Draft of a Book Chapter published in The Social Brain - Evolution and Pathology,
edited by Martin Brune, Hedda Ribbert & Wulf Schiefenhovel. John Wiley & Sons: Chichester, 2003: 315-338.

Theory of Mind Delusions and Bizarre Delusions
in an Evolutionary Perspective: psychiatry and the social brain

Bruce G Charlton MD


Bruce G Charlton MD
Reader in Evolutionary Psychiatry
Department of Psychology
University of Newcastle upon Tyne
NE2 4HH
England

Editor-in-Chief, Medical Hypotheses

Tel: 0191 222 6247
Fax: 0191 222 5622
bruce.charlton@ncl.ac.uk


The social brain and psychiatry

The phrase 'social brain' embodies the idea that the problems of living in a complex social group have been a dominant selection pressure in recent human evolutionary history (Humphrey, 1976; Byrne & Whiten, 1988; Brothers, 1990). One consequence is that many distinctively human behaviours can be linked with adaptations for social living.

The perspective of ‘the social brain’ has particular relevance to psychiatry, since 'psychiatric symptoms (eg. hallucinations, delusions, phobias, obsessions) are frequently dominated by social content, and a disruption of social relationships is highly characteristic of psychiatric illness. Indeed, it might plausibly be argued that the distinctive nature of many psychiatric illnesses - that thing that makes them 'psychiatric' - may be the combination of emotional pathology with social impairment. Certainly, the emotional and the social are intimately related at the level of brain function, since social reasoning depends upon evolved brain systems for monitoring and modelling emotional responses to social scenarios (Damasio, 1994; Charlton, 2000).

The following chapter will demonstrate how a human social evolution has been used to clarify and refine the diagnostic category of delusions. I will argue that two distinct types of delusions may be discriminated: ‘Theory of Mind’ delusions and ‘Bizarre’ delusions.


Delusional disorder

Delusional disorder (DD) may be described as a psychiatric condition in which a delusion is the primary symptom, and patients are otherwise ‘normal’ (Charlton & McClelland, 1999). The subject matter of the delusion is variable; with persecutory, jealous, grandiose, erotomaniac and somatic subtypes being recognised (APA, 1994). Furthermore, Delusional disorder is characterised by specifically social abnormalities of behaviour - such as morbid states of jealousy, love, self-awareness or fear of other people (Charlton & McClelland, 1999).

Delusions are false beliefs. However, this is an insufficient definition, and further attempts at definition are all somewhat unsatisfactory (Garety & Hemsley, 1994). Usually a delusion is defined as a false belief that is also strongly held such that it exerts a strong influence on behaviour and is not susceptible to counter-arguments or counter-evidence (or, at least, the delusion is unshakeable over a short timescale and in the absence of systematic attempts at belief modification). Furthermore, in order to distinguish delusions from 'religious' beliefs, a delusion is also supposed to be out of context with the usual cultural beliefs for that society (Sims, 1995).

Delusional disorder is an unusual diagnosis in general psychiatric practice, and delusions are most frequently seen to occur as only one element in more complex clinical syndromes. In other words, most delusions are observed along with other 'psychotic' symptoms such as hallucinations or incoherent speech ('thought disorder') as part of one of the classic syndromes of ‘madness’ such as schizophrenia, mania, psychotic depression, and 'organic' symptoms indicative of generalised brain dysfunction such as dementia or delirium.

But in Delusional disorder false beliefs occur largely in isolation as ‘encapsulated’ delusions. Such individuals do not have other primary psychological symptoms such as hallucinations, incoherent speech or qualitatively abnormal mood states (although the delusions may lead to secondary symptoms, for instance a belief in persecution may lead to secondary emotional change, such as fear or anger specifically in relation to the imagined persecutors). It therefore seems likely that the majority of people diagnosable with Delusional disorder are never seen by psychiatrists (Charlton & McClelland, 1999; Walston et al, 2000).


Theory of Mind (ToM)

It has recently been noted that the subject matter of Delusional disorders is distinctive, since the false beliefs are ‘social’ in content, and typically concerned with the assumed dispositions, motivations and intentions (DMIs) of other people. For this reason, Delusional disorders have been labelled ‘Theory of Mind’ delusions, because they seem to involve inferences (or theories) about what is going on in the minds of other people (Charlton & McClelland, 1999).

For example the commonest types of Delusional disorder are probably those relating to jealousy over sexual infidelity and those in which there is a false belief of persecution. Both are considered to be commoner in men. Jealous delusions may involve a man believing that his wife is concealing from him that she is having an affair with another man, while persecutory delusions typically involve a man believing that he is the victim of a hostile plot to attack and probably kill him. It has been suggested that these delusions derive from errors of inference relating to the contents of other people’s minds.

Since Delusional disorder is related to reasoning about the dispositions, motivations and intentions of other people, the mechanism by which such reasoning is performed in humans requires consideration. Theory of Mind is the ability - displayed by adult humans - of making inferences about the content of other people’s minds. Beyond this bald statement - conceptualisations of Theory of Mind vary widely between published accounts, and in different branches of biology. I suggest (for reasons argued elsewhere; Charlton, 2000) that the essence of ToM, its central adaptive importance and the reason why it evolved, is that the Theory of Mind mechanism is primarily concerned with making inferences concerning the dispositions, motivations and intentions of other people. It is not, therefore, a mechanism which evolved for making theories about the 'factual' or 'knowledge' content of other people's minds - although in language-using humans the ToM mechanism may be used for this purpose.

The ToM mechanism enables other people’s behaviour to be interpreted in the light of inferred DMIs. This is necessary because many human social behaviours are ambiguous unless interpreted with knowledge of 'intent'. For example, a clenched fist can be a threat, a salute, or a gesture of encouragement, according to the motivation of the fist-wielder. Discrimination between these different meanings requires an understanding of the social context of behaviour including the individual differences between human beings, and the different ways in which these different human beings interact.

For example only by knowing the DMIs of others can we distinguish between friends and foes, know who to trust and who to avoid - and in general build those alliances that underpin human society - especially in those small scale tribal societies in which human evolved (Walston et al, 1998).


Strategic social intelligence

The ability to make inferences concerning the DMIs of others can be termed strategic social intelligence (Charlton & McClelland, 1999; Charlton, 2000). It is strategic because it is used in planning future social strategies. Strategic social intelligence is therefore a kind of 'internal modelling', a way in which the brain can run 'simulations' of possible future scenarios and evaluate their outcomes. Most animals do not have strategic social intelligence used for planning, although many animals have highly developed tactical social intelligence (detecting and responding to social cues) for dealing with the here-and-now of face-to-face interactions within the same species.

Strategic social intelligence is an adaptation which is unique to humans and (probably) a few other species of recently evolved mammals with relatively large brains and complex social systems. Strategic social intelligence (SSI) is almost certainly found in chimpanzees, bonobos and other great apes, probably in dolphins and elephants, and perhaps in others. SSI is valuable in humans (and other species with broadly similar social systems) exactly because here-and-now behaviour cannot be interpreted at face value. No matter how expert we are at reading facial expressions, gestures and vocal intonation - we are still vulnerable to being deceived if we do not take into account the context of the social interaction and any evidence of the DMI of the individuals concerned.

For example, a smiling, charming and plausible stranger may knock on your door offers to give you 1000DM tomorrow if you will give him 100 DM today. It is strategic social intelligence which enables you to infer that this man cannot necessarily be taken at face value, and that he is more likely to be a confidence trickster than a benefactor. Damasio (1994) has shown that people with some types of neurological impairment - such as pre-frontal cortex damage and non-dominant parietal cortex damage - lack what I have termed strategic social intelligence. They demonstrate serious impairments of planning and judgement, especially in relation to social interactions - hence would be vulnerable to exploitation by deception, for instance they would probably take the above described confidence trickster at face value.


Strategic social intelligence and Theory of Mind

Strategic social intelligence is - like most biological systems designed by natural selection - useful but imperfect. And the ToM mechanism for inferring the content of other people's minds is not 100% reliable. Humans do not have direct access to the content of other people’s minds, and predicting the outcomes of social interactions is inevitably probabilistic. The validity of inferences about other minds can only be checked against the subsequent behaviour of individuals by (implicitly) asking the question: is subsequent behaviour consistent with the assumptions concerning dispositions, intentions and motivation?

Yet even this check on the validity of Theory of Mind inferences is flawed since inferences about DMI affect our interpretation of behaviour. For instance, if we make an inference that a person is aggressively hostile towards us, then we may look at their subsequent behaviour to discover whether his inference is correct. Yet the suspicion of hostility affects our interpretation of this behaviour. If we have already decided that Big Boris is hostile, our emotional state as we observe him is likely to be affected by this inference, and if subsequently he raises a fist towards us we are more likely to be frightened already and to interpret the fist as a threat. We may take the clenched fist as confirmation of Big Boris's aggressive hostility. Yet the interpretation of Boris's gesture as confirmation of a hostile intent may be a mistake if our original 'theory' of his mental state was incorrect.

The above example illustrates how humans make inferences about other peoples’ minds on the basis of information in their own minds. Some of this information involves propositional 'knowledge' about the external world perceived through the senses, but some of the information involves monitoring the internal world of emotions - ie. monitoring body states - both are necessary for understanding other humans.


The somatic marker mechanism

Humans use the state of their own bodies in understanding the contents of other minds (Damasio, 1994). From the work of Damasio and colleagues it emerges that the Somatic Marker Mechanism (SMM) is the primary mechanism for making Theory of Mind inferences (‘somatic’ refers to body, and ‘marker’ to the linking of body state information with perceptions - as described below). Hence the SMM underpins the function of strategic social intelligence.

The SMM was originally described by following studies of defective ‘social intelligence’ in neurological patients, especially those with pre-frontal syndrome and non-dominant parietal lobe damage. The essence of the SMM is that we make inferences about the DMI of other people by monitoring our own emotions. So we interpret another persons DMIs in the light of the emotions that those people induce in us. Patients with neurological damage that renders them unable to experience or monitor emotion will lose strategic social intelligence. They may be able to respond appropriately to here and now (tactical) social situations, but they cannot understand social context, predict social outcomes or plan adaptive social interactions. They have lost the ability to perform internal modelling of human interactions, to run 'simulations’ and evaluate probable outcomes.

Emotions are cognitive representations of body states (remembering that 'body' states also include brain states; Damasio, 1999). So that the emotion of fear is the state of a body that has been activated in a specific fashion by the sympathetic nervous system - with raised heart rate, blood flow diverted to muscles, erected hair etc. The brain continuously monitors these body states, and the emotion of fear comprises the brain representations of this body state. The SMM uses information on emotions in order to evaluate the significance of imagined social scenarios.


An illustration of the SMM in action

As an illustration, imagine that you perceive a large, aggressive man called Big Boris who is approaching you. You respond with the emotion of fear, which means that your sympathetic nervous system prepares your body for action, and the brain monitors this activated state and takes the fear into account when generating appropriate behaviour in response to the situation.

Your perception of the identity of Big Boris is integrated with the body state of fear in response to his approach, and this combined perception and emotion is laid down in long term memory. So, the memory now contains a combined perceptual-emotional representation of ‘Big Boris-fear’. The body state is the ‘somatic’ part (soma = body) and it is used as a ‘marker’ for the perception - hence the name of somatic marker mechanism. ‘Fear’ is the marker for ‘Big Boris’, and the distinctive character of the marker is that when the memory of Big Boris is reactivated, this also reactivates the emotional marker.

This type of long term memory becomes important in strategic social intelligence, for example when planning future interactions in relation to Bog Boris. Whenever you simulate or internally-model interactions with Big Boris, you will recall his identity. And in recalling Boris’s identity you will also re-enact the associated emotional 'marker' - in this instance the body state of fear that is linked to the identity of Boris. This re-enacted fear will influence your decisions in relation to Big Boris, so that you are more likely to consider him as an enemy to be avoided or eliminated than as potential friend or ally. Your inferences concerning Big Boris’s dispositions, motivations and intentions will therefore be based upon your emotional response to him.

This description of the Somatic Marker Mechanism demonstrates that the basis of Theory of Mind is the ability to use our own emotional states to make theories about the DMIs of other people. No doubt there are other mechanisms involved in human Theory of Mind inferences, especially since humans have abstract symbolic language, but Damasio’s work demonstrates that the SMM is the fundamental basis of the ToM ability - without the SMM strategic social intelligence is severely impaired. Theory of Mind is not, therefore, based on knowledge of other peoples thoughts, but assumptions about their nature and purposes. In other words, recalling Big Boris is fear-inducing for you, and your inference is that because Boris is a fear-inducing man, he is probably hostile.


A case study of persecutory delusions

This model of the Theory of Mind mechanism was developed partly as a consequence of studying individuals who suffered that type of Delusional disorder characterised by persecutory delusions. A case study of persecutor delusional disorder was undertaken in order to establish the characteristics of such individuals and to examine their reasoning processes (Walston et al, 2000).

‘Pure’ cases of persecutory delusions (ie. patients validly diagnosable as Delusional Disorder) are not easy to find, since such people only come to the attention of psychiatrists when the patients becomes psychiatrically ill due to the consequent fear of harm, or else when the patient becomes a danger to himself or others due to his reaction to their delusion.

Cases were sought by enquiry concerning the caseloads of 17 psychiatrists and 4 community psychiatric nurses. 34 cases were referred but only 4 fulfilled the study criteria of being 'pure' cases without other potentially obvious confounding psychiatric or neurological symptoms. The four cases were all men aged, between 32 to 43, who had suffered severe persecutory delusions for periods ranging from 6 months to 10 years. All were confirmed (by psychometric tests) to be of normal intelligence with intact cognitive functioning, and without any other formal psychiatric diagnosis. It is important to emphasise that the mental functioning, personality, conversation and social demeanour of these men was entirely normal, except in relation to the subject matter of the delusion.

It was found that all four men were able to lead normal social lives apart from their delusions, having good relations with family and friends - in other words their persecutory delusions were restricted to a specific group of supposed persecutors, and did not encompass everyone in the world. Furthermore, the subjects were all able to perform a range of visual and verbal social reasoning tasks - so called Theory of Mind tests - to a very high standard.

Through tape recorded interviews, a detailed account of their delusional beliefs was elicited, and the results were clear cut. Delusions of persecution were restricted to a specific group of imagined persecutors and to the hostile intentions of this group. All 4 men believed that they were being persecuted by a violent gang of male strangers. The delusional belief was restricted to the specific social category of people in the gang and the specific fear of persecution. The reasoning processes which led to these delusions were not irrational even though they were incorrect. It appeared that these subjects were systematically misinterpreting real but ambiguous information in the light of inferred hostile intent.

For example, one of the subjects saw a stranger enter his club, and assumed that the stranger was a member of the gang that was watching him. Or, the same subject saw someone carrying a bag and made the assumption that this bag contained a gun. In other words the stimuli were real, but were interpreted in the light of pre-existing assumptions concerning the hostile intentions of presumed persecuting gang members. It was the initial assumption that these subjects were being pursued by a hostile gang which was incorrect. Aside from this initial assumption, their interpretations of events was rational even when it was highly implausible.

Fear of violent attack from gangs of male strangers was probably consistent with a common source of threat in ancestral human environments (Walston et al, 1998). Certainly, evidence from twentieth century hunter gatherers, as well as chimpanzees, implies that alliances of unrelated males are a significant cause of premature death.


Interpretation of the Case Study

Delusional disorders seem to be a consequence of logical reasoning from false premises concerning other peoples’ mental states. They are based on false assumptions rather than logical errors. There may, in principle, be many causes leading to a person making false assumptions concerning other people's mental states; given that the system for making inferences relies upon monitoring subjective emotional states. But whatever the cause in each individual case, once established, such delusional beliefs appear able to sustain themselves by a circularity in reasoning based on specific emotions being linked to specific social categories - eg. misinterpretation generates fear which in turn leads to a misinterpretation which causes more fear.

Since delusional disorders are aspects of strategic social intelligence which involve the Theory of Mind mechanism, it is possible to explain many of the clinical and phenomenological features of delusional disorder on the basis of understanding the nature of the ToMM. The case study of persecutory delusions seems to confirm that delusional disorders occur in a context of non-pathological cognitive functioning, including an intact ToMM.

Indeed, the subject matter of several types of Delusional disorders seems specifically to be associated with important social challenges to reproductive success in the probable ancestral environment. Delusions are concerned with such matters as alliances of enemies (persecutory), fidelity of sexual partners (jealous), and vital questions such as other people’s perceptions of one’s own status (grandiose), appearance (somatic) and sexual attractiveness (erotomania). These represent some of the main categories of social competition in the human ancestral environment, in other words the main evolutionary selection pressures, and therefore some of the main functions of the ‘social brain’.


Characteristics of Theory of Mind delusions

1. Social subject matter of Delusional disorders

Humans are social animals, and the reproductive success of our ancestors depended crucially upon their ability to negotiate the social milieu and compete with members of their own species. Furthermore, human psychological mechanisms evolved under tribal conditions with small scale, face-to-face social interactions; and presumably they functioned well on average in these circumstances. But these same mechanisms now operate in a mass social environment populated mainly by strangers performing frequently unobserved acts, and in these conditions what was adaptive may become pathological (Charlton, 1998 & 2000)

The subject matter of delusional disorder bears a striking resemblance to the principal categories of social interaction that have evolutionary importance and require mental state inferences. In other words, delusional disorders apparently reflect the nature of social selection pressures in an ancestral environment. For example, homicide is a major cause of premature male death (hence, failure to reproduce) under tribal conditions (Wrangham and Peterson, 1995), and many homicides are the result of ‘gangs’ of males. Persecutory aggression by hostile alliances of unrelated males was probably therefore a highly significant feature of ancestral social life, and it makes sense that inferences concerning persecution by male alliances have the potential to act as a powerful influence on behaviour (Walston et al, 1998).

Similarly, a conjectural evolutionary scenario to account for erotomaniac and some somatic delusions can be derived from theories of human sexual selection (Buss, 1994, Miller, 2000). The major variable that influences a man’s attractiveness to women is status; and erotomania can be seen as a condition in which a woman becomes delusionally attracted to an unattainable but high status male (Enoch & Trethowan, 1991; Mullen & Pathe, 1994). By contrast, a woman’s physical attractiveness to men is primarily a matter of physical beauty (cues of youth and health; Buss, 1994) and in the somatic type of delusional disorder a common presentation is in a hypersensitive, insecure woman of reproductive age who has become preoccupied that she is physically unattractive due to some bodily impairment (such as a foul odour) or personal ugliness (eg. blemished skin, large nose). Somatic delusions of this type are reported to be unusual in women beyond reproductive age. And when somatic delusions of this type are found in men, it could be predicted that they will be more common among those who rely on their appearance for attracting sexual partners - for example homosexual men, or men of lower social status.

Such explanations are obviously highly general, and fail to account for the occurrence of pathologies inn specific individuals. Nonetheless, they make predictions about individuals diagnosed as suffering from psychiatric states, and these predictions can be tested - for example in studies such as the case study of persecutory delusions summarised above.


2. False beliefs are unavoidable when inferring mental states

The false beliefs found in delusional disorder are social, and involve mistaken mental state inferences - ie. misjudging the dispositions, motivations and intentions of other people. Such mistakes are inevitable, given the nature of the Theory of Mind Mechanism. Beliefs concerning the mental state of others cannot always be true because beliefs cannot be checked against objective criteria - there is no direct access to other minds.

And some circumstances might plausibly make such mistakes more probable. Inferences concerning the state and content of other minds depend upon information from one’s own subjective emotional responses. In other words, accurate knowledge of another mind depends on knowledge of one’s own body state. When a person's subjective emotional response is inappropriate or pathological, then the inference of mental state will probably be wrong. In principle, almost any cause of increased fear might be expected to predispose to persecutory delusions if there was already a somatic marker linked to a specific class of persons. Such fear may be an aspect of personality or circumstance, or due to a disease process, or drug side effects or withdrawal effect. For instance, I have described the emergence of persecutory delusions following the withdrawal of a neuroleptic (Charlton, 2000).

The relationship between specific emotional states and specific errors in inference leads to testable predictions - although understanding of the typology of emotional states remains incomplete. Persecutory delusions may specifically be associated with particular personality types, including certain attributional styles (Bentall et al, 1994). Another possible link between emotions and delusional disorder may also be seen in the reported association between low self-esteem (ie. perceived low status) and morbid jealousy (Mullen & Martin, 1994).


3. Beliefs concerning ToM inferences will be resistant to counter-argument

Beliefs concerning the state of mind of other people may be powerfully resistant to counter-argument, despite the fact that such beliefs arise from potentially insecure inferences. It might perhaps have been expected that such potentially insecure beliefs based on subjective emotional factors would be only weakly held - but in fact these are exactly the kind of beliefs held with greatest passion.

Presumably this paradox is explained by the fact that the human social domain is intrinsically competitive (Byrne & Whiten, 1988; Whiten & Byrne, 1997). Indeed, it is suggested that the ToMM evolved as a direct consequence of exactly this human versus human competition. Deception and concealment of hostile motivations and damaging intentions can be expected in the social domain.

Therefore, mistrustfulness is adaptive when it comes to judging the social explanations and reassurances of other people. Dishonesty from other people, in these matters, is to be anticipated - since most humans are potential rivals for limited resources (especially matings; Buss, 1994; Miller, 2000), and none of them share exactly the same social agenda. It therefore makes sense that beliefs concerning theory of mind will neither be labile nor readily abandoned despite their subjective basis. In a rivalrous social world where no-one can wholly be trusted, each person must reach their own conclusions about the motivations, disposition and relationships of other people, and must rely on their own judgements - however imperfect and unreliable.


4. ToM delusions are encapsulated due to the nature of the ToMM

When mental state delusions are a consequence of the ToMM (ie. dependent on the SMM) they depend upon a cognitive representation that incorporates a social identity with an emotion (Damasio, 1994, 1995).

The somatic marker is an emotion linked to a social category. When the memory of that social category (eg. Big Boris, or a specific gang of drug dealers) is activated, then the body state linked to it is re-enacted. In other words, because an emotion is linked specifically with a category of social identity that elicits that emotion, mental state inferences will be restricted to the particular person or group described by that social category.

This potentially explains why pure cases with delusions of persecution can nevertheless maintain friendly and co-operative social relationships with people outside of the social category of their presumed persecutors - people outside the specific social category do not elicit activation of the somatic marker emotion of fear. This seems to apply to both men and women, although the social categories differ. Probably, female persecutory delusions usually relate to familiar people, while male delusions relate to strangers (Walston et al, 1998).And analogously, female jealousy is mainly concerned with commitment of love and resources, while male jealousy is mainly concerned with sexual infidelity (see below). In both instances, the delusion is encapsulated, although the general social category differs between the sexes.


A case of morbid jealousy

Having developed the idea of Theory of Mind delusions by concentrating on the evidence provided by persecutory delusions, clinical case histories concerning delusions of sexual infidelity were examined to check whether they conformed to the features described.

‘Morbid jealousy syndrome’ describes a condition of inappropriate or excessive jealousy, specific to the sexual partner, and which dominates behavior; this becomes delusional when it involves a false belief in the sexual infidelity of the spouse or sexual partner. Morbid jealousy can occur in a pure form (ie. without the presence of another psychiatric diagnosis), in both males and females; although it is commoner in males (Shepherd, 1961; Enoch & Trethowan, 1991). What follows is true, although names and identifying details have been changed (Charlton, 2000).

Edward is a man in his mid-twenties. He had an uneventful childhood, was an average pupil and left school without taking examinations to serve an apprenticeship. Edward’s personality is cautious and careful, and people have commented on his neatness, punctuality and conscientiousness. Although somewhat shy, he has plenty of friends and an active social life. Indeed, he has strong attachments to his family, and a powerfully developed sense of personal responsibility. There is no history of psychiatric illness, nor current sign of psychiatric illness.

In his early twenties, Edward began a relationship with a younger girl called Frances that lasted several years. As the relationship progressed it became more stormy, with arguments centering around Frances’s desire for more freedom to go out with friends, and Edward’s increasingly possessive attitude to her and his criticisms of her sexually provocative style of dress. Edward became increasingly worried that Frances might be ‘seeing other boys and having sex. If she had sex with anyone else I could never have her back’. The worry escalated into a tormenting pre-occupation, and on one occasion Edward was driven to phone one of Frances’s friends to check that she was not seeing anyone else; on another occasion he went around the local night clubs to check on her whereabouts.

The situation became so bad that the relationship split up (a ‘trial separation’). However, Edward became even more distressed. One evening, Edward saw Frances in a bar, talking to a group of men and dancing in what seemed a provocative fashion. He left the bar ruminating on the possibility that she was seeing other men, and the thought ‘jumped through’ his mind that she may have had sex with them - although he pushed the thought aside. In an overwrought mood, he waited outside Frances’s home in a car to discuss their relationship. She sat by him in the car, an argument broke out and Francis tried to make it up by kissing Edward; but Edward exploded into sudden anger at her sexually provocative manner - and he strangled Frances to death.

Edward was immediately overwhelmed with remorse, drove for miles, and made a determined attempt at suicide. The interview took place in prison where Edward was awaiting trial for murder.


Sexual jealousy in evolutionary context

Jealousy in humans is a cultural universal, a complex and characteristic pattern of behaviour in response to specific cues, which serves an adaptive function concerned with paternal investment in offspring. Across the animal kingdom, jealous behaviour is found when males contribute resources to their offspring (especially after birth) and is a response to the problem of uncertain paternity in species where females potentially mate with more than one male (Wilson & Daly, 1992; Buss, 1994; Pagel, 1997).

Jealousy in men can be seen as an evolved psychological adaptation that operates to reduce the chance of sexual infidelity in a partner, and reduce the chance of misdirected investment (even the act of mating typically requires substantial investment of resources, and loss of the opportunity to invest these in courting other mates; Buss, 1994). If a male were to tolerate sexual infidelity and continue to invest resources into a rival male’s offspring, he would incur the ‘double’ genetic penalty of both failing to reproduce and ‘wasting’ resources on assisting a rival’s reproduction. Humans have few offspring, each requiring substantial investment of resources - any child sired by another man represents the loss of a substantial proportion of expected reproductive capacity (Buss, 1994).

Jealousy in women is significantly different in its motivation and intentions since female mammals do not suffer from uncertainty as to the identity of their offspring, and sexual infidelity per se is not a problem. The problem for a female is to secure investment to help in rearing offspring, and jealousy is primarily concerned with ensuring that the male partner directs his investment efforts towards the woman’s own offspring. So female jealousy is less concerned with the act of sexual infidelity and more with the danger of a male partner transferring his affections (and resources) to another female (Wiederman & Allgeier, 1993; Buss, 1994). Hence selection pressures have led to different cues that stimulate the emotion of jealousy in men and women: men primarily fear physical infidelity (the partner having sexual intercourse with another man) while women primarily fear emotional infidelity (the partner falling in love with another woman) (Townsend, 1995; Geary et al, 1995; Mullen & Martin, 1994).

The extreme of morbid jealousy such as displayed by ‘Edward’ would not usually be considered adaptive (see Sheets et al, 1997) since it could severely damage reproductive success: for example when it causes the breakup of a relationship, or death of one or both partners by homicide (Mowat, 1966). However, it remains possible that the threat or possibility of such extreme sanctions may serve as an effective deterrent; hence even intense jealousy may be adaptive on average, or under ancestral conditions.

Jealous delusions be considered as consequences of the ToMM since, although the content may be complex and varied, in pure cases the delusions seem to be consequences of internally-modelled social relationships and mental state inferences. Jealous delusions are not about what is happening here-and-now; but instead about what did happen, is happening elsewhere, or might happen in the future. In other words, delusions are provoked by imagined social interactions, ‘simulated’ scenarios of sexual infidelity.

Delusions of sexual infidelity are consistent with the four predicted characteristics of Theory of Mind delusions. For instance, false positive (or inappropriate) jealousy is inevitable at a certain frequency since imaginative construction of possible scenarios cannot always be based-upon or checked-against reality. Also, inferences concerning the intentions of a sexual partner are not directly accessible but can only be checked against behaviours whose interpretation is ambiguous. Jealousy is notoriously resistant to reassurance or counter-argument. There is often no objectively convincing way to contradict the delusional belief. This arises from the fact that jealousy evolved in a context of social competition where deception is expected as an element of that competition. Nonetheless, false beliefs of sexual infidelity are compatible with being encapsulated and specific to the sexual partner (Enoch and Trethowan, 1991). The encapsulation occurs on the basis that the ToMM involves a cognitive linkage between a particular social category and a particular emotion - outside that subject matter and that emotion, cognitive life may proceed relatively unaffected.


Bizarre delusions

Not all delusions are Theory of Mind delusions. Another important category of false belief is ‘bizarre’ delusions. Bizarre delusions include many of the most typical delusions seen in classic ‘schizophrenic’ patients (Sims, 1995). For example those ‘primary’ delusions in which a person suddenly becomes convinced of something false without any understandable logical link - ‘the traffic lights turned green and I knew I was the son of God’, or ‘My thoughts stopped and I realised that they were being drawn out of my head by X-rays’.

Some bizarre delusions arise from hallucinations or other abnormal bodily or mental experiences - for example ‘the voices’ may have told a person that he was the son of God, or he may believe that the funny feelings in his abdomen were caused by telepathy. These are bizarre ways of explaining bizarre experiences. However, whether bizarre delusions are primary or secondary, I will argue they share the common cause of global brain dysfunction. Hence, bizarre delusions have very limited relevance to the study of ‘the social brain’ - emphasising the importance of distinguishing between these two types of delusion.


Brain dysfunction and delusions

Everybody has experienced the kind of illogical thinking that leads to bizarre delusions, since this kind of progression of ideas happens in dreams. For instance, dreams may resemble the following: ‘I walked into the street and saw a lion and realised that to escape I needed to open a trapdoor hidden underneath the hedge, and the trapdoor opened onto another planet with purple skies and no gravity, but the lion had changed into a flowerpot…’

If we awaken from a doze, or just as we are dropping-off to sleep, we may recall that our thoughts were ‘falling apart’ and becoming illogical - this is a brief state of delirium due to ‘clouded consciousness’. The release from a normal coherent progression to a quasi-pathological and unpredictable association of ideas varies in severity on a continuum from occasional lapses of concentration to gross incoherence. The process can be observed by other people when a delirious patient exhibits a fluctuating state of consciousness, lucid and rational intervals interspersing drowsy or agitated periods of illogical thought.

Incoherent thinking and illogical reasoning is the consequence of ‘clouded’ consciousness, or generalised brain damage. Whenever thinking is impaired by ‘organic’ insult to the brain - when drowsy, pyrexial, when the brain is impaired by drugs or alcohol (or by withdrawal from drugs or alcohol), or has extensive pathological damage from by dementia, or has been damaged by trauma - then under such circumstances there is a greatly increased potential for impaired reasoning to lead to false beliefs.

Beliefs resulting from illogical thinking can be extremely bizarre, partly because the stream of consciousness is disrupted, and partly because the mechanisms for testing ideas for plausibility and consistency with other ideas is also damaged.


Characteristics of bizarre delusions

Bizarre delusions may be distinguished from ToM delusions in terms of several contrasting psychopathological criteria (Charlton, 2000).

  1. Bizarre delusions may have any subject matter

    Whereas theory of mind delusions are always about social phenomena; bizarre delusions might be about any subject or thing: social or environmental, physical or metaphysical, natural or supernatural.

  2. Bizarre delusional beliefs may survive objective refutation

    Theory of mind delusions stem from inferences concerning the mental states of other people, in other words ToM delusions arise from indirect inferences about entities which are not directly observable. Hence they may not be possible to refute because there is no direct access to other people’s mental states, not any objective way of demonstrating the dispositions, motivations or delusions of other people. But bizarre delusions may be held despite the evidence of direct observation.

    Evidence that any normal person would find compelling is not necessarily persuasive to someone with bizarre delusions. Because the reasoning processes are themselves impaired in bizarre delusions, then a chain of argument that would usually be considered to be conclusive evidence against a belief does not the necessary force to compel a change of belief.

    For instance, a person with psychotic depression and nihilistic delusions may believe that their internal organs have rotted away leaving them hollow. Such a person is holding a belief in the existence of a state of affairs that is incompatible with human life - yet this ‘fact’ of the delusion being impossible is not taken to be compelling. Indeed, this kind of patient may deny that they are alive at all - which again contradicts what would be considered to be the possibilities of objective fact.

    Whatever arguments or evidence that are brought to bear, the bizarre delusional belief may unshaken because, when brain function is impaired we cannot follow logic, and chains of reasoning are disrupted, so even objective evidence does not have the power to persuade.

  3. Bizarre delusions are not encapsulated by social category

    ToM delusions are characterised by false beliefs confined to a particular social category - as when the deluded person is only jealous of his wife (but not his sister), or only afraid of the local drug gang (but not the Freemasons). But since bizarre delusions are caused by impaired reasoning, bizarre delusions are not restricted to particular social categories, and delusional thinking is liable to be a feature of many domains of discourse. For example, bizarre delusions with a persecutory theme may encompass not just a specific group of persecutors, but the whole of humankind in a ‘conspiracy’ against the subject.

  4. Pure cases of bizarre delusions will not exist

    While ToM delusions can occur as ‘pure cases’ in people who are otherwise normal it would be predicted that there will be no pure cases of bizarre delusions. That is to say there will be no cases of people who have an encapsulated bizarre delusion with otherwise normal psychological functioning. In lay terms, all people with bizarre delusions will be overtly ‘mad’, or in some other way suffering from global brain impairment inevitably leading to a variety of psychological symptoms.

    Because bizarre delusions are a consequence of impaired reasoning processes, and impaired reasoning processes will be a consequence of global brain impairment such as delirium or dementia, then when bizarre delusions are observed there will always be a widespread impairment in brain function. Such a person will produce not just a single false belief, but a variety of psychological symptoms typical of that form of impairment. A person will bizarre delusions will not merely have a false belief, he will also exhibit symptoms such as impairments in concentration, altered mood, and poor performance on short term memory tasks, consistent with a diagnosis of delirium.

    Bizarre delusions will therefore only be found as part of a psychiatric syndrome - never as pure cases.


Bizarre delusions caused by organic brain impairment

The category of bizarre delusions is not explicable in terms of rationally misinterpreting normal perceptions on the basis of misattributed intentions, motivations, or dispositions. Bizarre delusions require either that the patient is rationally misinterpreting pathological psychological features such as hallucinations; or else the actual logical processes are irrational due to pathology: eg. ‘they threw an egg at my window, and this meant I was a homosexual, so I switched on my radio’.

It is uncontroversial that irrational thinking and abnormal psychological experiences are a common feature of organic brain disease - such as delirium, epilepsy or dementia. When a brain is dysfunctional or damaged then it is unsurprising that the brain cannot perform cognitive processing in the normal fashion. The same applies to sleep or near sleep states. False beliefs are to be expected in a circumstance when brain impairment has affected the cognitive processes by which beliefs are generated. There is reason to suppose that bizarre delusions are caused by global brain impairment, perhaps most commonly due to chronic and severe sleep disruption.


Bizarre delusions, delirium and illusory dreams

Chronic severe sleep loss and other forms of sleep disruption are significant clinical features in many psychotic patients, although they are seldom considered as potential aetiological factors for psychotic symptoms. Yet chronic, severe sleep loss can certainly cause delirium, and the probable mechanisms of this link have recently been elucidated (Charlton & Kavanau, 2001).

Memory circuits of the brain are reinforced during sleep, a process in which synaptic strengths are maintained at dedicated levels (Kreuger & Obal, 1993; Kavanau, 1994). Synaptic strength maintenance occurs largely through the action of self-generated, spontaneously occurring, slow brain waves (waves at frequencies less than about 14 cycles per second). This occurs both during rapid-eye-movement (REM) and nonREM sleep, though there are significant differences in function between the two phases. Maintenance is necessary since all synaptic strengths weaken with time due to "turnover" of essential molecules. Without remedial action during sleep, all memory circuits that were not being regularly ‘exercised’ by frequent use while awake, would gradually deteriorate and their encoded memories be lost (Kavanau, 1996; Stickgold, 1998).

Some of the memories being reinforced during sleep rise to the level of "unconscious" awareness, and these are the memories that provide the substance of our dreams. If our stored memories were valid in every respect, then our dreams would consist solely of "replays" of past or plausible events in our lives (roughly 85-95% of dream contents derive from authentic contents; Antrobus & Bertini, 1992).. On the other hand, when memory circuits are faulty, the events and perceptions in the resulting dreams may be distorted or largely illusory. The sources of illusory dream contents are at least three-fold: first, there are disordered synaptic strengths that owe to normal imperfections in the processes that store and maintain memories; second, there are the abnormal influences of pathologically altered brain waves; and third, there are the influences of sleep loss leading to incomplete refreshment of synaptic strengths.

The earliest manifestations of sleep deprivation, even after a single night, include significant impairment of cognitive performance and changes in mood. After only 48 hours most subjects report illusions and/or visual and tactile hallucinations, and these become more intense as deprivation progresses (Everson, 1997). The pathology underlying organic delirium additionally involves abnormalities in slow waves observable by EEG and characterized by deviations from normal frequency, form, magnitude or distribution (Slaby & Cullen, 1987).. Such pathological waves are presumably incapable of reinforcing memory circuits in the usual fashion. With a cumulative weakening of synaptic strengths in affected circuits, subsequent recall of such distorted memories produces hallucinations, delusions, and other hallmarks of delirium.

These alterations of mental state apparently reflect the use of incompetent circuitry that accumulates during the extended periods of sleep loss and/ or the effects of pathological brain waves. Just as illusory dreams in normal individuals often are the result of activation of incompetent circuits, the symptoms of organic delirium probably owe their origin primarily to the activation of incompetent circuitry of functionally pathological origin. And these mechanisms lead to the illusory content and illogical form of bizarre delusions (Kavanau, 1999; Charlton, 2000; Charlton & Kavanau, 2001).


The social brain and delusions

At least two types of delusion may be distinguished: ToM delusions and Bizarre delusions. Both types are false beliefs, and both types of false belief are typically resistant to short term and unstructured attempts at modifying them. Only the form and content of Theory of Mind type of delusions are related to the social evolutionary history of humans. By contrast, the form and content of bizarre delusions are products of pathology rather than adaptation. This illustrates the way in which evolutionary biology must be applied to medicine only with caution, because while some diseases reflect evolutionary and adaptive categories, other diseases do not.

ToM delusions may occur in multi-symptomatic syndromes such as schizophrenia, mania and psychotic depression as well as in pure cases. But what makes them potentially interesting to evolutionary biologists is that ToM delusions can occur encapsulated in pure cases, where the subject is free of other psychiatric pathologies (these are the Delusional disorders). In other words, ToM delusions are not necessarily pathological - their consequences may be pathological (eg. a person may suffer extreme distress, may kill themselves or another person as a consequence of their false beliefs). But the cognitive nature of the delusion is simply that of normal social beliefs.

A Theory of Mind delusion is a false belief which is the logical outcome of a false premise. The processes of reasoning are intact and unimpaired, but are operating on incorrect assumptions. For Edward (the jealous murderer described above) two plus two still equals four and the sun still rises in the East. Edward was also able to give accurate accounts of direct observations of objective data. However, his assumption that his girlfriend was having an affair was based upon an incorrect interpretation of indirect inferences concerning her state of mind. Although her behaviour appeared to him to be consistent with the assumption of her sexual infidelity, the fact of the matter was that Edward’s girlfriend was not actually having an affair - his belief was false.

ToM delusions happen to be false beliefs, but they are the result of normal brain processes operating on mistaken premises concerning other peoples DMIs. Mistaken premises concerning other people’s DMIs are inevitable given that these inferences are based upon unreliable evidence. ToM delusions are (probably) caused by many different factors in different individuals, such as the inevitable error rate of the ToM mechanism (especially when operating under modern conditions), and by emotional abnormalities - perhaps based on personality, or perhaps due to specific pathologies affecting emotions. The fact that inferences about the DMIs of other people depend on monitoring our own emotions, implies that anything which affects our body state may affect our understanding of social situations. This is a mechanism whereby changes in body chemistry, the influences of drugs, and the effects of health can all lead to changes in social functioning (Charlton, 2000).

The psychological mechanism leading to Delusional disorders is therefore identical with the mechanism of normal human ToM. This implies that almost all religious and or political beliefs (for instance) also have the form of ToM delusions - since these involve unwarranted assumptions about the DMIs of imagined entities such as gods, or abstract entities such as political parties and leaders. Indeed, all inferences concerning the DMI of other people are inevitably based on incomplete and inconclusive evidence; so religious and political beliefs are not unusual. But this may explain why such culturally-dependent and evidentially-insecure beliefs nevertheless generate such powerful emotional attachments.

By contrast, Bizarre delusions are the consequence of illogical thinking, can have any subject matter, and never occur in isolation. Bizarre delusions are found only as part of complex syndromes such as schizophrenia, mania, psychotic depression, dementia and delirium; conditions which include other primary psychiatric symptoms such as hallucinations, incoherent speech, and major mood changes. And bizarre delusions are caused by global brain dysfunction - such as delirium - especially when this incorporates severe and chronic sleep disturbance.

But false beliefs might also be the outcome of impaired thinking, of ‘illogical’ reasoning. Even correct premises would not necessarily led to correct conclusions since thinking is impaired. When reasoning is illogical, two plus two would not necessarily equal four, but might instead equal three, or five, or Adolf Hitler. The sun may rise in the West tomorrow, fail to rise at all, or have turned into a balloon.


Therapeutic implications

The suggested discrimination of delusions into ToM and bizarre types is not merely an abstract exercise - the therapeutic implications are considerable. For example, when treating a person with ToM delusions, it would be a mistake to try and eradicate the false belief using drugs, since the mechanisms leading to that belief are not necessarily pathological. Drugs might usefully alter the emotional state which makes a delusions distressing; for example a neuroleptic such as chlorpromazine might reduce extreme fear or agitation. But the false belief would probably remain intact, even if a person held that belief with less conviction, or did not feel compelled to take any action as a consequence of that belief (Charlton, 2000).

And since ToM delusions are the product of rational thought, then belief modification by rational persuasion is a possible line of therapy, and indeed ‘Cognitive’ therapies have been applied to these kinds of belief with some success (Kingdon et al, 1994; Dolan & Bishay, 1996). The main limitation of such rational persuasive therapies, however, is that it may not be possible to ‘prove’ the patient wrong, since the delusions may be based upon an inference concerning another person’s mind (Charlton & McClelland, 1999). The most fruitful approach might simply be to persuade the deluded person to acknowledge that there is room for doubt concerning the content of other minds, and that there are other hypotheses concerning the dispositions, motivations and intentions of others that are at least equally plausible, but which do not entail those beliefs which have led to that person’s referral.

Changing a person’s false beliefs by such techniques of persuasion would, presumably, be neither easier nor more difficult than changing a person’s religious or political opinions. That is to say - such persuasion is very difficult, but not impossible - and there are recognised techniques which improve the chance of success.

The treatment of bizarre delusions is a different matter altogether. At present bizarre delusions are treated with neuroleptics, which probably do not eliminate the false belief so mush as make the subject ‘indifferent’ to the belief (Healy, 1997). But if bizarre delusions are a manifestation of delirium in patients with a history of severe sleep loss and either EEG or clinical evidence of delirium, then management directed primarily at securing deep and restorative sleep would be expected to produce significant clinical improvement. The clinical benefit of neuroleptic and other tranquilizing drugs (such as lorazepam) currently used in the management of acute psychosis might turn-out to be attributable mainly to their sleep-promoting effects. This topic is given more detailed consideration elsewhere (Charlton, 2000).


Adaptive significance of psychiatric phenomena

There is no guarantee that the study of psychiatric phenomena will increase understanding of the social brain. But the fact that emotional and social systems are often disrupted in psychiatric illness implies that it is worth looking for plausible evolutionary and adaptive rationale for the patterns of symptoms and signs that are observed. Delusions are only one example, and the clinical features of many other disorders appear to be a consequence of historical selection pressure.

One characteristic that may distinguish between evolved syndromes and syndromes sharing an underlying pathology may be that evolved symptoms are often characterised by a link between form and content. Where a behavioural adaptation has evolved to solve a specific problem, then adaptive behaviours will usually be associated with a specific class of stimulus (Barkow et al, 1992).

For instance, anxiety is a pathological form of an evolved, adaptive emotional state (Nesse & Williams, 1996). The features of anxiety are adaptive when triggered appropriately, but in psychiatric patients the activation of the emotion may be too powerful, too sustained, activated without sufficient cause, or activated in an inappropriate situation. And among the anxiety disorders termed phobias, phobias of snakes and spiders are much more common than, say, phobias of lizards and ants, or of guns and automobiles. This very probably reflects the importance of snakes and spiders in human evolutionary history which has led to facilitated learning of fear to these specific categories of agent - however inappropriate the resulting behaviour may be in twenty first century England. People are not born with innate phobias, but it is easier to learn a phobia of stimuli that represented a significant threat in our ancestral environment than to learn a phobia of novel threats (Nesse and Williams, 1996).

Another example may be panic disorder, a disabling form of anxiety which is probably the adult variant of 'separation anxiety' (freezing and screaming) that is observed in infant children when they have become detached from the family group (Klein, 1980; Matthews and Charlton, 2000). Panic is a form of 'signalling' for rescue - almost literally a ‘cry for help’. Adults with panic symptoms seem to have been more prone to separation anxiety as children, and individual cases with pure Panic Disorder have reported that attacks occur when away from the family base, and that panic attacks include a powerful desire to be reunited with the family (Silove et al, 1996; Matthews and Charlton, 2000).

In conclusion, psychiatric illnesses may provide an important source of evidence for understanding the evolution of the social brain. Yet this field remains virtually unexplored. This field offers considerable scope for future research.

Acknowledgement: thanks are due to Florence Walston, David Healy, Hamish McClelland and Lee Kavanau for clinical information, analysis and ideas.


References

Antrobus, J.S. & Bertini, M. (1992). Introduction. (ed. Antrobus JS., Bertini M). The neurobiology of sleep and dreaming. Hillsdale, NJ, USA, Erlbaum, pp. 1-16

APA: American Psychiatric Association. (1994). DSM-IV - Diagnostic and Statistical Manual 4th edition, Washington DC, APA.

Barkow JH, Cosmides L, Tooby J. (1992). The adapted mind: evolutionary psychology and the generation of culture New York: Oxford University Press.

Bentall RP. Kinderman P, Kaney S. (1994). The self, attributional processes and abnormal beliefs: towards a model of persecutory delusions. Behavioral Research and Therapeutics. 32: 331-41.

Brothers L. (1990). The social brain: a project for integrating primate behavior and neurophysiology in a new domain. Concepts in Neuroscience, 1, 27-51.

Buss DM. (1994). The evolution of desire, New York, BasicBooks.

Byrne R.W. & Whiten A. (ed.). (1988). Machiavellian intelligence social expertise and the evolution of intellect in monkeys, apes and humans. Oxford: Clarendon Press.

Charlton BG. (1998). Psychopharmacology and the human condition. Journal of the Royal Society of Medicine 91, 599-601.

Charlton B. (2000) Psychiatry and the human condition. Oxford: Radcliffe Medical Press.

Charlton BG, Kavanau JL. (2001). Delirium and psychosis: an integrative model. Medical Hypotheses, in the press.

Charlton B.G., McClelland H.A. (1999). Theory of mind and the delusional disorders. Journal of Nervous and Mental Disease 187:380-3.

Damasio AR. (1994). Descartes error: Emotion, Reason and the Human Brain, New York , Putnam.

Damasio AR. (1999). The feeling of what happens: body, emotion and the making of consciousness. London: William Heinemann.

Dolan M & Bishay N. (1996). The effectiveness of cognitive therapy in the treatment of non-psychotic morbid jealousy. British Journal of Psychiatry 168, 588-593.

Enoch MD, Trethowan W. (1991). Uncommon psychiatric syndromes 3rd edition, Oxford, Butterworth-Heinemann.

Everson, C.A. (1997). Clinical manifestations of sleep deprivation. (ed Schwartz WJ.). Sleep science: integrating basic research and clinical practice. New York, Karge, pp. 34-59.

Garety PA & Hemsley DR. (1994). Delusions: investigations into the psychology of delusional reasoning, Hove, Psychology Press.

Geary DC, Rumsey M, Bow-Thomas CC & Hoard MK. (1995). Sexual jealousy as a facultative trait: evidence from the pattern of sex differences in adults from China and the United States. Ethology and Sociobiology, 16, 355-383.

Healy D. Psychiatric drugs explained London: Mosby-Wolfe 1996.

Humphrey, N.K. (1976). The social function of intellect. In Growing points in ethology (ed. PPG. Bateson & RA. Hinde). Cambridge, UK: Cambridge University Press.

Kavanau, J.L. (1994). Sleep and dynamic stabilization of neural circuitry: a review and synthesis. Behavioural Brain Research, 63, 111-126.

Kavanau, J.L. (1999). Adaptations and pathologies linked to dynamic stabilization of neural circuitry. Neuroscience and Biobehavioural Reviews, 23, 635-648.

Kingdon D, Turkington D & John C. (1994). Cognitive behavior therapy of schizophrenia. British Journal of Psychiatry, 164, 581-587.

Klein DF. (1980). Early experience with imipramine and anxiety. Comprehensive Psychiatry 12: 411-427.

Kreuger, J.M. & Obal, F. (1993). A neuronal group theory of synaptic function. Journal of Sleep Research, 2, 63-69.

Matthews S, Charlton BG. (2000). Phenomenology of panic attacks reflects human evolutionary history of separation anxiety. Irish Medical Journal. 93: 184-5.

Miller G. (2000) The mating mind: how sexual choice shaped the evolution of human nature. London: Heinemann.

Mowat RR. (1966). Morbid jealousy and murder, London, Tavistock.

Mullen PE, Martin J. (1994). Jealousy: a community study. British Journal of Psychiatry 164, 35-42.

Mullen PE & Pathe M. (1994). The pathological extensions of love. British Journal of Psychiatry 165: 614-623.

Nesse RM, Williams GC. (1996). Evolution and healing. London: Phoenix.

Pagel M. (1997). Desparately concealinf father: a theory of parent-infant resemblence. Animal Behavior, 53, 973-981.

Sheets VL, Fredendall LL & Claypool HM. (1997). Jealousy evocation, partner reassurance, and relationship stability: an exploration of the potential benefits of jealousy. Evolution and Human Behavior, 18, 387-402.

Shepherd M. (1961). Morbid jealousy: some clinical and social aspects of psychiatric symptoms. Journal of Mental Science, 107, 687-753.

Silove D, Manicavasagar V, Curtis J, Blaszcynsia A. (1996) Is early separation anxiety a risk factor for adult panic disorder? Archives of General Psychiatry 37: 475-482.

Sims, A. (1995). Symptoms in the Mind: an Introduction to Descriptive Psychopathology London: W.B. Saunders Company Ltd..

Slaby, A.E. & Cullen, L.O. (1987). Dementia and delirium. (ed. Stoudemire A, Fogel BS) Principles of medical psychiatry, New York, Grune and Stratton, pp. 135-175.

Stickgold, R. (1998). Sleep: off-line memory re-processing. Trends in Cognitive Science, 2, 484-492.

Townsend JM. (1995). Sex without emotional involvement: an evolutionary interpretation of sex differences. Archives of Sexual Behavior, 24, 173-206.

Walston F, Blennerhassett RC, Charlton BG. (2000). ‘Theory of mind’, persecutory delusions and the somatic marker mechanism. Cognitive Neuropsychiatry 5: 161-174.

Walston F, David AS & Charlton BG. (1998) Sex differences in the content of persecutory delusions: a reflection of hostile threats in the ancestral environment? Evolution and Human Behaviour, 19, 257-260.

Whiten A. & Byrne R.W. (ed.) (1997). Machiavellian intelligence II: extensions and evaluations. Cambridge: Cambridge University Press.

Wiederman MW & Allgeier ER. (1993). Gender differences in sexual jealousy: adationist or social learning explanation? Ethology and Sociobiology, 14, 115-140

Wilson M, Daly M. (1992). The man who mistook his wife for a chattel. In: Barkow JH, Cosmides L, Tooby J. (1992). The adapted mind: evolutionary psychology and the generation of culture New York: Oxford University Press, pp 289- 322.

Wrangham R & Peterson D (1996). Demonic males: apes and the origins of male violence Boston, Houghton Mifflin.


E-mail
bruce.charlton@ncl.ac.uk

HOME

also by Bruce Charlton
The Malaise Theory of Depression
Delirium and Psychotic Symptoms
Public Health and Personal Freedom
Psychiatry and the Human Condition
Awareness, Consciousness and Language
Injustice, Inequality and Evolutionary Psychology
Alienation, Neo-shamanism and Recovered Animism
Peak Experiences, Creativity and the Colonel Flastratus Phenomenon