User:Anthonyhcole/Sandbox: Difference between revisions – Wikipedia

Formatted for smartphone.

I was a happy, healthy toddler—playful, affectionate, curious, beginning to string words into sentences—when a botched and unnecessary medical intervention caused me life-long constant pain, and my psychology changed.

The pain comes from a spot halfway up my back to the left of my spine where there is a scar. The muscle beneath that scar is atrophied and the muscle around it is a little bulky.

It starts soon after I get up in the morning and engage that broad, flat anti-gravity muscle.

It’s “tonic” pain: rising and falling only slowly in intensity. The longer I’m up, the more it hurts and it takes hours for the pain to resolve after I lie down.

Most people in chronic pain experience periods of intense pain (like an endometriosis flare or moving an arthritic joint) between periods of less or no pain. With me, the pain is nearly always present and when the intensity changes it changes very, very slowly and predictably. My pain is more like a part of my nature, a trait, the way life feels, than the harrowing succession of alarming attention-demanding cruel insults typical of chronic pain.

This constant negative tone, this lens through which I experience the world, distorts everything that matters.

It slows my thinking speed, reduces my working memory capacity, impairs my concentration and undermines my self-control. It increases the intensity, frequency and duration of negative moods and it makes me neurotic. It numbs my social feelings and it leaves me isolated, inattentive and unpleasant.

I’ve been exploring your literature to see what you have to say about this.

Tonic pain: The pain literature doesn’t mention ongoing tonic pain in patients, or its impact on consciousness of pain which I address in the third section, below.

Cognition: The negative impact of pain on mental processing speed, working memory capacity, attention control, impulse inhibition, emotion regulation and other cognitive processes is well-attested in the pain literature.

Mood: Pain science has found the intensity, frequency and duration of negative moods like depression, anxiety and irritability are all amplified in pain.

Neuroticism: In the 20th century, science and psychodynamic theory defined neuroticism as an unhealthy exaggerated emotional response to noxious stimuli. Recently, though, neuroscience has found a brain process underlying this exaggerated emotional response to noxious stimuli—an exaggerated dorsal anterior cingulate cortex (dACC) response to noxious stimuli—and “neuroticism” is now undergoing redefinition.[1]

(The dACC plays an important role in the experience of suffering.)

Neuroticism now appears to be a two-step process caused by an excessively reactive dACC.

1. In a neurotic person, a social or physical insult (like rejection or a stubbed toe) produces an exaggerated dACC response, exaggerated suffering.
2. This excessive suffering triggers an emotional response whose intensity is proportionate to the exaggerated suffering intensity.

So, in the new theoretical model, neuroticism is no longer an excessively reactive emotional system but a healthy emotional system responding to an excessively reactive suffering system. If suffering is intense, a healthy emotional response will be intense.

What causes neuroticism; what causes exaggerated suffering in response to a noxious stimulus? One cause may be ongoing suffering. That is, if you are already suffering (from, say, chronic pain, sleep deprivation or hunger) that ongoing suffering may prime your dACC to over-react to a novel noxious stimulus.

Early psychophysics and personality studies found chronic pain is associated with heightened neuroticism. I don’t think that has been contradicted by later research.

Social feelings: In some settings, my social feelings (feelings like rejection, shame and empathy) are amplified. It’s a product of my neuroticism. But on other occasions, I am numb to social feelings. I haven’t yet figured out what determines whether my social feelings are amplified or anaesthetised but I do experience both.

Social engagement:
First, let me lay out three premises:

• I am excessively reactive to noxious stimuli, so negative facial expressions from others can hurt me a lot. A negative look is often, for me, more like traumatic abuse than the social slap on the wrist it seems to be for most people.
• I don’t convey appropriate feelings by facial expression. I can’t return a timely, sincere smile when suffering is swamping my sensorium. But the smile is an essential part of affective engagement, and failure to display a timely sincere smile elicits distrust in the observer.^[1]
• The human male face in pain triggers increased activity in the human observer’s amygdala and other brain regions. (The amygdala is active during the experience of fear and rage.) The female face in pain triggers reduced activity in the viewer’s amygdala and those other brain regions that are activated when viewing the male face in pain. This reduced brain activity in response to seeing the female face in pain may evoke compassion in the viewer. It does not evoke the fear and rage that the male face in pain evokes.^[2]

With those assumptions in mind, I’ll now try to explain my experience.

If you smile at me when I’m in pain, you will see my male pain and my failure to return a timely sincere smile, and I will see your automatic emotional response displayed on your face: distrust, fear and aggression. It’s an ugly emotional moment for both of us but especially so for me, because of my neuroticism.

I can’t look at you when you look at me, out of fear of being hurt by your expression, so, the interplay of emotional facial expression, the universal semaphore of displayed, exchanged feelings, is disabled in me and its absence marks me out as remote, shifty and strange and I miss important social cues.

No one is studying the impact of tonic pain and neuroticism on emotional facial semaphore and intersubjectivity.

Inattention: The present is usually so toxic, I retreat into distraction and absent-mindedness. I zone out. I dissociate. My surroundings are still available to the part of me that drives my car and opens the fridge door but deliberate, reflective, mindful me is mostly absent and lives by glimpses.

“Death is preferred over prolonged severe pain but even mild to moderate pain, if continued long enough, will bleed life of its pleasure, transforming the individual into a sufferer whose overriding goal is to drive this experience from consciousness.” — Kenneth L. Casey. 2019.^[3]

The impact of distraction on pain intensity and unpleasantness is well-attested in the pain literature.

Anti-charm: And then there’s emotional contagion. You feel my pain. It hurts you to be around me. I have the opposite of charm. This matters. There is something off about me. Long before we exchange words, you get a bad feeling about me.

You barely mention emotional contagion in pain, let alone its social implications.

______

So, I have found some fragments of me in your literature—my neuropsychological defecits, neuroticism, inattention, and negative moods—but the other fragments I discuss above—tonic pain as a unique class of chronic pain, insensitivity/hyperreactivity to social feelings, pain’s impact on eye contact and intersubjectivity, and the social implications of emotional contagion in pain—appear to have received no serious attention yet.

In 1968 Ronald Melzack and Kenneth Casey re-imagined physical pain as more than just a sensation,^[4] and their conceptual model still informs modern pain neuroscience and pain psychology. They described three dimensions of pain:

• sensory-discriminative: sense of the quality,^[5] location, duration and intensity of the pain
• affective-motivational: unpleasantness and urge to escape the unpleasantness
• cognitive-evaluative: cognitions such as appraisal, expectations, cultural values, distraction and hypnotic suggestion.

Here I discuss the affective-motivational dimension, the unpleasantness and the urge to escape or mitigate the unpleasantness.

Unpleasantness and the urge to mitigate unpleasantness is also called, in various contexts, “suffering”, “aversiveness”, “negative affect”, “negative valence”, “discomfort”, “torment”, “hurt”, “negative hedonic tone”, “dysphoria” and “distress”. I’ll mostly use “suffering” here.^[6]

What is suffering?
Suffering is the unpleasant, attention-consuming, aversive element of our threat-detection system. When we perceive a change in our biological or social state that threatens the integrity of our biological or social systems, that perception of threat is accompanied by unpleasantness and a motivation to mitigate or escape the unpleasantness, and, often, a specific drive aimed at mending or protecting the threatened system using apt behaviour.

These latter specific behaviours might include eating in a state of hunger, resting in a state of fatigue, protecting a damaged body part in pain, comforting a suffering friend in response to empathy, or making a phone call in response to a percieved social slight.

To be clear, suffering is found in three classes of feelings:

1. It is a dimension of negative homeostatic feelings like hunger, fatigue and hyperthermia. Negatively-valenced homeostatic feelings torment us with suffering until we satisfy them with specific behaviour aimed at maintaining the body in its ideal state. (In hunger: eating, in fatigue: resting, and in hyperthermia: stepping into the shade.)

Pain is a motivating homeostatic feeling; we respond to it by withdrawing from a harmful situation, protecting a damaged body part while it heals, and avoiding similar experiences in the future.

2. Suffering also plays a role in negative emotions (e.g., grief, anger, fear) and negative moods (e.g., depression, irritability, anxiety).

3. And it is an essential part of some social feelings (e.g., empathy, rejection, shame, loneliness).

Suffering likely evolved first and was enlisted by homeostatic feelings, emotions and social feelings as they emerged later in animal evolution.^[7] It is likely that just one neural network generates suffering, and every unpleasant feeling engages this one suffering network.^[8]

What does suffering do to us?
I am studying the effect of suffering on human emotion, cognition and social engagement and I have focussed on three causes of suffering, three negative homeostatic feelings—hunger, sleep deprivation and pain—because each of these has a body of scholarship addressing, to some extent, its affective, cognitive and social impacts.

Each of these distressing homeostatic feelings generates in humans the same set of symptoms, the same syndrome:

• Increased frequency, intensity and duration of negative mood states (e.g., wretchedness, anxiety, irritability) and negative emotional events (e.g., grief, anger, fear), and heightened affective response to noxious stimuli (neuroticism): things that hurt, hurt more.
• Slowed mental processing speed, reduced working memory capacity and impaired attention control, impulse inhibition and emotion regulation.
• Impaired social feeling.

Until someone finds an instance of suffering that does not cause this cluster of symptoms, I shall assume all suffering, regardless of its cause, produces this syndrome.

Even mild to moderate suffering, if it goes on long enough, creates a significant psycho-social problem for the sufferer but when ongoing suffering is severe its impact on these faculties is catastrophic.

I always knew there was something wrong with me. I have an identical twin: a perfect control. He played and made friends and I did not. He was happy, attentive, affectionate, sensitive, witty and loquacious. I was not. I kept hoping and waiting for nature to sweep me up and usher me through all the developmental stages I’d seen him effortlessly glide through but it never happened.

Throughout my childhood I’d felt discomfort in my back but didn’t pay it much attention until I smoked marijuana for the first time and I saw clearly in that instant that this discomfort was constant, intense muscle pain coming from a spot halfway up my back to the left of my spine, and I saw it was this that had been ruining me.

I “saw” this because marijuana connected my feelings with my consciousness and cognitions, and marijuana reduced the pain’s unpleasantness and intensity, and that sudden drop in unpleasantness and intensity, which I’d never experienced before, drew the pain to my attention.

I tried all the drugs and therapies but the most effective intervention was simply lying down for hours. Marijuana eased the pain but it took a serious toll in weariness and stupidity.

And if I rubbed a spot on my back at the centre of the pain it sometimes helped a bit. Later, at the beach, somebody touched me there and said, “What’s that scar?”

I asked Mum and she told me I’d had a birthmark X-rayed when I was a toddler to accelerate the birthmark’s involution.

Raised, bright red birthmarks usually involute—melt back into the skin and disappear—over childhood without any intervention but mine was close to the spine and doctors thought it might cause a spinal blood vessel malformation followed by paralysis and a slow, agonising death. It’s called Cobb syndrome.

It’s nonsense. When I looked in the 2000s there were very few cases in the literature. The likelihood of a birthmark being followed by a spinal arteriovenous malformation in the same dermatome seems no greater than chance.

Looking at the recent literature, it appears radiation of birthmarks as a prophylactic intervention for Cobb syndrome is no longer standard practice.

And the radiation intensity necessary to trigger involution is closer to imaging intensity than the intensity required to cause muscle damage, so I’m guessing the radiotherapist got the dose wrong.

_______

If the pain intensity rises more rapidly than usual (from extreme exertion, say) or falls more rapidly than usual (from, say, smoking dope) then it comes sharply into consciousness. But when the pain’s intensity follows its usual slow, familiar, non-alarming, predictable temporal course, when it creeps up on me and fades away slowly, I don’t notice it. The unpleasantness, however, is undiminished and, when it is intense, it crushes me.

This sensory (but not affective) inuring may be a cognitive process.

Pain science is familiar with analgesia caused by the excitement of sport or war where a player or combatant can temporarily experience no suffering and no awareness of pain in quite traumatic injury, like a severed tendon or a limb amputation. This is thought to be cognitive suppression of both the sensory and affective dimensions of pain.

Distraction, hypnosis and placebo, three more cognitive processes, can all modify both the affective and sensory dimensions of pain, or just the affective dimension depending on context.

I’ve never read an account of pain’s sensory but not its affective dimension being suppressed by a cognitive process.

Suppression of the sensory but not affective dimension of pain does seem to happen in some cases of brain damage, though,^[9] and Ken Casey describes a spinal pathway (distinct and remote from the ventrolateral spinothalamic tract, traditionally thought to convey pain to the brain) which carries pain’s negative affect but not sensation to the brain via a dorsolateral tract^[10] so this sensory but not affective inuring is, at least, neurologically plausible.

This sensory inuring in a familiar, predictable, unalarming, tonic, distressing homeostatic feeling may be addressed in the fields of consciousness or homeostatic feeling, I suppose. I’ve got a lot more reading to do. For now, though, it is just another piece of me I haven’t yet found in your literature.

This is where I put interesting stuff I don’t know what to do with.

• Thomas Beddoes (1806) A Manual of Health, or the Invalid Conducted Safely Through the Seasons, p 75:

  “Upon examining a particular child it has occurred to me many scores of times to ask the parent, ‘Pray, have you any more children?’

  ” ‘Yes but they none of them complain.’

  ” ‘Be so good as to bring them. I would wish to examine them myself.’

  “A child roars when suffering from a sharp pain but when pain creeps on them by degrees, when they find themselves in dull pain, they will rarely complain, and yet that is when I need to see them.”

  Quoted on page 166 in The Worst of Evils: The Fight Against Pain (2006) by Thomas Dormandy.

• Pain seems to make boys autistic and girls borderline.
• Borderline personality disorder (BPD) is a personality disorder (PD) characterised by significant distress.

“There is no doubt that the indicators of harmful emotional dysregulation, volatility, unpredictability and self-injury render BPD a legitimate mental disorder. It is unclear, however, why [DSM III] classified it as a personality disorder.

“Its trademark indicator, emotional dysregulation, is virtually the opposite of the rigidity that characterises a PD. Moreover, unlike other PDs, but like mood conditions, the symptoms of BPD are not egosyntonic [compatible with one’s view of oneself and one’s place in the world], cause great distress and lead to efforts to get rid of them.”

Alan V Horwitz, 2023. “Personality Disorders”. Chapter 5.

• Li, Tianbi; Decety, Jean; Hua, Zihui; Li, Guoxiang; Yi, Li (August 2024). “Empathy in autistic children: Emotional overarousal in response to others’ physical pain”. Autism Research. 17 (8): 1640–1650. doi:10.1002/aur.3200. ISSN 1939-3792.
• Autism seemed to demonstrate what happened when people developed without giving or receiving affection — Understanding Autism: Parents, Doctors, and the History of a Disorder. Princeton University Press. 2011-11-07. ISBN 978-1-4008-4039-7.
• “When depression is well marked its exact form varies greatly — grief finding causes for unhappiness in the past, fear which seeks them in the future, and a simple sense of wretchedness about the present seem the primary types.” … “In part, the mood expresses the individual temperament as determined by the interaction of inborn constitution with the sum of experience, remote as well as recent.” — Mapother, Edward (November 13, 1926). “Discussion on Manic-Depressive Psychosis”. British Medical Journal: 872-879.

• “… even when opium does not abolish pain, the pain no longer preys on the person’s mind.” Diocles of Carystus, a fourth century BC Greek physician, quoted in Thomas Dormandy, The Worst of Evils: The Fight Against Pain (2006), Ch. 2.
• “[A mid-career psychiatrist and brain imager] described how a person might have a very pure, identifiable and innate genetic lesion that disturbed their language functioning. Because of the person’s language problems, the psychiatrist pointed out, people in their environment would react differently to them. So, this very small and innate molecular difference would radically alter that person’s social surroundings. This environmental input might then lead to a measurable biological difference elsewhere in their brain which someone like this psychiatrist might measure …” — Fitzgerald, Des (2017) “Introduction”, Tracing autism: uncertainty, ambiguity, and the affective labor of neuroscience. In vivo. Seattle: University of Washington press. ISBN 978-0-295-74191-8.
• “In these decerebrated animals [animals whose cortex and thalamus has been surgically removed] a noxious mechanical or thermal stimulus regularly evoked a […] response that resembled the angry, defensive reaction of a distressed intact animal. The decerebrated animal would open its eyes with pupils dilated, turn its head toward the stimulated site, bare its teeth, and sometimes snarl and snap. Only noxious stimuli were effective in evoking this response.

  […]

  Because these reflex responses were evoked only by noxious stimuli and fully resembled the reaction of an intact, angry, distressed, and defensive animal to an unpleasant and threatening event, they were called ‘pseudoaffective reflexes.’

Casey, Kenneth L. (2019). Chasing pain: the search for a neurobiological mechanism. New York, NY: Oxford University Press. ISBN 978-0-19-088023-1. OCLC 1066088921. Chapter: 4

Back when these experiments were performed, scientists studied only male subjects.^[11]

I wonder if decerebrated female cats and dogs, like their male conspecifics, display fear and rage in response to pain. That is, is the female primative emotional response to feeling pain as scary as the male primative emotional response to feeling pain? If the male but not female primal emotional response to feeling pain is fear and rage, this may explain our negative (amygdala) response to the male but not female face in pain.

Just guessing here but the female reflexive primordial emotional response to feeling pain may be more like fear and grief. (I think that is so in humans, anyway.)

Fear and rage in others evoke fear in us. Fear and grief evoke a different emotion. Compassion, maybe? But not fear.

We need to study sex differences in the way we respond emotionally to our own pain and the way others respond emotionally to us in pain.

• Robert Spitzer, main author of DSM III, defines mental illness: “In DSM III, each of the mental disorders is conceptualised as a clinically significant behavioural or psychological syndrome or pattern that occurs in an individual and that is typically associated with either a painful symptom (distress) or impairment in one or more important areas of functioning (disability).

“In addition, there is an inference that there is a behavioural, psychological or biological dysfunction, and that the disturbance is not only in the relationship between the individual and society. When the disturbance is limited to a conflict between an individual and society, this may represent social deviance, which may or may not be commendable, but is not, by itself a mental disorder.” — Quoted in DSM: A history of psychiatry’s bible (2021) by Allan V. Horowitz, chapter 3.

• “Every single day [the patient’s] pain is experienced by the world around them.”

— Keith Meldrum

“… individual nociceptor activity is not always a faithful reflection of stimulus intensity. With prolonged stimulation, the spiking of some nociceptors may decline, or even cease, although the applied stimulus intensity is unchanged.” — Ken Casey, ibid, ch. 6

Here, Casey identifies a spinal pathway carrying negative affect but not sensation to the brain.

“These observations show that activity in uncrossed ascending spinothalamic fibres can lead to the unpleasant (hedonic or affective) aspect of pain but without the information that allows normal sensory identification. Apparently, affective but not normal sensory identification components of the pain experience can be mediated independently via spinal cord pathways other than crossed fibers in the ventrolateral spinal cord …” Ken Casey, ibid pp. 141-2 in ebook Reader (p. 27, in eBooks.com)

• Allan V. Horwitz on the drift of emphasis from “character” to “personality” with the birth of individualism:

“By the end of the ninteenth century, personality was a major source of interest both in Europe and the US.

“Personality referred to the typical ways that people behaved, thought, felt and related to others. Qualities related to charm – the ability to form friendships, likeability and the ability to project energy – replaced the earlier emphasis on duty, moral courage and integrity.

“As traditional and local bonds unravelled, social solidarity itself came to rest on the ability of these newly free individuals to integrate personally their diverse social roles.”

Horwitz, Allan V. (2023). Personality disorders: a short history of narcissistic, borderline, antisocial, and other types. Baltimore: Johns Hopkins University Press. ISBN 978-1-4214-4610-3.

Compare rates in chronic pain, itch, dyspnea, etc., with suicide rates in mental illness.

Audible audiobook. Book 2. Of the passions. (Audible chapter 5.)

As mentioned before, perceptions come in two forms: impressions and ideas. Impressions also come in two forms: in the form of original impressions and secondary impressions. Origional impressions are raw sensory experiences. They arise directly from contact with the external world without modification or intervention of ideas. Secondary impressions arise in the mind as a result of reflection. These impressions come to the mind arising [from an] idea (?) or through an idea evoked by an external impression. The passions and emotions, like them, are secondary impressions. Secondary or reflective impressions can be either calm or violent in nature. Those that are calm do not incite a need for action. They are quiet internal perceptions of a quality like beauty or satisfactions. Violent reflective impressions incite us to a response. To a reaction in the form of action. Love and hatred, grief and joy, and pride and humility are three couplings of violent reaction that incite a reaction.

The passions can also be classified as direct and indirect. Direct passions are those that are evoked by the immediate perception of pleasure or pain. Direct passions include desire and diversion, hope and fear, despair and security, and grief and joy.

Indirect passions are evoked in the mind through the medium of an idea.

Caspi and colleagues’ longitudinal study of antisocial behaviour among a cohort of men from New Zealand provides an example. They found no direct relationship between any genetic factor and antisocial behaviour. However, a large association emerged among those with the MAOA genotype who also had suffered maltreatment in childhood. Only maltreated youth with this genotype showed high levels of antisocial or aggressive behaviour by age 26. Allan Horowitz. Personality disorders. Ch. 7.

The suffering syndrome is found and is a major contributor to disability in all instances of distressing mental disorder.

Some mental disorders don’t necessarily come with suffering/distress. Certain tic disorders and personality disorders, for example, only qualify as mental illness because they interfere with the person’s functioning, but not necessarily with their hedonic tone. The suffering syndrome is not necessarily found in these non-distressing disorders but it is a feature of all distressing mental disorders.

Look, for example, at the extract below from the “associated features” of schizophrenia in DSM-5-TR. (Schizophrenia is a mental disorder strongly associated with distress.) Compare the symptoms I have underlined in that below text with the symptoms of the suffering syndrome, above.

(Spoiler: All the symptoms of the suffering syndrome, except exaggerated affective response, are found in the DSM associated features of schizophrenia.)

Individuals with schizophrenia may display inappropriate affect (e.g., laughing in the absense of an appropriate stimulus); a dysphoric mood that can take the form of depression, anxiety or anger; a disturbed sleep pattern (e.g., daytime sleeping and nighttime activity); and a lack of
interest in eating or food refusal. Depersonalization, derealization and somatic concerns may occur and sometimes reach delusional proportions. Anxieties and phobias are common. Cognitive deficits in schizophrenia are common and are strongly linked to vocational and functional impairments. These deficits can include decrements in declaritive memory, working memory, language function, and other executive functions, as well as slower processing speed. Abnormalities in sensory processing and inhibitory capacity as well as reductions in attention are also found. Some individuals with schizophrenia show social cognition deficits, including deficits in the ability to infer the intentions of other people (theory of mind).

Eugen Bleuler in 1911 addressed exaggerated affective response in his unmedicated schizophrenic patients:

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 toward the outer world is, then, a secondary one springing from hypertrophied sensitivity.” (p. 65)^[12]

Now, think for a moment about the distressing mental illness you are most familiar with. Do you see mental processing speed, working memory or attention problems? Problems with emotion regulation or impulse inhibition? Depression, anxiety and/or irritability? Problems with social sensitivity or social engagement? Affective hyper-reactivity (or affective disengagement like Bleuler’s patients)?

What is distress/suffering doing in mental illness? What is its role?

Recently, a historian of psychiatry told me, “Suffering is central to serious mental illness. Whether it is the cause or the effect, or something of both, is an open question.”

I’m sure it is an open question in his mind but the causal relationship between mental disorder and suffering is not an open question in psychiatry.

In psychiatry, at least in its bible the DSM, it is always the symptoms of mental disorder that cause distress, never distress that causes the symptoms of mental disorder.

Look at this from DSM-5-TR’s diagnostic criteria for major depressive disorder:

The symptoms cause clinically significant distress or impairment in social, occupational, or other important areas of functioning

This formulation occurs throughout DSM-5-TR,^[13] and it has been a feature of the DSM since its third edition in 1980 when the lead author laid down new essential criteria for every DSM diagnosis, including: the symptoms must be distressing to the individual or the symptoms must impair the individual’s ability to function.

I believe distress, in mental disorder, is causing the same devastating set of symptoms it causes in hunger, sleep deprivation and pain, and psychiatry, if it wants to heal this significant set of cognitive, affective and social impairments common to all distressing mental disorders, should find and address all sources of the patient’s distress. Don’t ignore distressing medical conditions such as insulin resistance, hormone imbalances, vitamin or mineral deficiencies/excesses, inflammation, infection, pain, malaise, etc..

But the symptoms that comprise the distress syndrome are not the only features of distressing mental illness. What about the symptoms that distinguish one DSM entity from another — mania, delusions, hallucinations, obsessions, etc.?

Well, they may be summoned by distress from a propensity in the patient’s biological inheritance, modified by life experience and social state: diathesis-stress, an old idea.^[14] That footnote marker [14] links to a pretty good primer on diathesis-stress, if you’re not familiar with this important theory of the etiology of madness.

If suffering is the stressor that elicits this eccentric behaviour, then eliminating ongoing suffering may at least to some degree ameliorate these eccentricities, these defining symptoms.

“Some researchers [claim] that a single dimension—similar to the g factor in intelligence, that provides a summary measure of general mental ability—accounts for all types of psychopathology across the lifecourse. ‘Today’s patient with schizophrenia was yesterday’s boy with conduct disorder or girl with social phobia and tomorrow’s elderly person with severe depression’, psychologists Avshalom Caspi and Terry E. Moffitt assert.” — Allan V. Horowitz, DSM: A history of psychiatry’s bible (2021), chapter 6.

Caspi’s and Moffitt’s proposal is in this 2018 American Journal of Psychiatry article. They discuss “the new idea that there may be one underlying factor that summarizes individuals’ propensity to develop any and all forms of common psychopathologies,” which they call p.

This p factor is suffering.