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Schizophrenia
Schizophrenia: 2.1B-D (Environ. Dysreg. Dis.) A Disorder
of Spacing? Stevens
& Price (2000) describe schizophrenia as a "spacing"
disorder. They argue that the genetic tendency towards schizophrenia
evolved in the context of rapid group splitting, group elimination, externally
medicated sexual selection, facilitated and contributed to the evolution of
language. They suggest that the schizotypal genotype is an adaptation
whose function is
to facilitate group splitting, achieved by the formation of a subgroup (or cult)
under the influence of a charismatic leader, who is enabled by his borderline
psychotic thinking to separate himself from the dogma of the main group and
create a new community with a new world view. (Group splitting has the
advantage of facilitate movement to a new habitat, leading to dispersal and
population growth.) Externally mediated mate selection, where
marriages are arranged for young people by their elders, introduces a form of
artificial selection. Therefore, these authors appear to be
proposing that the schizotypal genotype may benefit the Hierarchical/Ranking
(B) and Courtship/Mating (C)
Archetype Moore
et al (2006) reveals the considerable offspring benefits resulting
from being a warlord leader, suggesting that potentiation of the
Threat Response
Archetype A Disorder of By-product of Physiological Advantage?
Haukka
et al (2003)
consider whether schizophrenia may have in the past carried some
physiological advantage compared to the general population, but no longer do so
due to environmental changes. In their study on regional differences in the incidence of
schizophrenia, Haukka
et al showed that areas that had higher neonatal
mortality rates used to have higher incidences of schizophrenia. It has
been suggested that the schizophrenia genotype may impart a greater robustness
leading to increased survival. If this is the case, then this advantage
may have disappeared when factors that caused the higher neonatal mortality rate
disappeared. They also suggest that fertility rates may have declined as a recent
phenomenon in Western countries due to the cultural/economic trend of young
people delaying marriage and having children. The number of offspring
would be lower in schizophrenia populations because the onset of their disorders
would have consequences such as: reducing their marriage prospects, leading to
higher divorce rates & reducing their frequency of sexual intercourse.
If they had not delayed marriage or having children, a proportion would have had
offspring before the onset of their disorder. Haukka
et al found that the siblings of people with schizophrenia had significantly higher fertility
rates, but these rates did not compensate for the lower
fertility rate in those with schizophrenia. It was a Finnish cohort study of 870,093
individuals born over 10 years (1950-1959). Out of this cohort, 11,231
(1.3%) had schizophrenia and 24,319 (2.8%) were siblings. The fertility
rates of the patients with schizophrenia was half that of the general
population. Female siblings had slightly higher fertility than the
general population (1.89 vs 1.83 offspring) & male siblings had lower
fertility (1.57 vs 1.65 offspring). The proportion of genes inherited from these
families was calculated to be lower in each successive generation. A Disorder of Integration?
The first rank symptoms, which result from a disconnection
between the sense of individual self & the outside world, smack of the
disconnection symptoms found in the disorders
of integration proposed by Edelman
& Tononi (2000). Examples of symptoms where there appears to
be a breakdown between cortical connectedness are thought insertion,
withdrawal & broadcast (where the subject disowns his/her own thoughts
perceiving them to be someone else's or influenced by outside forces), ideas of
reference (where the subject makes inaccurate associations between external
events and him/herself) and delusions (where inaccurate attributions are made
& erroneous ideas develop). Cleghorn and Albert
(1990) argue that psychosis, and schizophrenia in particular, may be a
problem
in the integrated functioning of internal modular processing systems. They suggest that
neural networks subserving cognitive and emotional modules are desynchronised in their activation and inactivation
– a problem they term cognitive disjunction – and that this causes the symptoms of the disorder. They attribute both
positive and negative symptoms to “desynchronisation of widely distributed neurocognitive systems.” A Disorder of Over-Pruning
(The Developmentally Reduced Synaptic Connectivity
Model)? One model proposed where the central premise requires reduced integration
is that of synaptic
over-pruning.
Pruning is a normal developmental process where a selective
elimination of weaker connections occur to about 60% of maximal levels.
Most of this process is complete by age 2 in sensory cortical areas such as the
occipital & temporal cortex but is not complete until mid-adolescence
(or early adulthood) in association areas such as the prefrontal & parietal
cortex. Reflecting these changes is grey matter loss starting around age
5, becoming more robust in late childhood & adolescence, then tailing off to
lower adult rates in the 30s. McGlashan
& Hoffman (2000) use a neural network computer simulation to investigate
pruning.
There is investigatory evidence for reduced cortical
connectedness (a loss of connections between neurones with intact neuronal
numbers) in schizophrenia, in post-mortem histopathologic studies &
neuroimaging studies (cited
by McGlashan
& Hoffman 2000). Based on their research, they suggest that excessive reduction of synaptic connectivity due to over-pruning
may cause
Survival may select naturally toward maximal neuritic pruning with its attendant risk of over-pruning. This may account for the persistence of the schizophrenia genotype & familial association between creativity, genius & psychosis. Schizophrenia may therefore be the negative by-product of environmental pressure towards increasing intelligence. Schizotypal individuals in the population could be those who carry “at-risk” combinations of susceptibility alleles but who have not converted to overt schizophrenia – such cases must occur, since monozygotic twin concordance of overt schizophrenia is often observed to be less than 50%. In these cases reproductive fitness may be normal or somewhat subnormal (Hoffman & McGlashan 2004).
Burns (2004) proposes that schizophrenia is a disorder of the social brain, and it exists as a costly trade-off in the evolution of complex social cognition. He argues that paleoanthropological and comparative primate research suggests that hominids evolved complex cortical interconnectivity (in particular, fronto-temporal and fronto-parietal circuits) to regulate social cognition and the intellectual demands of group living. He suggests that the ontogenetic mechanism underlying this cerebral adaptation was "sequential hypermorphosis" and that it rendered the hominid brain vulnerable to genetic and environmental insults. He argues that changes in genes regulating the timing of neurodevelopment occurred prior to the migration of Homo sapiens out of Africa 100,000 – 150,000 years ago, giving rise to the schizotypal spectrum. While some individuals within this spectrum may have exhibited unusual creativity and iconoclasm, he suggests, this phenotype was not necessarily adaptive in reproductive terms. However, because the disorder shared a common genetic basis with the evolving circuitry of the social brain, it persisted. Thus schizophrenia emerged as a costly trade-off in the evolution of complex social cognition.
A Disorder of the Threat Response Archetype? Persecutory delusions may result from an excessive activation of the neural circuits involved with this archetypal function, that may be triggered by circumstances where the organism is or feels under severe threat. Of course, being in a severely disordered mental state is a highly vulnerable & regressed state. Generalised paranoia may have been adaptive for our ancestors. It seems intuitively understandable that these "survival" circuits would be triggered if the brain is malfunctioning, with activation of our most primal behavioural responses. Overactivation due to disinhibition might theoretically occur if some counterbalancing module is deactivated due to injury or acute (e.g. cerebrovascular event) or progressive neurological disease (e.g. dementia).
Delusional disordersDelusional male sexual jealousy
A Disorder of Theory of Mind (TOM) Modules? Charleton (2003) describes TOM as the brain circuitry that permits humans with making inferences concerning the dispositions, motivations and intentions of other people, to permit interpretation of their behaviour. It
has been argued that jealousy is a mate-guarding tactic which, if absent, is
likely to result in a man having fewer children because his wife may sometimes
be pregnant with the children of other men and because he will likely invest
much parental effort in children fathered by other men (Daly, Wilson and
Weghorst 1982; Symons 1979). Although jealousy is an uncomfortable,
undesirable state that can give rise to antisocial acts, it nonetheless is
likely to increase reproductive success and therefore be maintained by natural
selection. Sexual
jealousy is more intense in males than in females across a wide variety of
cultures, despite the enormous cultural differences in the situations that
arouse jealousy and the intensity and nature of its expression (Daly et al.,
1982). There are sex differences in the cues that arouse jealousy.
For men, cues to infidelity are more potent, while for women, losses of
relationships and resources are stronger (Buss et al 1992).
Citation suggestion: Dr Gary Galambos, Psychotic Disorders, Evolutionary Psychiatry Home Sydney Australia (http://www.ep.org.au/dis/psychotic.htm) [date accessed]The materials provided on this website may be freely cited but reposting on other websites, publishing or other reproductions, whole or in part, are subject to the written permission of Gary Galambos. Images may be reproduced provided the source is properly acknowledged.Site Copyright (C) 1999-2004 Dr Gary Galambos M.B.B.S. F.R.A.N.Z.C.P.Page last updated: 17 September 2006 | |||||||||||||||||||||||||||||||||||||||||||||||||
Schizotypal
personality disorder: 
