes -- Storage and evolution of memes in the brain -- External storage of memes: culture, media, cyberspace -- Culture and the individual -- What is mental health -- What is mental illness? -- Psychiatric diagnosis: toward a memetic-epigenetic multiaxial model -- Memetic diagnosis, memetic assessment and biopsychosocial epigenetic formulation -- Principles of memetic therapy -- Broad-spectrum memetic therapy -- Specific memetic therapies -- Genetic-memetic prevention -- Overview of specific syndromes -- Attention-cognition spectrum syndromes: delirium, dementia, impulse control syndromes, ADHD, antisocial personality, obsessive-compulsive personality traits, obsessive-compulsive syndrome -- Anxiety-mood spectrum syndromes: anxiety, panic, phobias, ASD, PTSD, borderline syndrome, dependent and avoidant personalities, social phobia, bipolarity and mania, depression-neurotic and syndromic, adjustment disorders -- Reality perception spectrum syndromes (imagination, dissociation, conversion, somatoform, misattribution somatization, psychosis) -- Pleasure spectrum syndromes (substance use/abuse, additions to substances and beliefs, fanaticism) -- Primary memetic syndromes: eating disorders, factitious disorders, malingering, meme-directed destructive behaviors -- Challenges for the future.
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Part 1
What Is Mental Illness? An Epigenetic Model
What Is Mental Illness? An Epigenetic Model
Hoyle Leigh and Hoyle Leigh Genes, Memes, Culture, and Mental Illness Toward an Integrative Model 10.1007/978-1-4419-5671-2_1 Springer-Verlag New York 2010
1. Genes and Mental Illness
Hoyle Leigh 1
(1)
University of California, San Francisco, California, USA
Hoyle Leigh
Email:
Abstract
The concept of mental illness evolved from possession by gods and an imbalance of body fluids (including the modern version of neurotransmitter imbalance) to a model that posits an interaction between genes and the environment. Environmental stress is known to play an important role both by altering the genes early in development and as a precipitating factor for illness in later life. Recent evidence suggests that the interaction between the genes and the environment is mediated by memes information encoded in neural connections which may be endogenous or exogenous.A gene meme interaction model of mental illness is proposed.
1.1 The Evolution of the Concept of Mental Illness
Alienist s used to treat mental illness and those afflicted were considered alienated or strange. There have been essentially two lines of thought concerning the causes of mental illness: alien and endogenou s. The alien causes may be a possessio n of the gods or the devil, or, more recently, microorganisms such as bacteria and virus. The endogenous causes may be an imbalance of the body flu ids the Hippocr atic blood, phlegm, yellow bile, and black bi le (thence the term, melancholia ) or the modern version of an imbalance among seroto nin, norepinep hrine, and do pamine. It is also generally accepted that severe environmental factors such as extreme heat or cold can cause mental aberrations such as del irium.
Certain types of mental dysfunction, such as maladaptive patterns of behavior and neur osis, have been also attributed to faulty learn ing or bad mode ling. Experimenta l neuroses and lea rned helplessness have been produced in animals by confusing re wards or inescapable punishm ent (Saunders et al., ).
Mental illness is known to run in families. With the advent of biological psychiatry, it was hoped, in the latter part of the twentieth century, that the etiologic genes of mental illness would be discovered. In fact, the diagnostic and statistical manual for mental illness adopted by the American Psychiatric Association in 1980 (D SM III) was based on the resear ch diagnostic criteria (Feighner et al., ) that were designed to isolate pure cultures of psychiatric illness for biological research.
At the time DSM III was introduced, the catechola mine theory of affective disorders (Schildkraut, ) was the prevailing theory of mood disorders, chlorproma zine the most commonly used antipsychotic, and the Human G enome Project was yet not even a gleam in anyones eyes. Exciting developments have since occurred in molecular biology and genetics and the Human Genome Project has been completed ahead of schedule (2003). Psychiatric research, at least in part fostered by the rigorous diagnostic criteria of DSM III and its slight modification, DSM IV (1994), has made breathtaking advances, taking full advantage of these and other developments during the Dec ade of the Brain , including neuroimag ing techniques. On the strength of these developments, a new theoretical model of psychiatric illness has emerged that is open and evidence based.
Many putative genes that code for vulnerability for psychiatric syndromes are evolutionarily conserved. This explains why schi zophrenia which is associated with low fertility rates in the afflicted has not become extinct. Crow () postulate that vulnerability to schizophrenia may be the price that Homo sapiens had to pay for the development of lang uage, i.e., the speciat ion of humans from their ancestral apes involves the same genes that caused the left hemisph eric dominance and language. Crow proposes that there are gradations in the genetic predisposition to psychosis, across diagnostic categories of schizoph renia and bip olar disorder.
Certain genes that endow vulnerability to anxiety, for example, the short allele of the serotonin transporter promo ter gene (more of this below), may confer sensitivity to the smoke de tector of anxiety activation (Nesse, ) and be evoluti onarily adaptive when humans dwelled in caves in fear of predator animals. In the modern world, however, such sensitivity to anxiety would be dysfunctional for the individual and thus be considered a psychiatric syndrome.
1.2 Gene-Environment Interaction and Brain Morphology and Function
The genes coding for predisposition to various psychiatric syndromes are currently being defined using various techniques including linka ge studies and gen ome scan. As far as psychiatric diagnosis goes, current state of affairs can be summarized as follows: For each diagnostic category, there are many susce ptibility genes, and a single gene or a few genes may code for the susceptibility for many different disorders. On the basis of genetic studies, Kendler et al. () proposed that psychosis be reclassified as: (1) classic schiz ophrenia, (2) major depressio n, (3) schiz ophreniform disorder, (4) bipolar-schizom a ni a, (5) schizo depression, and (6) he bephrenia.
What seems clear is that psychiatric disorders are syndromes, pheno menological convergence of a number of different genetic-pathophysiologic pathways. An analogy might be hypertension. Hyper tension is a syndrome that has definable signs and complications that can be treated with antihypertensive drugs. Hypertension, however, is pathophysiologically heterogeneous it may be nephrogenic, cardiogenic, neurogenic, endocrine, secondary to familial hyperlipidemia, stress-induced, etc.
1.3 GeneEnvironment Interaction: Serotonin Transporter Gene as an Exemplar
A single gene that codes for the vulnerability to multiple psychiatric (and medical) conditions is the serotonin transport er gene (SERT) and its promoter region polymorphism (5-HTTLPR). SERT is highly evolutionarily conserved and regulates the entire seroto ninergic system and its receptors via modulation of extracellular fluid serotonin concentrations. D NA screens of patients with autism, ADH D, bipolar disorder, and Tourettes syndrome have detected signals in the chromoso me 17q region where SE RT is located (Murphy et al., ).
Why does a single gene code for so many vulnerabilities? One simple answer may be that the gene codes for one or more basic evolutionarily adaptive predispositions that, in combination with other factors, may determine the development and severity of a psychiatric syndrome. When we look at the list of vulnerabilities above, it seems clear that there is a continuum, from anxiety to adaptive/maladaptive behavior to phobia to major depression, and/or to physical symptoms. The concept of endophen otype is useful in understanding traits associated with syndromes (e.g., eye-tracking abnormality in schizophrenics and relatives) (Gottesman and Gould, ) and might provide clues to a genotypic diagnosis.
Pezawas et al. (). What other factors, then, may further predispose the individual for a major depression? 
Fig.a
Differences in processing of emotional stimuli between s allele carriers ( darker arrows ) and homozygous l allele carriers ( lighter arrows ). Negative emotional stimuli are evaluated by the amygdale after preliminary analysis in the ventral visual pathway (not shown). Carriers of the s allele have markedly reduced positive functional coupling between the rostral anterior cingulate (rACC) and the amygdala, which results in a net decrease in inhibitory feedback from the caudal anterior cingulate (cACC), via connections between rACC and cACC ( short upward arrows ). Brain volume was also substantially reduced in s allele carriers in the rACC and, to a lesser extent, the cACC and amygdala. The consequence of these genotype-based alterations is an emotional hyperresponsivity to negative affective stimuli in s allele carriers ( large dark cloud ) compared with individuals lacking this allele ( small light cloud ), which may be related to an increased risk of developing depression. As found in a previous study, functional coupling between the vmPFC ( light circle on left ) and the amygdala was also increased in s allele carriers. (From Hamann, 2005, reprinted with permission)
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