User:Anthonyhcole/essay

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Introduction
I claim that functional mental illness, though presently thought to spring from a brain genetically predisposed to respond to environmental assaults with disorder, is simply the product of intense, sustained physical distress, and may arise from a perturbation of any part of the body; I claim that it is possible for a person to suffer intense physical distress while modern medicine is yet unable to detect anything in the body which might cause it.

How does being in constant physical distress affect a person? Below, using the example of constant pain, I answer that question, and on that answer build a new theory of mental illness. In Part One I describe the impact of pain on the person (distress, executive dysfunction, and neuroticism), and the impact of pain on social connection. In Part Two I argue that the mental illnesses ADHD, autism spectrum, schizophrenia, bipolar disorder, major depression and generalised anxiety disorder all share this symptom cluster comprising distress, executive dysfunction, and neuroticism; and I argue that this symptom cluster is the most disabling aspect of each of these disorders. Without it, these patients would not be ill – odd, possibly, but functional.

Since, in physical pain, the the primary symptom of this cluster (the symptom underpinning the others) is distress, it is reasonable to propose that distress is this cluster’s primary symptom when it is found in mental illness. I assert that distress, presently thought of as a byproduct of mental disorder, is the long sought cause of the affective, cognitive and social deficits and most of the functional, chemical and structural brain abnormality in mental illness, and that the primary source of distress in most cases of mental disorder may lie outside the central nervous system but beneath the skin.

It is probable that, beyond a certain threshold, all negative homeostatic emotions (fatigue, pain, nausea, thirst, air hunger, feeling sleep-deprived, feeling sick, etc.) entail distress, and that this distress causes executive dysfunction and neuroticism. However, with the exception of physical pain and sleep deprivation, very little work has been done on this. I begin by discussing the distress of pain and the mental illness I believe pain induces, autism.

What is pain?
The dominant scientific theory of physical pain divides the experience into three dimensions: sensation, affect-motivation and cognition.

By sensation they mean the feeling of the location, quality, intensity and duration of the pain.

The affect-motivation of pain has been divided into two components: (1) primary affect, the feeling that distinguishes pain from other homeostatic emotions like nausea and itch, and the unpleasantness and motivation associated with that feeling, and (2) secondary affect, consisting of emotions elicited by primary affect and largely determined by prior experience, present circumstances, and apprehensions and expectations about the future (Grahek, 2007). In this essay I use "distress" to denote the unpleasantness and motivation associated with pain and other negative homeostatic emotions.

With regard to cognition, pain science has focussed on the fact that thinking can change behaviour and modify secondary affect (emotions) and, consequently, primary affect. . This is called the “top down” effect. For example, allaying a person’s anxiety about a pain through education can measurably reduce the intensity of primary affect; and telling someone you’re giving them pain medicine when you’re actually giving them sugar pills can have the same effect

There is, however, another aspect to cognition in pain that has been virtually ignored by science and which I shall treat in this essay: the direct impact of pain on higher cognition, the “bottom up” effect. Several lines of enquiry have found that pain impairs working memory, and control of attention, emotion and behaviour.

An aspect of pain that has been completely ignored by pain science is its impact on the body’s primary affect system. It was proposed by Panksepp in 1998 and confirmed by Eisenberger, Lieberman and Williams in 2003 that social attachment in vertebrates employs the distress component of physical pain; below I discuss the possible impact of constant physical pain on human affective contact.

Some definitions
The warmth of the hearth may be pleasant but, beyond a certain temperature, heat becomes painful. This point is the pain threshold. The intensity of stimulus at which pain begins to be felt varies from person to person, and within an individual over time.

Will to endure: If I offer you $10 to hold your arm over a blow torch, you’ll refuse; but if your child’s life depended on it, you’d probably do it. Will to endure competes with impulse to escape. The urgency of your impulse to escape is modulated by several factors including stimulus intensity, while the strength of your will to endure fluctuates according to the salience and worth of your overarching (usually abstract) goals.

Your tolerance limit is the point at which the urge to escape overwhelms the will to endure, and you succumb to the more primitive of these competing motivators, and act to escape or reduce the unpleasantness.

Constant physical pain plus transitory physical pain
Distress is reflected in the brain as activity in, among other areas, the front (“anterior”) portion of the cingulate cortex (the ACC). This was suggested by the fact that surgical removal of the ACC relieves the distress of chronic pain and confirmed in 1997 by Rainville and colleagues, using PET scans of the brain.

Heightened pain-related activity in the ACC is experienced as heightened distress, and patients in constant pain, such as those suffering from fibromyalgia, Gracely et al., 2002), irritable bowel syndrome (Mertz et al., 2000 & Naliboff et al., 2001) sympathetically mediated pain (Apkarian, Thomas, Krauss & Szeverenyi, 2001) and atypical facial pain (Derbyshire et al., 1994), experience significantly higher distress and display significantly higher ACC activity in response to a given transitory painful stimulus compared to healthy controls.

Constant social pain plus transitory social pain
But physical pain is not your only source of distress. Social rejection activates the ACC and this activity is experienced as distress (Eisenberger, Lieberman & Williams, 2003). In a 2007 study, Naomi Eisenberger and colleagues found that subjects who report less regular contact with close and supportive others show higher ACC activity (and report more distress) in response to transitory instances of social rejection than subjects with higher levels of social support.

Constant pain plus transitory pain
So, transitory social pain is a more aversive experience for a person already suffering from chronic social pain, and transitory physical pain hurts more when inflicted on a person already suffering from chronic physical pain.

But if you are already constantly burdened by one form of pain (say, social, due to low social support) does this make you more vulnerable to the other type of pain (physical)? Naomi Eisenberger and Matthew Lieberman (2005) report that individuals with more social support experience less cancer pain, take less pain medication, are less likely to suffer from chest pain after coronary artery bypass surgery, report less labour pain and are less likely to use epidural anaesthesia during childbirth. So, if you suffer from chronically low social support you’ll be less able to tolerate transitory pain, social or physical. Following Eisenberger & Lieberman (2005) I shall call this state of generalised reduced tolerance for negative affect "neuroticism".

In constant physical pain are you less tolerant of transitory social as well as physical pain? That is, like low social support, does constant physical pain make you neurotic?

I’m not aware of any fMRI investigations into social vulnerability in constant physical pain but Sternbach and Timmermans (1975) found a significant reduction in neuroticism in chronic pain patients whose suffering was ameliorated by surgery, and concluded that “the neurotic features so often found associated with chronic pain are primarily the consequence of pain, and tend to dissipate with pain reduction” (p. 181). Here I will assume that in constant pain, social or physical, you’ll be less tolerant of transitory pain, social or physical.

Belonging
I believe constant physical and social pain both amplify the reward value of cues signaling belonging. Certainly, if social support (Eisenberger & Lieberman, 2005) or the presence of a friend (Brown et al., 2003; Seidman et al., 1957) raises your pain threshold or tolerance level, then I would expect cues signaling social support or love to be more rewarding to a suffering person than a pain-free person.

Empathy
That other important social feeling, empathy, seems to diminish as distress rises. This appears to be the case in me and all my friends. But it is by no means clear. It could be that feeling the affect of others remains intact or intensifies as our own distress rises, but caring (giving a damn) diminishes (Goulbert et al., 2005). Or perhaps, after being constantly distressed for a while, we learn to not recognise the negative affect of others, as a cognitive strategy for avoiding the additional suffering. FMRI studies of empathy, and psychological testing for care and concern in chronic pain patients may shed some light on this.

Self control, attention control and working memory
Eccleston (1995) has shown that chronic pain impairs control of attention: “…chronic pain patients suffering high intensity pain show significantly impaired performance on an attentionally demanding task when compared to low pain patients and normal controls” (p. 391); and Astrid von Bueren and colleagues (2005) have found that chronic pain patients exhibit marked deficiencies in alertness, vigilance, visual search and selective attention, compared to the pain free. Pain diminishes control of attention. Bruce Dick and Saifudin Rashiq, in their 2007 study, show that chronic pain impairs both attention control and working memory.

I believe the distress of pain disrupts not just working memory and control of attention, but self-regulation (emotion modulation and impulse inhibition) also; that is, the distress of pain interferes with all domains of executive function. I’m presently searching for peer reviewed proofs that physical pain impacts self-regulation but it may be that this function in chronic pain has not yet been tested. In 2005, Baumeister and de Wall showed that control of attention and self-regulation are impaired by contrived instances of social rejection.

I don’t think anyone has tested any aspect of executive function in chronically low social support.

For the purpose of this essay, I’m assuming that each form of pain, social and physical, impacts the same cognitive faculties: self-regulation, control of attention and working memory; and the closer you are to your pain tolerance limit, the stupider and more distracted and poorly controlled you are. Most people don’t need to see peer reviewed proofs to accept this proposition.

Pain and effortful thinking
If you’ve been in intense pain for a while, you’ll be used to being thought of as lazy. But physical chores may not be the only ones you avoid. In intense constant pain, attending to what matters as opposed to what’s interesting or attractive, and exercising self-regulation and working memory in an uninteresting task will not only be impaired, as described above, but more distressing and aversive. For me and others I interact with on chronic pain forums, this is a phenomenological fact. Its scientific veracity will have to wait. Until then I’m assuming that in intense constant pain it will require a greater effort of will to initiate and persevere with tedious and aversive cognitive chores, as they will hurt the suffering much more than they will the pain-free.

But in pain, if you can become absorbed in an attractive, engaging higher cognitive task, you may lose sight of your pain to such an extent that you no longer suffer (Eccleston, 1995). If losing yourself in a task reduces or eliminates pain, this loosens the toxic grip that distress has on executive function, while you are absorbed within the confines of that task. Hence, in intense constant pain, you may be able to rise to the highest level of World of Warcraft with unimpaired executive function, but be utterly incapable of completing a tax return, no matter how hard you try.

Pain and the passions
Here I must introduce a couple of Greek terms, for which I cannot find an English equivalent. The ancient Greeks defined thymos as the part of the soul comprising boldness, pride and the desire for honour, recognition and supremacy. It is the motive force behind war and slavery. A faint echo of this meaning can be heard in the personality psychology term surgency; and the nearest vulgar English word is spiritedness, as in “a spirited debate” or “a spirited stallion”. Provoked, unbridled thymos can manifest as anger, rage and murder.

According to Plato (428/7 – 348/7 BC), thymos resides in the soul alongside epithumia (the bodily appetites), and these two passions are governed by Logos (reason). He likens thymos and epithumia to a pair of unruly winged horses under the rein of their charioteer, Logos. The destination of this ensemble is, according to Plato, Heaven, where pasture is found which is suited to the highest part of the soul.

But according to Epicurus (341 – 270 BC), our goal is ataraxia, which he defined as robust tranquility: the bliss of the beloved baby at the breast - warm, comfortable, safe; the bliss of one free of fear who enjoys the loving embrace of family, friends and the wider community. Epicurus was a materialist, in the sense that when you’re dead, you’re dead. He believed that the soul's yearning for ataraxia, not Heaven, motivates Logos to keep a tight rein on thymos and epithumia. For Epicurus, Heaven is the love of other people.

Pain has two important effects on thymos. It increases irritability – your likelihood of feeling angry – and, because pain undermines executive function (Logos), it impairs the ability to modulate the intensity of anger and the ability to inhibit the expression of it. What happens when in pain, irritable thymos is ruled by an enfeebled Logos? In some cases, anger, rage and, in the extreme, assault and murder. But more usually, when Logos is incapable of taming thymos so that thymos positively colours and energises social relations, hunger for belonging prevails and you simply crush thymos entirely. After one too many destructive outbursts, you break your own spirit.

Evoking aversion
Have you ever been with a bunch of people when a charming person arrives and lifts the mood of the whole group? Some people just radiate good feeling. That’s contagion of joy or pleasure (Hatfield, Cacioppo & Rapson 1994). In 2000, Peter Totterdell at the University of Sheffield, UK, found a significant association between the happiness of professional cricketers during a match and the average happiness of their teammates, regardless of other factors such as whether the match was going in the team’s favour. He found a similar effect among nurses and office workers. It has also been shown that if a college student suffers from mild depression their roommate will become progressively more depressed the longer they live with them, and that emotional displays by bank employees have a direct impact on the moods of their customers.” (Bond, 2008). People who feel good get lots of invitations. Everybody wants them around.

If you’re struck by high intensity constant pain you’ll have the opposite effect. The invitations dry up pretty quickly. You’ll be a downer, a pain to have around. Of course, it depends on the intensity of your distress. The watershed seems to be the point at which you can’t smile convincingly and eye contact becomes uncomfortable.

The genuine smile
In 1862, the French physician Guillaume Duchenne, using mild electric current to map the anatomy of facial muscles, noted that the muscle around the eye, the “orbicularis occuli”, is recruited in the genuine, spontaneous smile of enjoyment, but not in the fake smile. In 1992, when studying the ability of different age groups of children to contrive fake expressions, Ekman and colleagues noticed that most could deliberately contract the inner but not the outer portion of this muscle, though the whole muscle was engaged in a natural smile. They therefore considered just the actions of the outer part of the orbicularis occuli essential for distinguishing the genuine smile. Ekman named the genuine smile the “Duchenne smile”. Most people can distinguish at a glance a genuine smile.

I assert that intense constant pain will switch off your ability to readily display a Duchenne smile.

When someone smiles at you and you don’t respond with a timely Duchenne smile, how does it make them feel? According to Duchenne (1862/1990, p.72), failure to display a timely genuine smile “unmasks a false friend”. Conversely, a Duchenne smile conveys the impression of sociability and, in males, generosity (propensity toward altruism; Mehu, Little & Dunbar, 2007). Your ability to display a timely Duchenne smile signals your worth as a friend.

The face in pain
Simon et al. (2006) found fMRI support for their hypothesis that the “male pain expression triggers an emotional reaction characterised by a threat-related response” (p. 309). That is, seeing a male face in pain activates the fight-flight system in the brain of the observer. With good reason. In humans, pain can instigate a disposition towards aggression (Berkowitz, 1993, p. 14). Seeing a male in pain is seeing a male prone to poorly modulated aggression. Rats given electric shocks turn and bite their neighbours; so this tendency towards aggression in pain is evolutionarily quite ancient, as may be the tendency in humans to fear and hate males in pain.

The female face in pain evokes an opposite response in the brain of the observer (Simon et al., 2006). The fight flight system in your brain will exhibit a drop in activity when you see a female face in pain. I imagine this would feel like love and trust, maybe compassion. I believe pain may evoke pathos or thymos in the sufferer and this is determined by pre- or perinatal testosterone level, so that the expression of pathos predominates in female sufferers and thymos in male sufferers; and the observer responds appropriately. I discuss this in more detail below.

Social grooming
Robin Dunbar (1996) describes the role of social grooming in primates. When one primate grooms another, the level of endogenous opioids in the groomed’s nervous system rises. This feels good to the groomed who favours the groomer in terms of shared resources and protection. Grooming is the currency of the monkey troupe economy. Dunbar theorises that, in humans, this endorphin-raising kneading, pinching and scratching of our ancestors has evolved into conversation (gossip in particular) and that we raise each other’s endorphin levels, and so build, monitor and maintain our network of allegiance and friendship, with gossip. But conversation without the unfakeable natural smile, body language and easy eye contact of painlessness or good feeling will not raise the endorphin levels of your interlocutor. Indeed, it will bring them down.

Endorphin-raising in conversation also depends upon the quality of your contribution – your ability to please with attentive listening and timely, interesting, relevant, sensitive, empathetic, and good humoured contributions – and in constant pain this too, thanks to impaired executive function and social sensitivity, and generally feeling awful, will be negatively impacted.

In intense ongoing pain your ability to display a timely Duchenne smile will be impaired and, according to Duchenne (1862/1990), inertia in displaying a genuine smile unmasks a false friend; if you’re a male in pain, according to Simon et al. (2006), your face will evoke the fight-flight response in others; and concentration, working memory and control problems will interfere with the quality of your conversation. In intense constant pain your ability to build, monitor and maintain a network of affection and support will be impaired.

Attachment
Given the above, it may be reasonable to predict that people in constant pain would feel insecure in their relationships. In a study soon to be published in the journal Pain, Davies and colleagues find exactly that, though they interpret this correlation as proof that insecure attachment style causes widespread chronic pain.

Personality
Theorists have described at least five “dimensions” of normal personality. The dimensions are conceived of as continua and individuals differ according to where they are on each continuum. David Buss [1991] characterises these dimensions:
 * “extroversion/surgency” (proclivity to rise in a social hierarchy),
 * “agreeableness” (willingness to cooperate),
 * “conscientiousness” (capacity for reliable work and enduring commitment),
 * “neuroticism/emotional stability” (ability to handle stress), and
 * “openness/intellect” (propensity for innovation or astuteness in solving problems).

Let’s look at how constant, high intensity, trait-like pain might affect where you are placed on these five personality dimensions.


 * Extroversion/surgency: Since chronic distress can induce social withdrawal, it may locate you nearer the introvert end of this spectrum; and your ability to scale social hierarchies will be impaired by your poor empathy or caring, damaged executive functions and heightened neuroticism.
 * Agreeableness: Willingness to cooperate may not be impacted at all by pain but your ability to may be impaired by your executive dysfunction and loss of empathetic rapport with others.
 * Conscientiousness: This is competency and willpower. Your dysfunctional executive powers will ensure you are placed at the less conscientious end of this continuum.
 * Neuroticism/emotional stability: Already covered under Distress + distress above.
 * Openness/intellect: Impaired working memory and control of attention will affect your astuteness in solving problems.

Anhedonia
Here I shall include a history of the concept and an exploration of the likelihood that constant physical suffering might produce it.

Motivation
The distress dimension of pain includes the urge to escape the suffering. Here I shall address the effect that a perpetual urge to escape may have on the normal motivations of human life.

Consciousness
There's a lot to be said about pain and consciousness. I'm not there yet.

Social withdrawal
Like a wounded wolf or a lab rat with formalin injected into its hind paw, a human in pain withdraws from social engagement (Osborn & Smith, 1998). The wolf to her lair, the rat to the darkest corner of her cage, and the human to her room or, when social contact is unavoidable, to somewhere inside herself.

Parenting in pain
White et al. (2009) report that “Previous research has suggested that women may withdraw or reduce their parenting activities when they are in pain and this study supported the previous research.”

So?
In high intensity constant pain you’ll feel bad to be around, you’ll be lazier, grumpier, stupider, needier, less controlled and less empathetic or caring; and deft modulation of thymos and epithumia to fit social circumstance will be impaired. As a consequence of all this you’ll suffer marital disharmony and a general loss of affection from those around you. But you’ll be more neurotic, so this social catastrophe will hurt you much more than it would a pain-free person. Your diminished executive function will make cognitive chores more difficult and aversive so, if your heart isn’t in your job and it requires normal executive function, you may lose your job. You may well lose it anyway just because you can’t get on with your co-workers.

"'If I have matters right, the consequences of pain will include direct physical distress, unemployment, financial difficulties, marital disharmony, and difficulties in concentration and attention…' Harold Merskey 2000"

What happens when this catastrophe befalls an infant?

The common symptom cluster
ADHD, autism spectrum, schizophrenia, bipolar disorder, major depression and generalised anxiety disorder share a cluster of symptoms comprising distress, amplified affective response, and executive dysfunction. Each disorder has one or two additional symptoms which distinguish it from the others. For example, in autism spectrum: poverty of affective contact and behavioural rigidity, in schizophrenia: delusions or auditory hallucinations, in ADHD: hyperactivity. When there is no additional symptom - when the mental illness consists solely of distress, hypertrophied affect and impaired self regulation, working memory and attention control - the diagnosis may be schizotypy or ADD.

Presently there is no universally agreed upon aetiology for either the disorders themselves or that symptom complex which they share. I propose that the symptom which is primary in the shared complex is distress, and that the cause of this distress may lie outside the central nervous system but beneath the skin. Now I shall test the explanatory power of this hypothesis in the case of autism.

Description and prevalence
The word ‘autism’ has two distinct meanings. The first is Eugen Bleuler’s (1911, p. 14) “inclination to divorce oneself from reality”. He put this symptom alongside disordered thinking, blunted affect and ambivalence (dithering) at the core of the syndrome he labeled ‘schizophrenia’. The second meaning of the word ‘autism’ is the syndrome, described by Leo Kanner in 1943, emphasising behavioural rigidity (stereotyped behaviours, obsessive need for sameness and lack of spontaneity) and impaired affective contact. Why would one be inclined to divorce oneself from reality, avoid affective contact and hate dissonance between environment and expectation? Bleuler answered the question in 1911:

"'Particularly in the beginning of their illness, these patients quite consciously shun any contact with reality because their affects are so powerful that they must avoid everything which might arouse their emotions. The apathy towards the outer world is then a secondary one springing from a hypertrophied sensitivity.' Eugen Bleuler 1911 P. 65"

In the 1980’s Kanner’s syndrome was rarely diagnosed (4 in 10,000; Lotter, 1966), late language development (no single words by age 2 and no strings of words by 3 years of age) was a cardinal symptom, and only 25 per cent of patients had an IQ of 70 or above. In the 90s, though, more diagnoses were given to children with late language development but normal or high IQ. These were called ‘high-functioning’ autistics. Also in the 90s, patients with normal or high IQ and normal language development were identified. These are said to suffer from ‘Asperger’s syndrome’ to distinguish them from high-functioning autistics (Baron-Cohen, 2003):


 * Kanner’s syndrome with late language development and IQ below 70: classic autism
 * Kanner’s syndrome with late language development and IQ above 70: high-functioning autism
 * Kanner’s syndrome with normal language development and IQ above 70: Asperger's syndrome

Since the latter two groups seem far more alike than different when examined in adolescence (Gilchrist et al., 2001), for most researchers, Asperger’s syndrome is just another label for high-functioning autism (Happe, 1994).

To fit a diagnosis within the autism spectrum, symptoms must be present before age 3. Reliable diagnosis can be made from age 2. If a child begins life developing normally and, between ages 15 and 30 months, starts to lose acquired communication and social skills, and receives a diagnosis within the autism spectrum, the condition is called regressive autism. If autistic symptoms descend upon a child after age 3, the catastrophe is called childhood disintegrative disorder.

When there is a severe and pervasive impairment in the development of reciprocal social interaction or verbal and nonverbal communication skills, but the criteria are neither met for autism nor any other mental disorder, the diagnosis is ‘pervasive developmental disorder not otherwise specified’ (PDD-NOS).

It is now believed that autism spectrum disorders affect approximately 60, and narrowly-defined autism 10-30, per 10,000 children under 8. Methodological differences between studies, changes in diagnostic practice, and public and professional awareness are likely causes of apparent increases in prevalence. “Whether these factors are sufficient to account for increased numbers of identified individuals, or whether there has been a rise in actual numbers affected, is as yet unclear… The prevalence of autism in the adult population is not known” (Medical Research Council, 2001, p. 18).

Etiology
I propose that autism, whose most obvious symptom is a disturbance of shared feeling, is the product of constant, high intensity physical pain, a feeling which no one wants to share.

The refrigerator society
Beginning in his original 1943 paper, Kanner frequently referred to the coldness of the parents of autists. In a 1949 paper he said these children were “left neatly in refrigerators which did not defrost. (Their) withdrawal seems to be an act of turning away from such a situation to seek comfort in solitude” (p. 425). This led, in the 50′s and 60′s, to the theory that autism was caused by “refrigerator mothers”. Then, in 1964, Bernard Rimland argued against the social imposition of autism and in favour of a neurological explanation with Infantile autism: The syndrome and its implications for a neural theory of behaviour. The counter-punch came three years later from the refrigerator mother theory’s most persuasive proponent, Bruno Bettelheim (1967). In 1969 Leo Kanner pointed out that he had always spoken “of this condition in no uncertain terms as ‘innate’. But because I described some of the characteristics of the parents as persons, I was misquoted often as having said that ‘it is all the parents’ fault’.”

Peter Hobson’s book, The Cradle of Thought (2002), contains a poignant comparison of videoed interviews with two girls: one typical, the other autistic. His description of not only the clumsiness and detachment of the autistic girl but his own awkwardness and inability, despite his best efforts, to behave in a warm and natural manner with her – but not with the typical girl – says it all. Autistic children make normal people feel and act uncomfortable, and a convincing affectionate display, for most parents, is impossible.

"'Many writers, Eisenberg & Kanner (1956) among them, have observed that the non-intellectual aspects (the coldness) of the parents’ personalities may be aggravated by the non-responsiveness of the child. …But why do these reasons apply only to the parents of children with infantile autism?' Rimland, 1964, 31."

My analysis in Part One supports a plausible explanation for society's lack of affectionate display towards autists: If the child is in intense constant physical pain, it will be unpleasant to be around, and provoke unease and aversion, not warmth. The parents respond to the non-responsiveness or even perceived hostility of the child with coldness and even hostility of their own.

Testosterone
"'…there is a critical time period early in life, usually within the first few days after birth, during which testosterone exposure is essential to elicit aggression in adulthood.' (Simpson, 2001, p. 32)" This quote refers to mice. The work connecting foetal or perinatal testosterone level to aggression in humans is scrappy and ambiguous. I’m still looking for solid proof but foetal or perinatal testosterone level may determine society’s response to the suffering person. It works like this:

Children in pain can be irritable. (Berkowitz, 1993a). Boldness depends on foetal or perinatal testosterone level (Jacklin, Maccoby & Doering, 1983). So a child’s irritability is mediated by pain, but his propensity to direct anger outward towards others as aggression is a product of his pre- or perinatal testosterone level.

One toddler in constant pain with a history of higher pre- or perinatal testosterone is more likely to act aggressively toward you or look aggressively at you and evoke fear and dislike (like Chucky). Another in pain, but low in pre- or perinatal testosterone, will display pathos, and evoke compassion (like Bambi). That is, it is pre- or perinatal testosterone level that determines whether the child reacts to pain with thymos or pathos, and whether the parents respond to them with fear and loathing or compassion. One child in pain is simply much more aversive than the other, and the parents respond accordingly: most chronically distressed boys are viscerally (perhaps unconsciously) feared and hated and denied the life-giving, unfakable Duchenne smile, and most girls in pain are extended compassion.

If developing boys struck with intense constant physical pain are burdened with a hostile social milieu, and distressed girls tend to evoke compassion, then distressed boys will suffer more from the same source of chronic distress than distressed girls (physical pain + social pain vs. physical pain + compassion).

The gut
Wakefield (1998), suggested the measles-mumps-rubella vaccine may induce autism – and put thousands of British parents off vaccinating their children. DeStefano (2002) has soundly discredited Wakefield’s methods. It just happens that autism frequently descends upon people in the first 18 months of life, so the odds are high that this will occasionally coincide with early childhood vaccination at around 13 months. But Wakefield’s association of some cases of autism with gut pathology (Furlano et al., 2001; Horvath et al., 1999; Torrente et al., 2002) may be correct. Some autism spectrum patients have a history of intestinal disorders (Molloy & Manning-Courtney, 2003) and suffer. The remainder, too, suffer – from some other source of undiagnosed or ignored intense trait-like pain.

When Richard Sandler and colleagues (2000) treated autists suffering from GI symptoms with the antibiotic vancomycin, eight out of ten showed significant improvement in gut symptoms, behaviour and communication, and most returned to baseline when treatment was discontinued.

"'Several hypotheses to explain the etiologic association between the GI tract and the brain in autism have been proposed, including absorption of opioid peptides, overgrowth of neurotoxic bacteria, dysfunction of secretin or its receptors, and dysfunction of serotonin or its receptors' Molloy & Manning-Courtney, 2003, p. 170)." I would say autism is a consequence of intense constant suffering which happens in some cases to emanate from the gut. In their March 2009 article Kiah Bertoglio and Robert L. Hendren conclude that “Because of the high variability in behaviors, biologic findings, and response to treatment, many specialists are assuming a theory of many different autisms, each of which may have a somewhat different etiology and response to treatment.”

Eye contact
"'The face in pain is highly salient to observers, who ranked eyes the most important cue…' Amanda Williams 2002 p. 449"

Poor eye contact is a feature of autism (Phillips, Baron-Cohen & Rutter, 1992; Hobson & Lee, 1998). “People with (autism spectrum conditions) focus their attention more on the mouth region when processing faces, while typical controls rely on the eye region that provides more information about the emotional states of others” (Ashwin, Wheelwright & Baron-Cohen, 2006, p. 78-9). It has been argued that autists’ lack of sustained eye contact is due to their complete indifference to people, that looking into someone’s eyes is as emotionally charged for an autist as looking into a letter box.

The soundness of this argument has been challenged by the results of a 2005 study by Kim Dalton and colleagues at the University of Wisconsin. They compared the brain activity of autism spectrum patients and normal control subjects when looking into the eyes of a person in a photograph and, in the patients, found heightened activity in regions associated with fear, and no change of activity in those regions for normal controls: “Amygdala activation was strongly and positively predicted by the amount of eye fixation among the autistic individuals for both study I and study II but not among the control individuals in either study I or study II” (p. 523). Eye contact strikes terror into the hearts of autists. Dalton and colleagues propose that autists avoid eye contact in order to avoid this “negatively valanced overarousal to social stimuli” (p.524)]. But how can eye contact be so frightening? If autism is a product of affective hypersensitivity (as Bleuler observed) induced by constant, high intensity physical pain (as I argue), then from the discussion in Part One it is possible to construct a valid explanation for this feature of autism:


 * When you look into the eyes of most males in pain, and some females in pain, you feel disquiet and aversion (Simon et al. 2006).
 * What does the distressed person see when she or he looks into your eyes? Disquiet and aversion. This is a significant facial rejection cue, pre-language, potent, hurtful and hard to hide.
 * The distressed person’s vulnerability to negative social cues will be high, so the exchange of looks will be excruciating.
 * Most males and some females in pain elicit this response from everybody and they learn pretty quickly to just not see faces.

This is a reasonable and logically valid explanation for why autists fear mutual gaze: they cop many more negative looks, and negative looks are vastly more painful for them than they are for normal people. This argument is sound, provided it can be demonstrated that constant physical pain induces heightened vulnerability (ACC reactivity) to negative social cues, and that has yet to be established.

Inability to engage in eye contact is a major social disability. According to Franz de Waal "Another point [we share] in common with the chimpanzee is the critical role of eye contact. Among the apes it is a prerequisite for reconciliation. It is as if chimpanzees do not trust the others' intentions without a look in the eyes. In the same way, we do not consider a conflict settled with people who turn their eyes to the ceiling or floor each time we look in their direction. P. 43."

Seeing another’s feelings
You can often see, just looking at someone, how they feel (happy, angry, enthusiastic, reluctant, tired, nauseated, etc.), what they intend or are about to do (from their stance and gesture and where they are looking); even their attitude toward another person or thing. Ian Hacking (2008) calls these situations – where you can see another’s feeling, attitude or intention – “Köhler’s phenomena”, after Wolfgang Köhler, one of the founders of Gestalt psychology.

"A kindly boss is upset when he has to reprimand an employee. Quoting Wolfgang Köhler: 'Viewed from without, the official’s activity is a picture of perturbation. We see he is upset. We don’t infer, in the common case, from the way he looks and acts when he is upset. We usually ‘see‘, to use Wittgenstein’s word, via his behaviour, that he is upset; which is not to deny that sometimes we have to infer (guess, divine) that he is upset.'

"Köhler has many more illustrations. They include that of following a person’s gaze. 'If my attention is attracted by a strange object, a snake for instance, I feel directed toward it and at the same time a feeling of tension is experienced. A friend, even if he has not recognised the snake, will see me, and especially my face and eyes, directed toward it. In the tension of my face he will have a visual picture of my inner tension. In its direction he has a direct picture of the direction in which I experience the fear.' Another example from both Köhler and Wittgenstein is that of a child reaching out to touch a dog but not daring to do so. We see what the child wants to do and also see it’s a bit too scary." Ian Hacking 2008

Professor Hacking notes that autists are blind to Köhler’s phenomena. What could be behind the blindness to Köhler’s phenomena in autism? I propose that the answer is absurdly simple. Autists are in constant, high intensity pain and so are afraid and not welcome to look at others’ faces – especially their eyes. And when you don’t look at people, you can’t see Köhler’s phenomena. When your social world is devoid of sustained Duchenne smiles and consists entirely of cold, angry, fearful or disapproving facial responses from others, your perception of the state of others is shut down, to protect you from heightened distress.

Intersubjectivity
"'....nothing pleases us more than to observe in other men a fellow-feeling with all the emotions of our own breast; nor are we ever so much shocked as by the appearance of the contrary.' Adam Smith 1759 1.1.14"

See a loving mother and her healthy baby. Watch them giggle, coo, gurgle, nod. Mother smiles, baby notices and smiles. Mother's smile instantly broadens, and baby beams. They chuckle together, eyes effortlessly engaged. Whose heart is not warmed by this spectacle? Merleau-Ponty talks of:

"...an intersubjective ‘system’ forming between (persons), which is unbroken by reflective objectification [...] Their actions interlock and engage, each motivated and coordinated by and through an orientation to the other, but without conscious positing and reflective awareness of either self or other. They do not think about the other. They respond to them and are absorbed in a common action. Each action by the one calls forth an action in the other, which calls forth an action from the first, and so on.

"Such pre-reflective interactions are also theorised by Mead (1967), who refers to them as a 'conversation of gestures'." Crossley, 1996, p. 32

Peter Hobson (2002) who proposes that intersubjectivity is the evolutionary precursor to language and thought, notes that autists do not engage in intersubjectivity. My theory predicts this. If autists are in pain, then actual face to face intersubjectivity is terrifying and excruciating; like scraping a claw on sunburn. Let’s use the analogy of grooming. Say we are engaged in a mutual grooming session, but your skin is sorely inflamed and your fingers are numb claws. Good grooming is a combination of gentle kneading and sometimes quite fiercely intense pinching and scratching. It is a sensitive, responsive combination of these that raises your partner's endorphin level in a grooming session. But all you can offer is pinching and scratching, and all you can bear is the very gentlest touch. That is, you can’t offer me chuckles or smiles or receive from me a look of disapproval. Intersubjectivity is never going to happen.

Theory of mind
The ability to form, maintain and recall a multi-dimensional image (a rich, layered meaning) of the mind of another person is impaired in autism. ‘Theory of mind’ is a posited faculty or ‘module’ of cognitive function that enables one to see that others have their own view of the world which may differ from one’s own in attitudes, intentions, feelings and understandings (Baron-Cohen, 1985). This faculty combines the ability to see and hear others with sufficient acuity to detect often subtle and fleeting changes of expression, the ability to feel an attitude, intention or emotion associated with those expressions, the ability to grasp the understanding of another, and the ability to apprehend that understanding and feel a composite of those attitudes, intentions and feelings later, when one sees again or remembers that person: theory of mind relies on a combination of perception, empathy, social feeling and memory.

Constant pain disrupts all of these functions.

Executive function
Executive function is impaired in autism. (Russell, 1997). Simon Baron-Cohen’s argument against the primacy or necessity of executive dysfunction in autism springs from the fact that some autists are capable of superior ‘systemizing’ (his term, meaning ‘pattern-finding’) within the confines of their quite circumscribed special interests. Baron-Cohen sees unimpaired executive function in autists when they are focused on their subject of obsessional fascination. For an explanation as to how this could be possible while executive dysfunction is a necessary feature of autism reread Pain and effortful thinking, above. Constant pain causes executive dysfunction in any task that is not fascinating or engaging, which is the exact nature of the higher cognitive deficit in autism.

Stereotypies
Hand-flapping and other repetitive behaviours are consistently reported by autists as being comforting: they are said to relieve distress. Anyone watching an autist engaging in these behaviours “sees” that this is so.

Insistence on sameness
Insistance on sameness is a cardinal symptom of autism. I asserted above that stretching working memory, and exercising executive control over attention, emotion and behaviour is hurtful for people in constant pain, unless it is a fascinating distraction from pain. When a break in routine is required, or a change of surroundings is imposed, automatic behaviour is no longer effective; such a change of circumstances demands conscious, deliberate engagement with the environment, flexible thinking, and rapid learning of novel data. Autists and people in intense constant pain, find taxing executive tasks such as these distressing.

Möbius sequence
Above I describe a cascade of events behind reduced eye contact in autism. It begins with the autist’s inability to return another’s Duchenne smile, the other is disturbed by the autist’s unresponsiveness and this disquiet – disapproval even – is displayed on the other’s face. The only facial cues the autist gets are negative ones; he quickly learns not to attend to faces; and suffers the consequences of not seeing faces: blindness to Köhler’s phenomena, inability to engage in intersubjectivity, and impoverished theory of mind. If this analysis is correct then we should expect to find poor eye contact, blindness to Köhler’s phenomena, inability to engage in intersubjectivity, and impoverished theory of mind in Möbius sequence, a brainstem disorder which prevents the patient from displaying emotional facial expressions. Despite (I presume) the absence of affective hyperreactivity and “negative magnetism” of physical pain, we do find a significantly higher frequency of blindness to Köhler’s phenomena, inability to engage in intersubjectivity, and impoverished theory of mind in Möbius patients (Bandim, et al., 2003; Johansson, 2001; Gillberg & Steffenburg, 1989).

Congenital blindness
By the same logic, congenitally blind children, despite (presumably) the absence of affective hypersensitivity and the repulsiveness of pain, may be expected, because of their inability to engage in visual intersubjectivity, to have a higher than normal incidence of autistic symptoms. Rachel Brown (Brown et al., 1997) visited six schools for the visually impaired in England and studied twenty four children totally blind or near-totally blind from birth, between three and nine years of age.

"'It turned out that no fewer than ten of the twenty four children we studied satisfied the clinical criteria for autism – a proportion that is 400 times as great as one would expect in sighted children… Then we made close comparisons between nine of the blind children who met the criteria for autism and nine sighted children with autism who were of similar age and IQ … only two of the nine blind children displayed the quality of social impairment that was characteristic of the sighted but autistic children, a quality that involves the special feel one has of a lack in emotional contact.' Hobson 2002 p. 195"

Extreme social isolation
(Romanian orphanages)

Psychophysiology
Auditory mismatch negativity (MMN) is the brief drop in the brain’s electrical activity when it detects an unexpected change in an otherwise familiar and predictable stream of sounds. It happens about a fifth of a second after the odd sound. In 2008, Gomes and Gravel showed that when a person has autism and is concentrating on something other than the stream of sounds, their MMN is significantly smaller than that of healthy subjects. In 2003, Bruce Dick and colleagues showed that if a person is in chronic pain and concentrating on something other than the stream of sounds, their MMN response (to a difficult-to-detect odd sound) is significantly smaller than the same person in less or no pain. Pain produces a similar MMN response to that found in autism.

Psychophysics
Pain threshold in autism. The DSM-IV-TR says that many autists have a higher pain threshold than normals (American Psychiatric Association, 2000), although Nader and colleagues (2002) note that the facial expression of pain in response to venipuncture is more pronounced in autistic than matched non-autistic children. One thing that affects your pain threshold for various stimuli is pain itself. Chronic pain may move your pain threshold up or down, depending on the type of chronic pain and type of novel stimulus. Every chronic pain condition I have looked at has an effect on pain threshold. That is, chronic pain induces pain threshold abnormality. The precise underlying physiological pathology which is causing the pain (and, hence, the autism) will determine whether an autist has a higher or lower than normal pain threshold.

In some chronic pain conditions it may be necessary to inflict more intense stimulation to evoke novel pain than would be required for pain free subjects. But once the pain threshold has been passed and pain is being evoked, the chronic pain patient should be less tolerant than normals. Hence, in the above example (Nader et al., 2002), although autists generally display a higher pain threshold, once pain is being evoked (by venipuncture) facial display expresses more unpleasantness.

Brain structure and function
This is the deal-breaker. If the brain morphology and function of autism can be explained in light of chronic pain, this all stands up. I'm too scared and lazy to confront this just now.

Summary
My theory of autism explains Kanner's observation concerning the coldness of his patients' parents, while supporting his argument for the innateness of autism. It explains poor eye contact, blindness to Köhler’s phenomena, absence of affective contact or intersubjectivity, executive dysfunction, impaired theory of mind, stereotypies, insistence on sameness, pain threshold anomalies, the role of perinatal testosterone level, and the odd psychophysiology. It accounts for every feature of autism. No other theory comes close.

Schizophrenia
The cognitive faculties impaired in schizophrenia are "attention, speed of processing, working and long-term memory, executive function, and social cognition;" that is, the same cluster impaired by autism and pain (and probably every other distressing homeostatic emotion). Bleuler observed that his schizophrenic patients' blunted affect was a product of "hypertrophied sensitivity."