The prevalence of eating disorders poses
an apparent paradox to evolutionary theory,
because prevalence rates correlate inversely
with the availability of food, and because
amenorrhoea counteracts reproductive success.
Behavioural observation of patients with anxiety disorders suggests that these disor-
ders--as a group--reflect exaggerated responses to
internal or external signals
of perceived danger or
The autonomic part of the anxious response pattern prepares the organism
for one of several behavioural options to terminate the anxiety-eliciting situation,
namely flight,immobility, submission, or aggression.
In gregarious species like primates and humans, some fear reactions may have an altruistic
connotation in that a fear reaction of one individual may alarm others about impending
Alarm calls are found in many primate species and can be truly seen as altruistic
behaviour because the call is clearly at the cost of the alarming individual, which runs the
risk of attracting the attention of predators, and because the alarming individual has no
immediate pay-off from warning its conspecifics.
In any event,fear(the term referring best to the 'normal' adaptive variant) and anxiety
(reflecting pathologically exaggerated fear in terms of duration,intensity
or situational appropriateness) clearly belong to a
group of defence mechanisms, much like submission and depression do.In contrast to
depression,it is intrinsic to the anxiety disorders that anxiety attacks usually cease
automatically, and often aim more directly at eliciting care from others (like in PD or
agoraphobia). Moreover, situations causing anxiety can better be avoided than those
leading to depression. Whether or not some form of altruistic behaviour is reflected in
anxiety disorders is open to speculation. Arguably, altruism is part of OCD-associated
pathology, where others (usually closely related individuals) may benefit from exagger-
ated hygiene or repetitive control of potentially dangerous situations.
Phobic fears of specific situations, objects or persons are so widespread that they
inevitable constitute a significant part of human nature, much of which is inherited from
our primate ancestors. For example, during normal human ontogeny, separation from
the primary caregiver, heights, or strangers are among the strongest fear-evoking situa-
tions,to which the human infant is biologically prepared to respond. Not only are these
fear responses particularly prevalent during certain developmental periods; separation
distress occurs soon after birth,fear of heights emerges when the infant starts to crawl,
fear of strangers when the toddler begins to give up physical closeness to the mother for
brief periods of time, and so forth. These fear reactions are operate on actual sources of
fear that were persistent enough in the environment of evolutionary adaptedness (EEA)
to be selected. Their way of functioning has been likened to the principle of a 'smoke
detector' mechanism, which works optimally if the threshold is low enough to reliably
produce a response to potentially life-threatening Stimuli at the cost of some raise alarms,
but high enough to limit the costliness of too many energetically
expensive false alarms. Here,it needs to be emphasized that not responding to a genuine threat
(for instance, in a predation situation)is most expensive, because
it may cause death of the individual;thus, behaviour too dauntless would readily be
eliminated by natural selection, and a lack of fearfulness would not translate into greater
In primates including humans, phobic fear reactions are not only acquired through
direct conditioning experiences, but also through vicarious experiences,in which an
individual witnesses the response of another individual to fear-relevant stimuli. These
are probably the most important mechanisms of how biologically predisposed fears
become actually manifest. For example,fear of snakes is most likely not 'innate' in
primates, but requires observation of fear responses of conspecifics to the sight of a
snake. However, although conditioning seems to be necessary, biological preparedness is
also likely involved, because no such reactions can be experimentally conditioned when
using flowers instead of snakes as conditioned stimuli. Even though these conditioning
models may be more valid for between-species fears than same-species (social) phobic
fears,it is most obvious that normal fear-conditioning and pathological phobia and
other anxiety disorders lie along a continuum. This is true for all psychopathological
signs and symptoms, and anxiety disorders are paradigmatic in this respect.
Normal fear conditioning takes place early in life. For example, a young primate may
easily acquire fear of snakes through attending to its mother's reaction. The extraordinary
importance of physical closeness for young primates and humans supports the assump-
tion that individual differences in attachment exert long-lasting effects on how young infants and children learn to cope with fear-inducing situations.If,for instance,the
primary caregiver is unresponsive to the infant's needs or even unavailable,insecure
attachment is likely to develop. Consequently,
ambivalently or avoidantly attached infants are
more vulnerable to develop anxiety disorders later
in life. In line wlth this, patients with various forms
of anxiety disorders have experienced early losses
more often than controls,report rejection by parents
more frequently, or have experienced extremely
inadequate caregiving more often compared
to controls. This makes sense in light of the hypothesis that insecurely attached
individuals are prepared through adverse early experiences to develop mistrustful inner
working models and to see the world as a hazardous place.
Gene-environment interactions leading to anxiety disorders seem to predispose these
individuals to assume behavioural strategies aiming at harm avoidance and acquiring
defence strategies associated with internalizing symptoms (which explains the frequent
comorbidity of anxiety disorders with depression).In line with this assumption, carriers
of the short polymorphic version of the serotonin transporter gene have been found
to develop depression or anxiety disorder after negative life events more often than
individuals who lack this allele variant.
Early experiences may,therefore, 'shape' the responsivity of neurobiological circuits
involved in fear responses. For example, evidence from brain imaging studies suggests
exaggerated sensitivity of the amygdalae to fearful stimuli in patients with PTSD or SAD.
In addition,the reduced control over fear responses may be augmented by a diminished
emotional evaluation of threat signals (projected from the amygdala to prefrontal cortex
areas), and insufficient integration of representation of past experiences (via the
hippocampal formation).In other words,in sensi-
tized individuals,irrespective of whether sensitiza-
tion is genetically predisposed, acquired through
aversive experience or both,the amygdala may lose
the inhibitory control through which it normally contains the approach of novel objects I
or other organisms (including individuals of the same species).Instead the amygdala,
responds in a dysregulated or hyperactive fashion such that benign environmental
stimuli may be perceived dangerous. All this may result in exaggerated avoidance behav-
iour and subjectively overwhelming feelings of intense fear in vulnerable individuals.
Conceivably, humans may be particularly susceptible to dysregulation of fear circuits
for several reasons, which may account for the high prevalence rates of anxiety disorders.
Firstly, since humans are exceptionally social, but physically vulnerable,they may be
inclined to constantly check their environment for potential sources of threat(both from
outside and from within the social group). This may not only include predatory or phys-
ical threat, but also threat of social status and loss of resources.In support of this
assumption,the neuroanatomical structures involved in the evaluation of potentially
dangerous situations have increased in size over evolutionary time, WⅡich underscores
theirimportance in terms of survival and reproductive success. Secondly, newborn
humans critically depend on intense nurturance and care, such that a stable affectional
bond with a primary caregiver is outstandingly vital for survival.If, however, stability of
an affectional bond is unattainable or disrupted (for example, by loss of the primary
caregiver), a hypersensitive and constantly overaroused fear system may result. Such a
situation may dramatically worsen,if physical or
emotional abuse is involved with which an imma-
ture human infant can hardly cope. Thirdly, humans
have evolved the capacity to anticipate future
scinario, which on one hand, was certainly highly
adaptive with regards to foreseeing food shortages
or other potentially perilous situations including
changing alliances between contenders ; on the other
hand, exaggerated anticipation of threat and danger
seems to be immanent to various forms of anxiety
disorders , which may ,in part , explain why patients often report fear of recurrence of
anxiety (anticipatory anxiety). Finally,it could be that in modern societies the dimin-
ished necessity to cope with fear-inducing situations--simply due to a reduced number
of dangerous encounters with poisonous animals or predators--renders the neurobio-
logical system involved in evaluation of potential hazards more labile and 'unprepared' to
accurately respond to real-life confrontation with spiders, snakes or heights. However, a
notable exception could be potential or actual harm caused by conspecifics.In modern
societies,individuals frequently meet other people, whom they have seen never before,
and whose intentions are much harder to determine than in familiar people. This may
cause particular problems for those individuals who have developed mistrustful inner
working models and are cognitively biased towards assuming malicious intents in others.
In fact, patients with anxiety disorders frequently complain that others can virtually see
what is wrong with them, and feel being observed or stared at(in contrast to delusional
beliefs, patients with anxiety disorders do not report in corrigible conviction that this is
true; continua between extreme anxiety and paranoid ideation may, however, exist).
Although the preceding paragraphs have dealt with anxiety disorders as if they were
different manifestations of a singular diathesis,they differ,to some extent,in neurobiol-
ogy and precipitating events.
PD is perhaps the most primitive of the anxiety disorders. For example, PD has been
interpreted as false suffocation alarm, because carbon dioxide inhalation or lactate
infusion may produce panic attacks in vulnerable
(healthy)individuals. Moreover, PD occurs more
frequently in individuals with heightened PCO2 levels, e.g. during sleep, during the
premenstrual period and in patients with respiratory disorders. On the other hand, PD is
less common in physiological states associated with lowered PCO;,including pregnancy
and delivery. Although there is some evidence that the genetic vulnerability is most prominent in PD compared to other anxiety disorders, additional environmental factors
such as loss of an attachment figure may be equally important in that such events may
lower the suffocation alarm threshold. Panic attacks may therefore be seen as the extreme
version of a preparatory set of physiological changes typical of immediate flight or
escape behaviours. Anticipatory anxiety is often the result of recurrent panic attacks.
Thus, at the cognitive level PD involves the mental representation of future negative
events.In neurobiological perspective, PD probably involves hyperexcitability of norepi-
nephrine pathways and reduced serotonergic and GABA-ergic dampening of limbic
structures.In light of the putative association of PD with separation distress, a link with
abnormal oxytocin turnover is conceivable.
Agoraphobia, which often accompanies PD,reflects an exaggerated response to avoid
(claustrophobia). Agoraphobia,like PD,IS probably
the pathological extreme of an evolutionarily
conserved behavioural pattern that is common to many animal species and helps to
protect the organism from entering unknown terrain that could yield a predatory threat
or hostile attacks from conspecifics. Whether or not agoraphobia differs from PD in
neurobiology or simply represents a more severe and complex form of PD is debatable.
Shared genetic vulnerability between agoraphobia and PD and associations with similar
precipitating life events may support the latter assumption.
SAD is characterized by intense fear of social situations in the presence of an authorita-
tive person. Social phobia can be interpreted as an exaggerated submissive gesture
triggered by situations that may potentially lead to humiliation and loss of social status.
There are some phenomenological parallels
lap with normal blushing, which,in extreme forms,
develop into erythrophobia,the fear of reddening
of the skin as a visible signal of the subjective
state of embarrassment. SAD causes a dilemma, especially in its generalized form, because
fear and anxiety usually elicit care and comforting behaviour in others, which the affected
individual cannot tolerate In fact, heightened attention from others may even aggravate
the phobic reaction. The difference to other anxiety disorders is that in SAD patients tend
to exaggerate the evaluation of mental states of others. Unlike patients with autism or
schizophrenia who have difficulties in representing mental states of others (reduced
mentalizing in the former,inaccurate hyper-mentalizing in the latter), patients with social
phobia are well able to appropriately reason about other persons' mental life;in specific
situations, which are perceived as posing a threat to social status and reputation, however,
they negatively interpret social signals of others and may over-anticipate a personally
appalling outcome of social encounters. Research in animals and humans strongly suggest
a central role of amygdala dysfunction in SAD. This dysfunction may be mediated by
reduced availability of GABA and serotonin as well as by impaired regulation of affiliative
behaviour and social attachment via oxytocin. Moreover,reduced inhibition of amygdalar
function through glutamatergic prefrontal efferents (via GABA-ergic interneurons) has
been identified as potential proximate causation of SAD.
GAD is,in contrast to phobic anxiety, not explicitly associated with particular precipi-
tating events. GAD rather reflects an overall tendency towards hypervigilance, probably
forming a continuum with avoidant personality
disorder.It is the least heritable anxiety disorder
and therefore depends even more than the other
anxiety disorders on early aversive subjective experiences and learned behaviour. Chronic
hyper-excitability,restlessness and increased muscle tension is likely to involve the HPA
axis, which may induce secondary physical problems including chronic arterial hyperten-
sion and other stress-related disorders.
Within the broader spectrum of anxiety disorders, OCD stands out by its marked
repetitive and stereotyped behavioural subroutines. From an ethological perspective,
OCD-associated behaviours resemble displacement activities (compare Chapter 5) and
stereotyped behaviours observed in animals under physical restraint.In OCD, however,
the repetitively displayed behaviours clearly address harm-avoidance by checking,
washing, ordering or hoarding.Interestingly, OCD manifests or worsens in biologically
relevant situations such as pregnancy and following childbirth. OCD-associated behav-
iours are thus abnormal by their excessiveness, but probably qualitatively not distinct
from adaptive harm avoidance strategies. Even though anticipation plays an important
role in many anxiety disorders,the cognitive mechanism of mentally generating future
scenarios that may cause harm to self or others is decisively at the core of OCD. Humans,
unlike most other animals, have evolved the capacity to cognitively represent imagina-
tions of past and future events by using semantically and autobiographically stored
memories. This is certainly selectively advantageous, because future threats or needs can
be dealt with in advance (e.g. by collecting food without being hungry). The difference to
hibernating animals is that the cognitive represen-
tation of possible future scenarios is not instinct-
driven (hibernators collect food even if they have
never experiences winter time before), yet much more flexible.In other words,this kind
of cognitive representation is independent of situation and content,i.e. one can create
social or non-social future events as mental images.In the case of OCD,it would seem
that it is exactly this mechanism that is over-active and--despite insight into the
bizarreness of obsessive thoughts and compulsive behaviours--difficult to control.
At the neurophysiological level, OCD not only involves abnormal serotonergic activity,
but also increased dopaminergic transmission, which may cause an imbalance of phylo-
genetic older 'habitual' systems and phylogenetic younger 'flexibility' systems. Flexible
responses involve the capacity of selecting the relevant sensory input, shifting the atten-
tional focus, making the best choice of behavioral alternatives, and sometimes suppress-
ing salient responses in favour of less salient ones.In primates and humans,the
dorsolateral prefrontal cortex,the orbitofrontal cortex,the cingulate cortex,the supple-
mentary motor cortex, pallidostriatal structures, and parts ofthe thalamus contribute to
the execution of flexible behaviour, where striatum and thalamus operate as filter of
incoming information and project back to different areas of the frontal cortex. These
brain regions have been found hyperactive in OCD. Moreover, enhanced brain activity in the anterior cingulate cortex,in the prefrontal cortex,the dorsolateral prefrontal cortex,
and dorsal prefrontal cortex has been shown to be associated with episodic memory
retrieval in healthy individuals,'prospective memory,that is,the ability to keep in mind
something that needs to be carried out in the future, and,in part, with anticipatory anxi-
ety These findings underscore the assumption of a significant role of exaggerated cogni-
tive risk anticipation in OCD.
Similar mechanisms may also contribute to PTSD, however, with the difference that the
manifestation of PTSD is, by definition , proceed by
a severe traumatic event---in OCD,real danger ma
have never been encountered. Furthermore,in
PTSD,re-experiencing a traumatic event that lies in the pastis at the core of the sympto-
matology, and much less so the mental imagination of future (novel)traumatizing scenar-
ios. Remembering past situations associated with threat or actual harm is certainly
adaptive in that it helps to avoid similar future negative experiences;in PTSD, however,
this mechanism is pathologically hyperactive to the extent that it may actually preclude
adaptive responses, but instead gives why to phylogenetically primitive fear reactions such
as 'freezing' and dissociative states (regarding catatonic/dissociative behaviours, compare
Chapter10). Similarto OCD, however,in PTSD intrusive thoughts and memories are
perceived as uncontrollable, and usually generate strong autonomic arousal, chronically
heightened vigilance, and persistentfeelings ofimpending danger.It would seem that
individuals with PTSD are unable to disentangle past, present, and future threat scenarios
in that they re-experience in the present what frightened them in the past. Hence, at the
physiological level, PTSD represents a hyperactivity of the alarm system associated with
chronic up-regulation of the HPA axis, which,in turn,impairs integration of traumatic
experiences and appropriate memory consolidation. Moreover, even though the amygdala
is hyperactivated during recollection of traumatic events, normal threat evaluation is
impaired such that the affected individual is less well able to distinguish between relevant
and irrelevant stimuli as potential sources of danger.In addition,the communication
between right('emotional') and left('rational') hemisphere seems to be functionally
disrupted in PTSD, such that traumatic memories may be experienced as ego-alien,
because the emotional aspects of the traumatic experience cannot be appropriately
verbalized.It is plausible to assume that the changes at the physiological and
neuroanatomical level in PTSD are the more severe the earlier the individualis confronted
with a traumatic experience. Early childhood trauma,for instance, may induce pervasive
alterations of neural circuits underlying emotion processing and emotion regulation.In
light of the lateralization of the functions, severe early traumatization may affect more
strongly the right rather than the left brain.
In summary, anxiety disorders represent pathologically exaggerated defence mecha-
nisms, which primarily manifest at the emotional, but also at the corresponding and
interconnected behavioural and cognitive level. Anxiety disorders differ to some extent in
their genetic underpinnings and environmental causation. All anxiety disorders have in
common, however,that they can be triggered by social experiences and are influenced by
different modalities of associative (social)learning. Unlearning the conditioned response
is sometimes hard to manage , such that preventive measures including prevention
of early traumatization and strengthening of resilience are crucial aspects of any
One of the hallmarks of schizophrenia is, however, that patients have profound difficulties in social interaction, which often precede the manifestation of the first psychotic episode.
Children who as adults develop schizophrenia not only present with neurological
soft signs, but also with increased prevalence of socially abnormal behaviour including extreme shyness, withdrawal or aggression towards peers.
These behavioural abnormalities may be paralleled by children's difficulties in understanding other people's behaviour in terms of their mental states.
Ethological research into non-verbal behaviour of schizophrenic patients has revealed that they are reduced in their ability to promote Social interaction
even in one-to-one interview situations.
Schizophrenic patients with pronounced negative symptoms more often display behavioural patterns suggestive of avoidance or 'cutting-off' social contact altogether, whereas others, particularly those with paranoid ideation may be more likely to show subtle cues signalling threat such as 'staring'.
Interestingly,the non-verbal behaviour of patients with schizophrenia may sometimes appear indistinguishable from behavioural patterns found in depression, which in a general vein can be interpreted as correlates of submissive behaviour.
Whether or not children who later develop psychosis are more frequently insecurely
attached to caregivers is a matter of debate; as adults,the majority of shizophrenia patients report early attachment bonds in a dismissive or unresolved style, which correspond to insecure-avoidant or disorganized attachment.
It is, however, conceivable, similar to the case of autism,that disruptive neurodevelopment in the child exerts negative effects on early social interaction including the formation of an affectional bond between infant and primary caregiver.If such gene-environment correlations play a role early in childhood development of individuals who later become psychotic, additional aversive events to the point of physical or emotional abuse may be more likely to occur in problematic familial environments, and,in turn, may increase vulnerability for psychosis via chronic activation of the hormonal stress axis.
Evolutionary hypotheses regarding schizophrenia have revolved around the apparent paradox why such devastating disorders exist at all, despite the marked reproductive disadvantage of affected individuals by 30 to 70 percent particularly males.
Similar to other disorders, it has been proposed that a selective advantage of traits
may exist, of which only the extremes of variation are disadvantageous.
The number and diversity of evolutionary hypotheses of schizophrenia, however, are unparalleled in other major psychiatric disorders. They span as divergent aspects as advantages of schizotypal traits in relation to group selection, schizophrenia as a trade-off of human language acquisition or creativity,reduced risk of cancer in relatives of schizophrenic patients, schizophrenia as extreme negative variation of sexually selected traits, and effects of maternally imprinted genes.
Many of these explanatory approaches are implausible because they implicitly assume that schizophrenia is a homogenous 'disease entity', or that the risk for schizophrenia is conveyed by a single gene or several genetic polymorphisms with large effect size.
Neither assumption is currently supported by empirical evidence.
For example, schizophrenia is probably not the result of a single balanced polymorphism where the risk for schizophrenia (and reduced fecundity of affected individuals) is compensated by advantageous effects within the brain (e.g. benefit for the social group conveyed by schizotypal personality traits in relalives of affected individuals), or outside the brain (e.g.reduced cancer risk, greater resistance against infectious diseases or increased survival rates in relatives of schizophrenia patients).
However,there is some evidence for a recent positive selection in the human lineage at several loci including those coding for DISCI, dysbind in and neuregulin, of which the exact functional significance is as yet unknown.
An intensely discussed evolutionary hypothesis of schizophrenia has linked the disorder to a failure to establish functional dominance and language in one or the other hemisphere of the brain.
It has been proposed that cerebral dominance is under control of only a few regulatory genes, and that polymorphisms at one or several of these loci would not only reduce cerebral dominance but also convey a risk for schizophrenia.
In support of this hypothesis it has been found that children who later develop psychotic disorders are more often ambidextrous and have more language disorders and behavioural disturbances than children who as adults do not become psychotic.
Moreover, some studies have revealed a reduced cerebral asymmetry in schizophrenic adults compared with healthy subjects, and sex differences in normal asymmetry have been found disrupted in schizophrenia.
With regards to the representation of language,it is assumed that under normal conditions the organization of language is segregated such that the spatial or 'logical' component is represented in the non-dominant hemisphere and the temporal or 'phonetic' aspect in the dominant hemisphere, both of which normally interact via the corpus callosum.
Accordingly,'firstrank' symptoms in schizophrenia could reflect a disruption of the
normal transcallosal connection of the two hemispheres.Imprecise coordination of the logical and the phonetic aspect of language could produce symptoms such that an individual perceives his or her own thoughts as alien.
However,there is no unequivocal link of handedness and language, nor has cerebral dominance been successfully linked to oligogenetic effects. Furthermore,this hypothesis does not explain symptoms other than formal thought disorder or delusional beliefs.
In any event,the hypothesis points to the interesting observation that sexual selection could be involved in the pathogenesis of schizophrenia, since age at onset and symptom severity differs between the sexes.
Age at onset is usually earlier, and symptom severity is greater in men, and both features may be associated with the normally greater asymmetry between the cerebral hemispheres in men, which fails to be established in schizophrenia.
Several studies have shown that developmental instability is pronounced in patients
with schizophrenia. Normally, genes involved in neurodevelopment help to 'buffer'
against negative effects of multiple mutations, pathogens and toxins. Variation at these loci may lead to increased 'fluctuating asymmetry' (FA),that is, a near-normally distributed asymmetry of bilateral characters that are on average symmetrical in the population.
In schizophrenia, FA is greater in twin pairs concordant for schizophrenia than in
discordant pairs, which suggests that greater FA may indicate an imprecise expression of the developmental design due to genetically or environmentally caused developmental disruption.
This could explain,for example, why patients with schizophrenia have a greater number of minor physical abnormalities such as hypertelorism that could be indicative of an incomplete early cell migration.
Other characteristics putatively associated with a developmental instability in schizophrenia are greater homozygosity of blood alleles,lower premorbid intelligence,reduced cortical volume, and a relative instability of functional and anatomical lateralization of brain functions in schizophrenia.
FA is under partial control of sexual selection, as small FA is usually perceived more attractive than large FA.
It could therefore be that,in a very general vein,the broad spectrum of schizophrenia represents the unattractive extreme of variation of sexually selected traits including FA,language,intelligence, and social cognitive capacities that may be important for successful courtship behaviour.
In fact, many behavioural signs and symptoms and epidemiological findings seem to support this assumption,including the onset of the disorder at the point when mating and courtship behaviour normally peaks.
Competition for potential mates is pronounced for males compared with females, and the peak of mating effort is at a younger age for males, which could explain the earlier onset of schizophrenia and the more severe course and outcome in men.
By contrast,the need to attract suitable mates reaches a second peak in women near the end of their reproductive cycle, which may account for the higher prevalence of erotomanic delusions in women .
If the schizophrenia phenotype represents the low-fitness extreme of sexually selected traits,it is also plausible why patients with schizophrenia have lower than average reproduction rates.
In line with this hypothesis,it has recently been discovered that age at onset of schizophrenia varies with proximity to the equator:the closer people live,the earlier the onset.
One possibility for this finding could be that factors such as increased exposure to pathogens and higher levels of polygyny create a pressure towards mating at a younger age.
This, in turn, may lead to earlier expression of schizophrenic signs and symptoms produced by a stress-induced dopamine overshoot in the ventral striatum, where the need for intensified (premature) courtship behaviour serves as non-specific stressor.
Such a scenario may also explain why the search for replicable allelic variation involved in the pathogenesis of schizophrenia has been unsuccessful.
Since stabilizing selection tends to reduce deleterious mutations,it could be that an individual's higher than average number of fitness-reducing alleles leads to the expression of the schizophrenia phenotype, but that many of these alleles are evolutionarily transient.
However,the emergence of new fitness-decreasing mutations may contribute to an
equilibrium through which the average prevalence of schizophrenia in a population is maintained.
Taken together,the polygenetic inheritance of schizophrenia and the heterogeneity of the disorder can be understood as the negative side of sexually selected fitness-enhancing additive genetic variance.
Consistent with,though not identical to the hypothesis of schizophrenia as the
maladaptive extreme variation of sexually selected traits, some physical and behavioural characteristics indicate that genomic imprinting may play a role in the expression of schizophrenia-associated features. Generally speaking, several characteristics seem to support the assumption that maternal imprinting leads to a pattern of general undergrowth and 'Femaleness' of the brain in schizophrenia.
This could include reduction of grey matter,reduced lateralization, and overactive mechanisms involved in social cognition--- the opposite of what is found in autism.
These general evolutionary hypotheses of schizophrenia are,in part,flawed by the fact that they hardly cover all clinical aspects of schizophrenia. Thus, in addition to these broad approaches to understand the heterogeneous nature of the schizophrenia spectrum phenotype,it is useful to analyse individual symptoms based on evolutionary theory. Of note,it is explicitly assumed that signs and symptoms are pathological exaggerations of variation of adaptive mechanisms that arise from a disturbed interplay between one or more levels of the triune brain .
The distinct deficit in social competence in schizophrenia, which often precedes the
manifestation of the first psychotic episode,is paralleled by deficits in social cognition.
This deficit is perhaps triggered by a dopaminergic overstimulation of mesolimbic circuits, which one-sidedly influences the emotional positive symptoms of schizophrenia,for example, tend to be hypervigilant , in particular regarding
gaze monitoring of others, and to interpret social cues as threat.
They may also over-attribute mental states of others, often in a way that they falsely infer malicious intents of others, clinically expressed as persecutory delusion or delusion of reference.
Excessive mental state attribution may also contribute to some aspects of formal thought disorder.
For example, a patient who incorrectly assumes that his or her interlocutor shares his or her knowledge--- perhaps due to the patient's fragile ego-boundaries associated with thought transference--- may present with loose associations or derailment. Moreover,the tendency in some patients to form too many hypotheses about the mental states of others, while at the same time being unable to choose among these hypotheses the most plausible one, may lead to secondary negative symptoms, perhaps as self-protection from over-stimulation and arousal.
Consistent with this assumption, patients with schizophrenia fail to correctly attribute mental states 'on the spot' despite their tendency to over-infer mental states.
Over the course of the illness, negative symptoms often increase (whereas positive symptoms are still present, but less emotionally valent), accompanied by a decreased potential of the prefrontal cortex to be activated by dopamine.
Thus,in chronic schizophrenia, patients evaluate social situations less, and have even more difficulties in inferring mental states of self and others.It is at present unclear whether this 'mentalizing' deficit in schizophrenia is as selective as it seems to be in autism.
There is at least convincing evidence that patients with schizophrenia also have difficulties in integrating contextual and autobiographical information when judging mental states on the basis of observed behaviour.
Another frequent clinical finding in schizophrenia is the striking lack of awareness of
illness and insight.It would seem that impaired insight is related to patients' difficulties to reflect upon their own states of mind.
Patients also frequently experience so-called passivity symptoms,for example,that a patient's own action is perceived as being influenced by an external agent.
Thus,it is conceivable that disturbances in the neural network underlying the representation of self and others may be central to many 'core' symptoms associated with schizophrenia.
The neural basis for the ability of mental state attribution or 'mentalizing' and self-
representation is now well known It comprises several interconnected regions of the frontal,temporal, and parietal lobes, among which adaptations, perhaps unique to primates, such as the mirror neuron system, play a crucial role in simulating actions and behavioural dispositions of significant others.
In addition,it has been speculated that the paracingulate sulcus, which separates the anterior cingulate cortex (ACC) from the medial wall of the prefrontal cortex and is inconsistently present in humans, represents an evolutionary novelty involved in social cognitive processes. Furthermore,the infraparietal lobule, which consists of the angular gyrus and the supramarginal gyrus, is probably involved in self-other distinction and representation of the self as acting agent.
Similar to prefrontal cortical midline structures,the infraparietal lobule myelinates late during ontogeny and is only rudimentary in great apes, suggesting that selection has operated on these particular brain areas involved in self-reflexivity and mental state attribution.
These brain regions have been found to be functionally and/or structurally damaged in patients with schizophrenia.
Apart from formal thought disorder, many aspects pertaining to the content of delusional beliefs appear to be tightly linked to scenarios that were selectively important in the human evolutionary past.
This does certainly not preclude influences on delusion formation from an individual's personal background, but the uniformity of delusional content across cultures suggests that universal patterns relating to survival and reproduction are mirrored in delusions.
For example,the content of persecutory delusions differs between men and women
regarding the number and sex of persecutors, as well as regarding the degree of familiarity with the perceived persecutor.
Whereas men usually feel more often threatened by groups of strange males, women more often feel persecuted by individuals from their personal environment. Both deluded men and women primarily report fears of being physically injured or assaulted. The rationale for these sex differences in persecutory delusional content could be that the main source of ancestral threats for men in the environment
of evolutionary adaptedness (EEA) were indeed strange males from other
tribes; by contrast, women, under ancestral conditions,formed the core of the kin-based highly cooperative social group, such that expulsion from the community was a real threat for women living in the EEA.
This assumption is further supported by data from chimpanzees, our closest living relatives,in which territorial competition and warfare between troops of rivalling males has been reported to be high, perhaps similar to what happened in ancestral human conditions. Moreover, until quite recently, similar scenarios were described in extant hunter-gatherer or horticultural societies, where a substantial number of men (up to 25 per cent) and women (up to 13 per cent) died premature violent deaths.
Similarly, delusions relating to mating effort and reproduction differ markedly
between men and women, and again,these patterns are highly uniform across cultures.
Since parental investment differs between men and women with women investing more than men in potential offspring,the former were selected to be choosier in terms of mate choice.In other words, women are, on average, more likely to seek socially high-ranking men as potential partners who are willing to invest in offspring.
In contrast,in established pair-bonds, paternity is less certain than maternity
such that strategies to ensure sexual fidelity were more strongly selected in males. These divergent selection pressures for males and females are strikingly mirrored in erotomania, the delusional conviction of being loved by another person, and delusional jealousy.
Erotomania is much more common in women, who usually choose socially high-standing men (politicians, physicians, actors, sportsmen, etc.) as 'love objects'.
Women with erotomania often try to 'convince' their love objects of their own mate value and tend to harass them. This form of following is, however, different from what is found in stalking behaviour. Stalkers are much more often men who pursue their victims sometimes using violent means.
Erotomania is uncommon among stalkers, however, jealousy (both delusional
and non-delusional)is frequently involved in stalking.
There is probably some
phenomenological overlap between stalking behaviour and delusional jealousy.
Delusional jealousy is much more frequently observed in men compared with women.
It can be seen as the counterpart to erotomania, aimed at partner retention and securing sexual fidelity.
Finally, many signs and symptoms commonly subsumed under the term catatonia can be interpreted as contextually abnormal and exaggerated fear response,fight-flight ambivalence, or behavioural patterns relating to submission or assertive behaviour.
Catatonic stupor,for example, strongly resembles a primitive fear reaction,
which markedly resembles tonic immobility seen in many animal species.In tonic
immobility, which is most likely elicited by impeding predatory threat where flight is
impossible,the animal stops moving to avoid detection. At the same time,it shows
heightened alertness,reduced vocalization, unfocused gaze, analgesia, and abrupt onset and offset of the behaviour,followed by a ferocious struggle to escape. Further similarities are found regarding autonomic instability.
In tonic immobility, heartrate initially rises and then drops below baseline, which can also be observed in catatonic stupor.
The parallels between catatonic stupor and tonic immobility as (primitive) fear responses---represented in the most ancient parts of the triune brain--- are also supported by the fact that catatonia responds well to anxiolytic treatment with benzodiazepines and can be worsened by dopamine depleting drugs.
In addition, patients with catatonic stupor often report in retrospect extreme feelings of overwhelming anxiety during the catatonic state.
Catatonic stupor may be preceded or followed by states of extreme hyperactivity or
excitement, sometimes associated with assaultive behaviour. However, catatonic excitement is usually poorly coordinated, which may reflect a primitive behavioural escape response in situations in which the source of the perceived danger is hard to recognize.
Other behavioural symptoms labelled catatonic, such as waxy flexibility, abnormal
imitation and echoing movements including automatic obedience, can be interpreted as contextually abnormal submissive behaviours,the counterpart of which are represented by behaviours suggestive of exaggerated resistance to requests such as negativism.
The pathophysiological underpinnings of these inappropriate expressions of fear,
fight-flight ambivalence, and communicative behaviours are incompletely understood.
Dysfunction of the prefrontal cortex is probably involved, as bilateral lesions to the ACC produce akinetic mutism. Inhibition of imitative behaviour also implicates the distinction from self and other, such that it is conceivable that dysfunction of the infraparietal lobule contributes to catatonic behaviours. Moreover,there is possibly a lack of inhibitory control of the amygdala via the orbitofrontal cortex, which is reciprocally connected with the limbic system.
Little is currently known about the role of the amygdala in catatonia, but given its impact on fear and aggression related behaviour, and the response of catatonic symptoms to anxiolytic treatment,it can be presumed that this structure is central to the aetiology of catatonia.
In addition to the assumption of an inhibitory deficit it could also be that catatonic behaviours can be elicited in individuals Who are vulnerable to overstimulation of these brain areas.
In this context , it is important to note that many catatonic symptoms are indistinguishable from catatonic symptoms are phenomenologically dissociative symptoms, and that a terminological indistinguishable from dissociative symptoms, and that a terminological distinction is more due to convention rather than neurophysiological differences.
This notion is essential, because it throws light on the possibility that patients with early traumatization are perhaps more susceptible to develop dissociative/catatonic states if experiencing retial, because it throws light on the possibility that traumatization or other situations associated patients with early traumatization are perhaps more susceptible to develop dissociative/catatonic states if experiencing re-traumatization or other situations associated with unbearably intense fear.
Finally, catatonic behaviours (like all symptoms found in schizophrenia) can frequently be observed in other psychiatric disorders,foremost depression and bipolar affective disorder, which is,from an evolutionary point of view not surprising, given the importance of these behaviours for submission and appeasement strategies.