Wednesday, 1 November 2017

PSY 3002 Lecture Notes 2017-18

PSY 3002-1 – Evolutionary Psychology - 2017-2018
Bruce G Charlton

Nature of course
Application of evolutionary biology to understanding human behaviour.
Especially focused on the aspect of natural selection called adaptation – and not on the ‘origin of species’.
Adaptation is about traits – that is any specific attribute of an organism that enhances relative reproductive success.
Size, shape of structures, a mechanism, whole organism behaviours, instincts, motivations and abilities.
Traits are the kind of things that are shaped in artificial breeding of animals and plants – noticed by Darwin because began to be done in middle 1700s in Britain. Breeding speed of horses, weight of cattle, size and sweetness of apples, yield of wheat; behaviours of working dogs, plumage and homing ability of pigeons. 
Adaptations include camouflage of insects, hard protective shells, weapons and venoms etc.
Differences in evolutionary history leads to different traits and behaviours in men and women – eg. average different life expectancy, health and disease, priorities in seeking a mate, levels of violence.
Some aspects of the human mind evolved in response to natural selection over past generations – shaped the way humans think and behave in some circumstances – Evolutionary Psychology.
Set books
Dylan Evans and Oscar Zarazate - Introducing Evolutionary Psychology. Icon Books (less than 2 quid on Amazon)
DM Buss Evolutionary psychology: the new science of the mind  - probably best book overall - Also contains an introduction to evolutionary theory
L Barrett et al. Human Evolutionary Psychology – more advanced Master’s level text
Evolution and Human Behaviour – find in University e-journals
Other reading as we go. 
Evolutionary psychology is the most controversial science – so we will jump straight in to a currently controversial topic: male female differences in the workplace. Target paper – essential reading for first lectures – very long!
Kingsley R Browne. Sex and temperament in modern society: a Darwinian view of the glass ceiling and gender gap. Arizona Law Review. 1995; 37: 971-1106
  1. Interesting
  2. Controversial
  3. Almost book length; heavily referenced
  4. Serves as an intro to Evol Psychol (written for lawyers)
  5. Has been quite often cited (more than 150 times) – so can read a variety of responses to the paper.
  6. Can use to discuss the role and limitations of Evol Psychol
Glass ceiling (GC) refers to observation that women are found in the highest level positions in hierarchical organizations at a lower proportion than they are found in lower level positions.
E.g. lower percentage of women CEOs than junior managers, or professors than junior lecturers.
Note: ‘Glass ceiling’ prejudges the cause of this observation – claiming that there are invisible discriminatory barriers against promotion of women.
Gender gap (GG) refers to observation that women employees earn less than men employees.
Note: This gap is reduced by considering only full time employees, and further reduced – or reversed – as further controls are introduced – e.g. precise jobs, levels of qualifications, years of service, productivity measures, hours worked/ antisocial hours etc.
Therefore note: Glass Ceiling difference is real – although much diminished by affirmative action preferences for hiring and promotion since 1995; but Gender Gap difference is not a real phenomenon if comparisons are made with relevant statistical controls.
Summary of the argument in Browne 1995:
  1. There are significant psychological differences between men and women: personality, priorities, motivation, risk taking behaviours.
  2. These psychological differences are produced by biological differences during human evolutionary history, due to differences in men and women’s biological and social roles, hence selection pressures.
  3. These differences in male-female human psychology are mainly caused by genetic leading to hormone and brain differences.
  4. Sex roles are not merely imposed by society – there is a biological basis.
  5. Sex differences in relation to work in modern societies – such as the GC and GG – are also seen in many other types of society throughout history and in the modern world. (Human Universals); and also in other societies of other mammalian species.
  6. These biological differences are sufficient to explain the GC & GG without need to invoke explanations such as prejudice against women or socially-imposed sex roles.
  7. This analysis does not tell us what – if anything - to do about the GC and/ or GG. Does not tell us that GC and GG are explained by boil diff, but just that they could be.
  8. However, the biological explanation does challenge the rationality of some existing laws – since some laws assume that men and women are psychologically identical on average, and therefore that the identical treatment of men and women will lead to identical outcome.. In contrast Ev Psychol suggests that identical treatment of men and women would be expected to yield non-identical outcomes.
Biological Differences -> Same conditions -> Different outcomes
PSY 3002-2 – Evolutionary Psychology and Medicine 2017-18
The fundamental assumptions of Natural Selection
Bruce G Charlton
Malcolm Potts. Sex and the Birth Rate. Population and Development Review, 1997; 23: 1-39.
Menlaos Apostolou. Sexual selection under parental choice. Evolution and Human Behavior, 2007; 28, 403-409.
Scope and limitations of evolutionary psychology.
Ev Psychol explains adaptations, or generates hypotheses for them – but is the trait under investigation an adaptation?
For example, it needs to be argued that the explanations of the GS and GG in the Browne paper are indeed important factors involved in determining promotions and salary.
Assumption men and women the same? Not plausible – proper Q is what direction and how big differences.
Browne’s hypotheses stand up to testing by a great deal of evidence of many types.
In some societies there may be other social factors that are equally or more important. Or the main factors may be simply unknown, or denied, or outside of the scope of science - if that is believed to be possible. For example, in hunter gatherer tribes, magic and witchcraft are frequent explanations for all sorts of problems. 
Natural selection provides retrospective answers: because adaptations are formed over many generations, and only when selection pressures are stable and sustained over many generations. For example, a population will usually only become taller if height is an advantage for several generations.
However, sometimes selection may be very rapid – for example when a new deadly disease kills everybody who is not resistant – then, assuming resistance is heritable/ genetic, the next generation will be much more resistant. So that adaptation may evolve in only one or very few generations. This may have happened to Native Americans with tuberculosis and/ or smallpox.
Adaptations are only beneficial on average – and not for everybody in all circumstances. E.g. Tallness may be an advantage most of the time, but when there is a famine, smaller individuals may survive better.
In populations, there may be overlaps in traits, For example, on average men are a few inches taller than women – but some women are taller than some men. However, small average differences in a trait may lead to large differentials at the extremes, so all the very tallest people are men. 
Also, if genetic differences and environmental factors could all be controlled for, then all men would be taller than all women…
Modern Society and reproduction
Modern society has changed very rapidly, especially over the past 200 years since the Industrial Revolution. Yet humans are mostly adapted for a very different kind of society.
There are differences in technology, and also social differences.
One major technological factor which has affected adaptive traits is fertility-controlling technologies, such as contraception and abortion. The massive effect is described in Potts (1997).
Because humans lack the adaptive instincts to reproduce in the modern environment, in all developed nations where fertility control technologies are available and accepted the Total Fertility Rate is below an average of 2 children per woman – which means that these humans are going extinct!
But this is also affected by social factors, because certain religious groups have continued to have above-replacement numbers of children – either because having many children is part of the religion, or simply because fertility control technologies are forbidden (and people continue to have sex).
But only certain, traditionalist, religious groups have many children – most religious people do not. And no non-religious modern groups have above replacement fertility (only a few individuals); and this tells us that religion is an uniquely powerful motivator; it suggests that populations without religion may not be biologically sustainable under modern technological conditions! In short, it may be that modern secularism is highly non-adaptive and will lead to extinction of most modern populations (unless something changes – which it probably would).
Arranged Marriages
The work of Menelaos Apostolou has shown that in all traditional societies for which data is available – including the anocent-type societies of hunter gatherers, animal herders and simple farmers – the parents play a very large role in arranging marriages – i.e. in choosing mates; especially for women. 
In other words, human evolved in a situation of arranged marriages – and the modern method of each person trying to find their own mate is one for which we are Not equipped by natural selection.
In other words, our instincts are adapted for a society in which marriages were – to a greater or lesser extent – arranged by parents; and it would not be surprising if our instincts were Not adaptive for modern societies.
In other words, from the perspective of evolutionary psychology it is not surprising that so many people make such bad choices of sexual and marriage partners; because ‘doing what comes naturally’ often leads to wrong choices.
This research is a very good example of the way in which evolutionary psychology can put a completely new perspective on modern problems. (Although social factors, media etc. very relevant)
PSY 3002-3 Evolutionary Psychology & Medicine 2017-18
Bruce G Charlton
Recent human evolution - Effects of the agricultural and industrial revolutions on human psychology
Greg Cochran & Henry Harpending (2009) -
Bigger population means that beneficial mutations are more frequent. As population increases, natural selection becomes faster.
Human pop went from approx
60 000 years ago - ¼ million
3,000 years ago – 60 million (240 X increase)
1800 - 1 billion
1927 – 2 billion
Now - 7 billion
World population 100X bigger – beneficial mutations 100X more common.
Spread very rapidly, despite larger population, because the growth of spread is exponential (like an epidemic).
Agricultural Revolution
Transition from hunting and gathering to agriculture; Perhaps the biggest change in human life in the history of the world.
Agriculture produces 10-100X more food per acre/ hectare.
From approx 12 000 ya herding of goats then sheep, cultivation of wheat and barley
Sheep 11 000 ya
Cattle (India) 8 000 ya
Agriculture spread over almost all world except marginal areas such as extreme north and south, jungle, savannah.
New selection pressures:
  1. Denser populations, larger populations
  2. Increased numbers and rate of infectious diseases – many zoonoses. Selection for resistance
  3. Societies became hierarchical/ unequal, specialized jobs, ‘government’-co-ordinated.
  4. Large inequalities in power, wealth, reproductive success.
  5. Downward social mobility over generations – rich replace poor.
  6. Agriculture selects heritable psychological traits: perhaps higher intelligence, more conscientious personality, and ‘taming’ (reduced impulsivity and violence). 
  7. Diet: more carbohydrates, and invention of alcoholic drinks – selection for coping with these
  8. Mortality rates determine RS. Selection favours factors that produce increased health and survival of offspring.
PSY 3002-4 – Evolutionary Psychology and Medicine – 2017-18
Bruce G Charlton
Recent human evolution – effects of the industrial revolution on human psychology and health
Reference: Edward Dutton & Bruce G Charlton – The Genius Famine (2016)
Industrial revolution
(Recapitulated from previous lecture)
By 1800, first in England, signs of a new kind of society; further change in selection pressure.
1300 – 4 million
1400 – 2 million (after Black Death)
1600 – 4 million
1800 - 8 million
1850 - 16 million
1900 - 32 million
Much more food – partly from improved agricultural efficiency and productivity – the Agrarian revolution, beginning about 1700. Better quality animals from selective breeding, crops, new machinery, new crop rotations, soil improved by manure and lime etc.
Partly from the Industrial revolution providing wealth used to buy food from abroad.
New selection pressures:
Greatly reduced child/ adolescent mortality rates all-round; but especially among the poorest where child mortality had been close-to total - leading to rapid increase in population. (child mortality reduced from more than 60% to one percent in most developed countries)
Upward mobility. For first time in history, from about 1850 the poorer, less intelligent, those with less education had higher reproductive success (more surviving viable children) than upper classes – especially among women. 
Will (all else being equal) tend to reduce average heritable intelligence and conscientiousness.
(Because both intelligence (80%) and personality traits (50% plus) are substantially heritable.)
Modern Fertility
Modern fertility rates driven by technology (contraception, abortion) and secular (non-religious) societies – both have reduced TFR to less than two in all native populations of developed societies.
Fertility rates (not mortality rates) now drive population growth – large differences = large and rapid demographic transformation = rapid natural selection:
TFR – S Korea, HC China 1.2 – Niger, Somalia c7 - c five-fold
Median Age – Japan, Germany c 47 – Niger, Uganda c16 – c 3X

Current natural selection of humans
Very rapid (large populations, widely varying RS/ fertility)
World population is growing, population of developed nations is declining (below replacement fertility) – associated with heritable physical and psychological differences.
Some places and peoples in world the population is rapidly expanding, other places it is declining (although obscured by increasing longevity – leading to increasing median age). 
Species-level demographic replacement – rapid human evolution observably happening decade by decade.
Effects of reducing Intelligence
Increasing intelligence is positively correlated with health, lifespan, salary, educational attainment
But these measures are concerned with differentials/ differences – not absolute levels.
Increasing evidence of decline in ‘g’ general intelligence, as measured by long term trends in ‘objective’ (non-exam based) measures such as simple reaction times, skull asymmetry, working memory.
Would tend to reduce health and longevity, all else being equal.
Conscientiousness has similar correlates to intelligence – health, lifespan, jobs, educational level
But personality does not have objective measures – human rated.
Effects harder to observe.
Mouse Utopia hypothesis
That the high rate of child mortality in humans (more than half) serves to eliminate deleterious genetic mutations that occur spontaneously each generation.
Because this reduced so much after the Industrial Revolution would expect mutation accumulation with each generation.
Would expect various, random types of genetic damage to become more common.
May affect intelligence, personality, and physical health
Hypothesis is nicknamed the ‘mouse utopia’ scenario
May be that the Ind Rev created the selection pressure which will sooner or later destroy itself!
PSY 3002-5 Evol Psychology and Medicine 2017-18
Ageing and memory, intelligence, personality
Bruce G Charlton
Michael A Woodley, Guy Madison, Bruce G Charlton. Possible dysgenic trends in simple visual reaction times… The Mankind Quarterly 2014; 55: 110-124
Recent natural selection has led to an ‘ageing population’ – increase in media age (mid-forties) – proportion of the very old – effects on psychology, direct and indirect.
1985-2014 – treble the number of people aged 90plus (currently half a million – nearly 1 percent of population). At least half of these will suffer from some form of dementia.  
Theories of ageing
  1. Inevitable: Biologically speaking is natural/ inevitable – need to explain NOT ageing, or the delay in ageing.
Damage to an organism (from many causes) tends to accumulate through life – unless it is repaired.
  1. Reproductive Success: Natural selection operates to optimize reproductive success, not life span – and beyond a point, building organism for increasing lifespan will reduce reproductive success.
The problem for an organism is that there is a trade-off between being ‘built to last’ need for energy and resources for current needs such as surviving, reproducing, investing in offspring etc.
  1. Longevity: Humans are among longest lived animals because children take such a long time to reach independence and sexual maturity. To rear about six children, women (and to a lesser extent men) need to be built to survive to about fifty years old (life to 70 years is like a safety margin to aim at.).
Psychology of ageing
  1. Memory – gets worse
  2. Intelligence – declines
  3. Personality changes
  4. Increasing numbers of people with dementia – cumulative, progressive degenerative generalized brain diseases increasing in incidence with age: tomorrow’s lecture
  5. Psychological effects physical disease (heart, lung, cancers etc.)
  6. Increase prevalence of psychological disease esp depression
  7. Effects of increased usage of prescribed drugs – blood pressure, antidepressants, sleeping tablets etc. 
Several aspects of memory usually decline with age:
Decline most in ‘Episodic memory’ for autobiographical details, sequenced in the correct order – eg. Who, What, When, Where, Why?
Also Working memory ability declines – to do mental tasks that require holding several facts in mind and manipulating them – eg measured by reverse digit span. May be a consequence of reduced processing speed which is approx. measured by simple reaction times.

Intelligence – specifically underlying ‘fluid’ intelligence (rather than ‘knowledge-based’ crystalline intelligence, which may continue to increase into late middle age).
Intelligence can be measured by IQ tests, and by tests such as simple visual reaction times or more elaborate processing speed tasks.
sRT – a light comes on, must press a button as quickly as possible. Usually takes about 250-350 milliseconds
IQ raw scores tend to decline with age – from twenties or thirties onwards, especially scores for fluid intelligence – eg problem solving, or ‘fluid intelligence’ = mental agility.
But crystallised intelligence (also knowledge and expertise based - such as vocabulary, general knowledge) may accumulate and increase into middle age or early old age.
Reaction times get slower with age, almost as soon as adult maturity (and maximum fluid intelligence) has been reached.
Looking at simple reaction times, it seems that average intelligence begins to decline from about age 16 - 24 (older in men) – and declines by more than one standard deviation by the mid 60s– which is roughly equivalent to 15 IQ points.

Personality traits are stable in rank order throughout life – ie. In 100 people, the most extravert aged 20 will probably remain the most extravert in that group, aged 60.
But the average measure for personality traits will change in the whole group through adult life.
In other words, personality usually changes throughout adult life. Personality changes (unlike intelligence decline) may be adaptive rather than due to ageing – at least until middle age – because different personality types are adaptive at different stages of the normal lifespan.
Big Five - OCEAN
Openness - decreases
Conscientiousness – increases to middle age then decline
Extraversion - decreases
Agreeableness - increases
Neuroticism – probably stays about the same (inconsistent results)
Demographic changes (due to changes in selection pressure in modern societies) are leading to multiple functional declines due to age.
PSY 3002- 6 Evolut Psychology and Medicine 2017-8
Evolution and Dementia: Vascular, Lewy Body
S Boyd Eaton et al (1988) Stone Agers in the Fast Lane. American Journal of Medicine. 84: 739-49
Reference: Search – “Longevity Medicine Review” interview Joseph Knoll – speculative piece
Humans not built to last much beyond 65 – mostly fulfilled their contribution to RS, and high cost in resources and repair systems of building humans to last extra decades (e.g. building a Rolls Royce costs ten times as much as a basic car). 
Increasing proportion and numbers of people with dementia.
A variety of cumulative, progressive degenerative generalized brain diseases - increasing in incidence with age. (Age 65 about 5% with dementia, age 90 about 50%).
 ‘Global’ cognitive decline - Affects 3 or more cognitive functions such as: Memory, Intelligence, Language and Executive function (planning, judgment, sequencing), emotions/ personality
Many effects on behaviour – reduced ability at work and self-care; change of personality (may become violent); deterioration of behavior (hoarding, hiding, wandering); change in sleep patterns (nocturnal activities); usually patients have no insight because reasoning ability declines as part of syndrome
Vascular/ multi-infarct dementia
Degenerative change due to many small ‘strokes’ due to blocked blood vessels (arteries) or small bleeds. Destroys multiple small parts of the brain by blocking blood vessels, and induced bleeding.
 Atherosclerosis –accumulation of damage plus parasitic/ (local neoplastic) evolution of arterial lining cells.
Atheroma – a yellowish lump/ plaque grows from the lining of the artery. Contains damaged lining cells and white blood cells, cholesterol crystals, then becomes calcified and hardened.
Then local excess growth of plaque narrows/ blocks artery
Plaque breaks up into blood stream – Emboli/ particles – block arteries – transient ischaemic attacks/ mini-strokes
Attract blood clots – block arteries
Plaque may break, artery wall rupture - and cause bleeding into brain
Arterial damage can be prevented by lowering blood pressure; blood clots can be prevented with low dose aspirin
Lewy Body Dementia
Part of Parkinson’s Disease syndrome.
Lewy bodies are abnormal microscopic protein deposits found inside nerve cells.
Dementia with LD presents with fluctuating (better and worse over period of hours) psychiatric symptoms such as visual hallucinations and persecutory delusions, and features of Parkinson’s disease.
Pathology - Loss of neurons in substantia nigra (black substance) – Seems to be an inevitable side-effect of the dopamine system for drive and motivation the production of dopamine is toxic to these cells in brain.
Suggests LBD is a side effect of the dopamine system which is useful (and increases fitness) in early life by supporting drive/ motivation and concentration – becomes harmful in later life.
Not eliminated by natural selection in later life, because elderly people have many degenerative problems affecting many body systems (heart, lungs, joints, skin etc) and are likely to die from something or another…
  1. Probably, Lewy body dementia occurs gradually, and invisibly, from early in life
  2. Age of occurrence depends on rate of degenerative change (varies between people) and length of lifespan (also varies).
  3. If people lived long enough, everybody would eventually get LBD Dementia
To slow the rate of LBD Knoll recommends taking small dose of Selegiline / L-Deprenyl from early adult life – inhibits breakdown of dopamine therefore has dopamine enhancing action. Whether this would work is not known. Caffeine and nicotine are probably also preventive.
Conclusion – dementia seems to be an almost inevitable consequence of ageing.
The older you get the more likely you are to have dementia.
More older people in modern populations.
May sometimes be a maladaptive consequence of processes that are helpful – indeed necessary – in early life. Revealed by modern increased lifespan beyond the maximum seen in ‘the wild’.
PSY 3002-7 Evolutionary Psychology and medicine 2017-18
Bruce G Charlton
Evolution of Anxiety and Fear
REF: IM Marks, RM Nesse. Fear and Fitness. Ethology and Sociobiology. 1994; 15: 247-261.
What is anxiety/ fear?
Anxiety is a kind of fear
- some say anxiety is about potential threats,
fear about actual threats,
but tend to be used interchangeably.
Both are unpleasant increase in arousal - probably a universal biological category, cross-cultural, once of the basic emotions an adaptive response – a defence mechanism - improves chances of survival – ultimately reproduction.
(Reproductive success is the bottom line – approx.. average effect of a trait on differential production of viable offspring)
Benefit-Cost trade-offs
Anxiety is an adaptation, a defence mechanism - but too much or too little anxiety – or anxiety in a wrong situation is maladaptive.
Vigilance of a squirrel or blackbird. Too much, reduces food intake, too little increases risk of predation.
Also modified by learning – unfamiliar versus familiar environment.
Anxiety as a defence mechanism
Anxiety is a defence mechanism: against:
  1. predators
  2. conspecifics (same species) and
  3. the environment.
Anxiety disorders in psychiatry are examples of when an adaptation (evolved pattern of behaviour that enhances reproductive success) becomes a pathology – quantitative aspects of a trait, or inappropriate situation.
Anxiety as an emotion
 Anxiety involves multiple body systems as well as the mind –
Cardiovascular, Respiratory, Gastrointestinal, Musculoskeletal…
‘Arousal’ induced acutely in a few seconds by sympathetic nervous system (mostly noradrenaline neurotransmitter) and over tens of seconds by adrenaline hormone in blood, released from adrenal glands. Also cortisol is released from adrenal gland in response to stress – acts over timescale of days.  
Using Antonio Damasio’s concept of emotions – anxiety is the representation of the body state changes caused by these phenomena. Also includes changes within the brain – one part of the brain representing changes to others. Therefore anxiety and brain and body manifestations – and treatment of anxiety can work on brain, body, or both.

Evolved fears
Many fears are non-associative – i.e spontaneous and innate. Instinctive fears.
These are often evolved eg. Fear(specific phobias) of snakes, spiders, heights, the dark, of being alone, of strangers – When not automatic, we are prepared to learn these fears.
Tend to be prone to false positives – unnecessary fear
We do not learn these fears – on the contrary we learn to overcome them.
Anxiety disorders may be more a failure to learn to overcome fears, rather than learning of fears.
Evolutionarily unfamiliar threats – cars, guns, drugs – tend to be prone to false negatives; ought to fear them more than we actually do.
In modern life anxiety is very common – probably the most common psychiatric symptom – and agents to treat anxiety are probably the most common psychiatric drugs. Is this an example of evolutionary mismatch?
Ancient anxiety system too sensitive for modern conditions; and/or triggered by non-threats (snakes and spiders) and not triggered by real threats to survival (cars, alcohol).
i.e. a mismatch.
Medical problems with anxiety include the anxiety disorders (excessive or inappropriate anxiety); but little known/ studied hypo-phobia – too-low-fear can also be a problem.
Some people have hypo-phobia as a heritable and lifelong personality trait; others by forms of brain damage (e.g. amygdala, Right-sided parietal stroke damage, affecting judgment.
PSY 3002-8 Evolutionary Psychology and medicine 2017-18
Anxiety and Fear - Six Defences
Bruce G Charlton
Key concept: Mismatch
REF: Chris Cantor. Post-traumatic stress disorder: evolutionary perspectives. Australian and New Zealand Journal of Psychiatry. 2009; 43: 1038-1048
Key concept: Mismatch
Contemporary human life is very different from the ecological and social environment in which humans evolved.
e.g. Animals in a farm or zoo behave differently from wild animals in their natural habitat crowded hens pecking/ cannibalism – beak trimming.  – same with modern humans compared with out hunter gatherer tribal ancestors
High intelligence and Conscientiousness was adaptive in English Medieval times and increased RS, but in modern times they reduce RS – reversal from adaptive to maladaptive. 
Anxiety defences were evolved under very different conditions than currently prevail – expect anxiety often to be non-adaptive, sometimes maladaptive.
A hierarchy of 6 key defences to fear-provoking threats
  1. Avoidance
  2. Attentive immobility
  3. Withdrawal (‘flight’)
  4. Aggressive defence (‘fight’)
  5. Appeasement (mainly for conspecifics/ same species)
  6. Tonic Immobility (frozen, unresponsive)
  1. Avoidance
    EG tortoise inside shell. Hedgehog.
    E.g. anxious patient avoids dangerous situations, – taking refuge, hiding somewhere safe. Agoraphobic person who will not leave home.
  2. Attentive immobility
    Temporarily frozen, alert, vigilant, poised)
  3. Withdrawal
    Includes escape, running-away, ‘flight’
  4. Aggressive defence
    Gets angry, lose temper, try to confuse or intimidate attacker. (Both predator and prey try to avoid injury)
  5. Appeasement
    Mainly for conspecifics/ same species.
    Pacification, conciliation, submission
    Approach attacker and submit to them – ‘Stockholm Syndrome?
  6. Tonic Immobility
Imminent predation - Prolonged frozen state, passive, aware but maybe unresponsive (famous in chickens).
May simulate disease
Lose sensitivity to pain, may feel depersonalized – detached from self. E.g. PTSD - shell shock, after rape. Some shared features with catatonia (eg waxy flexibility)
Some of the main general causes of disease
(A version of the ‘surgical sieve’):
  1. Genetic
  2. Neoplastic
  3. Degenerative
  4. Infectious (pathogens and parasites)
  5. Trauma
All may have evolutionary implications or consequences.
  1. Genetic – e.g. disease may have evolved – with mismatch, or genetic damage to adaptation.
  2. Neoplastic – cancer is due to natural selection of epithelial cells, evolving to overcome the body’s defences and become a parasite.
  3. Degenerative – diseases of ageing – due to limitations on lifespan, due to evolutionary constraints from the optimisation of reproductive success.
  4. Infectious – linked with evolution of resistance to parasitic diseases.
  5. Trauma – may be repaired by evolved mechanisms, selective trauma may reveal evolved function of specific systems – eg. selective brain damage.
Conclusion – there are many ways that natural selection may be related to disease; but most diseases are not directly due to evolutionary causes.
PSY 3002-9 – Evolut Psychol & Medicine 2017-18
Bruce G Charlton
Phobias, Hypophobia and Panic
Poulton R, Menzies RG. Non-associative fear acquisition. Behaviour Research and therapy. 2002; 40: 127-49
Matthews S, Charlton BG. (2000). Phenomenology of panic attacks reflects human evolutionary history of separation anxiety. Irish Medical Journal. 93: 184-5. (Baron of Jesmond)
Already discussed: Often evolved by natural selection as defence against a significant threat to RS in the ancestral environment.
This explains the form and content – but not the severity of the disorder. Phobias are (usually) Exaggerated Defence Mechanisms.
May be mismatch, and probably other factors involved such as individual personality and experience.
? Maladaptive if lack of anxiety - increase accidents etc.
Too little anxiety leads to increased rate of injuries and accidents, therefore it is a disease/ pathology.
But does not lead to psychiatric complaints – shows up in physical injuries/ deaths due to high risk behaviour –easy to miss unless looked-for.
First shown in relation to fear of heights in children. Fear of heights in children emerges when they begin to crawl – which make sense biologically.
A group of adult height-phobics at age 18 reported zero serious falls at age 9. But absence of fear of heights in adults (hypophobia) associated with higher rates of serious falls reported for childhood.
If fear of heights was a disease, it would lead to increased injuries/ death – but it does the opposite.
If fear of heights was primarily learned, then falls would lead to increased fear of heights – and a positive association between falls and fear of heights - but the association is in the opposite direction.
Therefore fear of heights is adaptive, effective at reducing or preventing injuries from falls. Lack of fear is maladaptive trait.
Opposite of Phobias – Insensitive/ Weak Defence Mechanism
‘Fear of heights’ varies between individuals more like a personality trait - real-life experience of falls does not make much difference to phobia or hypo-phobia of heights.
Specific phobias – eg for heights - are heritable; found at a much higher-than-expected rate among genetic relatives.
Rapid build-up of anxiety
Physical symptoms prominent – hyperventilation, palpitations, shaking, nausea
Fear of a catastrophic outcome - heart attack, stroke-brain haemorrhage, epileptic fit, collapse
Superficially sounds like a disease, implying fitness reducing. But panic is seen apparently universally and all cultures.
Also, panic is a distinctive and complex package/ syndrome of features – which looks somewhat like an adaptation.
Complex, costly and yet common behaviors may have evolved – because they have persisted probably some advantage to outweigh disadvantages.
Evolutionary Theories of Panic
Hypothesis - Donald F Klein. Separation anxiety
Suggestion that panic is an adult form of separation anxiety.
Separation anxiety/ distress occurs when an infant is separated from its mother and cries loudly, as signal - needs assistance.
Childhood separation anxiety is predictive of adult panic disorder.
And adults with Panic disorder have an increased prevalence of reporting childhood separation anxiety.
Exaggerated and inappropriate Defense Mechanism?
But - Against this is that adult panic may be silent – freezing, shaking, collapsing – which would not be an effective signal. 
Also Panic doesn’t seem to fit closely with any of Cantor’s six categories – aspects tonic immobility, eg. Dissociation - but does not freeze. Trigger is more like agoraphobia and may lead to Avoidance.
No single, solid hypothesis, but a couple are plausible. 
PSY 3002-10 Evolutionary Psychology and Medicine 2017-18
Evolution of OCD & PTSD 
Bruce Charlton
Brune M. The Evolutionary Psychology of Obsessive-Compulsive Disorder. Perspectives in biology and medicine, 2006; 49: 317-29.
Look at Chris Cantor paper again for PTSD
Two common causes of disorder are 1. Mismatch; and
2. Hyper/ hypo/ inappropriate activation of evolved Defence mechanisms – This is the subject of today’s lecture.
May be from mismatch, or from any cause of disease.
Obsessive Compulsive Disorder
Definition: Cognitive and Behavioural elements.
Cognitive: repetitive unpleasant and unwanted thoughts (but not hallucinations, recognise obsessions as subjective) – not regarded as perceptions. 
Behavioural: Ritualised, repetitive behaviours
OCD probably an exaggeration of an evolved, adaptive mechanism to ‘model’ cognitively the future consequences of present action – secondary emotions; like anxiety compared with fear.
All healthy humans have a harm-avoidance, risk-minimizing defence mechanism to avoid severe dangers from present actions; in OCD this is exaggerated and this inflicts costs – wasting time, energy and resources – presumably, therefore, tending to reduce RS. 
I have a hunch that there is a further Mismatch-caused amplification of OCD tendency by technology and modern knowledge. For example, technology with invisible effectiveness – locks, switches, valves; or the germs as a cause of contamination infection, but germs being invisible. 
Hypothetical causes of OCD:
Underpinned by theory of mind ability, and episodic memory – autobiographical and sequential memory. These enable meta-representations that is, representations of representations (= cognitive modelling).
A mental model of entities and causes to run ‘simulations’ of possible futures.
It is an adaptive advantage – enhances chance of survival – to be able to predict and avoid harmful consequences of present actions. This mechanism was presumably a product of natural selection. However, in OCD this system malfunctions. 
Post-traumatic stress disorder (PTSD)
Diagnosis PTSD: Delayed/ protracted response to severely stressful or traumatic event (war, disaster, torture, violence) – latency of weeks/ months < 6 months. Symptoms of e.g. re-living, intrusive memories, flashback, nightmares – but not full delusions.
A type of exaggerated memory - emotionally overwhelming recall of past scenarios. 
Conceptualizing the cause of PTSD
Memory for events is laid down with memory of emotions experienced. When events are recalled, emotion is re-experienced – and this may be a very strong emotion. (Damasio ideas – forthcoming lecture)
When body is in the same emotional state, events are more easily recalled (state-related learning). So memories are cued by place, mood, various reminders. Strength depends on severity of trauma.
Memory for events depends upon their perceived salience with relation to survival and reproductive success. Major traumas are naturally perceived as salient.
Therefore PTSD is probably based on an evolved, adaptive Defence Mechanism; but too strong and inappropriately activated.
The PTSD story is rather similar to OCD story – exaggerated normal adaptive defence mechanism
But whereas OCD is about modelling fear of the future, PTSD is about learning from fear in the past.   
PSY 3002-11 Evolutionary Psychology and Medicine 2017-18
Bruce G Charlton
AK Moskowitz. ‘Scared stiff”: catatonia as an evolutionary-based fear response. Psychological Review. 2004; 111: 984-1002
Catatonia has long been regarded as having significant similarities to Tonic Immobility and to be rooted in extreme anxiety – such ideas go back about 150 years– this article explores the strengths and limitations of this argument.
Core symptoms of Catatonia are
  1. Stupor
  2. Immobility
  3. Mutism
But also catatonia displays other more complex and active ‘motor’ aspects – catatonic excitement – e.g. purposeless hyperactivity or hostility, stereotypical movements, copying and negativism…
Catatonia occurs in schizophrenia, melancholia, mania and as a drug side effect (especially with antipsychotics and SSRI antidepressants).
Association between catatonia and anxiety has been mostly ignored But:
  1. Recently the nature of catatonia has become clearer – not just a part of schizophrenia, but a non-specific syndrome found in about 10 percent of acute psychiatric hospital patients. 
  2. Catatonia is usually curable with high dose benzodiazepines such as lorazepam – and these are anxiolytic drugs.
  3. Detailed interviewing reveals that many catatonic patients report intense inner anxiety and awareness.
Tonic Immobility - TI
Tonic immobility caused by prolonged stillness and unresponsiveness in the face of threat.
Exacerbated by restraint, entrapment and also inversion.
This immobility is associated with typical catatonic features of muscle rigidity with waxy flexibility, and mutism.
TI may last minutes or hours – and may end in death (as may also happen with catatonia).
In TI, as in catatonia, the immobility may suddenly cease with abrupt hyperactivity, purposeless excitement, or flight or assault.
Adapted to confuse or deter predators – ? some predators only respond to movement, some avoid diseased prey.
Causal factors
Because in catatonia, the perceived threat comes from ‘within’ (e.g. psychosis, drugs), the source of danger cannot be localised, cannot be escaped from – organism feels trapped - triggering the TI response?
Moskowitz suggests TI comes from fear – present threat, catatonia from anxiety – potential threat.
Why does TI and catatonia sometimes end in death (‘malignant catatonia’)?
An obvious cause of death typically cannot be found on post-mortem.
Perhaps a prolonged and severe sympathetic nervous system activation with extreme anxiety (eg malignant catatonia shaking, racing heart, hyperventilation, high temperature)– but eventually the opposite parasympathetic (‘vagal’) over-drive is triggered; with slowing of heart, and potential for heart stopping.
Literally ‘scared to death’.
Catatonia is a relic of Tonic Immobility, which is an evolutionarily ancient defensive strategy; an inappropriate expression of this strategy adapted to defend against predation; caused by the perception of being under extreme threat – but in catatonia the perceived threat is inner (caused by severe psychosis, illness or drug action).
Suggestion: extreme anxiety due to perception of:
  1. Inescapable but amorphous danger
  2. Feeling of defeat and entrapment
  3. Sensation of imminent doom.
PSY 3002-12 Evol Psychol & Med 2017-18
Emotion – ideas of Damasio
Bruce Charlton
Lecture suggests a general model for an important psychological mechanism of psychiatric symptoms which explains why psychiatric disorders have both emotional and social aspects, provides links to evolution, and a way of conceptualizing drug actions
  • Ideas of Antonio Damasio
  • Psychiatry and the Human Condition 
    Problem of psychiatry for me – understanding how drugs interact with behavior. How can eating chemicals make you feel better, function better?
    Emotions represent body states. i.e. Emotions are brain’s representations of the internal environment.
    Strength of emotions depends on body. These depend on brain representations of viscera & muscles, and this is a quantitative dependence.
    Example of fear/ anxiety
    One of the emotions is fear. This is relevant to the anxiety based forms of psychiatric illness.
    Fear can be conceptualized as a primary emotion
    Anxiety as a secondary emotion.
    Primary emotions are characteristic body states occurring in response to perceptions, for example the primary emotion of fear in response to seeing a tiger. Primary emotions occur in many animals even very simple animals.
    The primary emotion is a motivational state, a generalized disposition towards certain types of behavior rather than others eg a fearful animal is more likely to run away (or fight) than to seek food or engage in a mating ritual. A hungry or lustful animal has different priorities. 
    Secondary emotions and Cognitive modelling
    Secondary emotions are characteristic body states that occur in response to cognition, in other words they are body states enacted by cognitive modelling.
    Cognitive modelling means imaginatively enacting experiences – the imagining a tiger triggers the emotion of fear; imagining food stimulates hunger.
    So a secondary emotion would be the bodily state of anxiety that might occur in response to thinking about a tiger - in response to modeling in one’s own mind the situation of being attacked by a tiger.
    Because emotion is learned with event remembered. Laid down emotion is a somatic marker – body state associated with memory.
    Because the emotion experience is learned with the event – the laid down event is a Somatic Marker – i.e the body state stored as a memory. 
    Secondary emotions probably only occur in humans and other animals capable of conscious thought - such as chimpanzees.
    Evolved Strategic Social Intelligence – Probably the basis of ‘theory of mind’ (or ‘mind-reading’ so called) and explains why ToM problems associated with ‘mind blindness’ associated with autism (some brain damage) – leads to emotional problems.
    This evolved as an aspect of social intelligence – specifically Strategic social intelligence – about other people, other places, other times.
    This is (probably) the basis of the Theory of Mind (ToM) ability – and explains why ToM problems are associated with emotional deficits – as in Autism as a developmental disorder, or Asperger’s syndrome.
    Severity varies between extreme ‘mind-blindness’ – when emotional deficits prevent an understanding of here-and-now social situations (autism, brain damage eg right sided stroke) to more subtle deficits in social interpretation of past events, and planning of future interactions (Asperger’s, prefrontal cortex damage).
    The emotional state/ body state is the same for primary and secondary emotions - however primary emotions are triggered by perceptions while secondary emotions are triggered by cognitive modeling. This explains how emotions such as anxiety can occur even in the absence of stimulus.
    Secondary emotions enable us to do effective cognitive modeling and elicit the appropriate emotional response to what we are thinking about, which enables planning and good judgment.
    A model for psychiatric drugs
    Damasio’s ideas link the social behavior and emotions - because we use emotions to judge social situations.
    The nature of psychiatry: Emotion and social problems are probably the commonest features of psychiatric illnesses.
    Anything – eg. a drug - which changes the body state, or the brains perception of body state, may affect emotions.
    If a drug such as diazepam/ Valium blocks the physical changes of anxiety relax muscles - then body state change will be monitored by the brain and reduce the perception of anxiety.
    Standard Cognitive model
    Event leads to Perceptions, Event laid down in LT memory and resulting in behavior. Abstract, cognitive recall of the idea – That something happened.
    (Remember I was attacked by a tiger)
    versus Damasio’s Cognitive model including emotions
    Event causes Primary Emotion – body state/ emotion – these are laid down in LT memory Together, as a Package. The body state is the Somatic Marker of the event. When recalled, both the event and the associated body state are activated. The original emotion is re-experienced as a Secondary Emotion with the memory of the event. So we recall the events with its emotional context. We remember, and re-live the Experience of the event.
    (Remember being attacked by the tiger and it felt like this.)
    PSY 3002-13  Malaise theory of depression 2017-18
    Bruce G Charlton
    Reference -
    “Malaise theory of depression”
    An example of how an evolutionary hypotheses was discovered, developed and tested.
    Hypothesis – Malaise is one of several causes of depressive symptoms (‘depression’ on its own, or in context of immune-activiating illnesses, or the large/ loose category of Major Depressive Disorder);
    Malaise may also be a contribution to causing more severe Clinical Depression (e.g. melancholia/ endogenous depression and psychotic depression).
    Sickness behaviour and depression
    People with depression often feel ill, and say they are ill.
    Several symptoms of major depressive disorder are similar to ‘sickness behaviour’ – ie general behaviour characteristic sick mammal.
    Described by vet called Hart 1988 – fatigue/ reduced energy, somnolence (sleepiness), slowing (psychomotor retardation), anhedonia (esp eating and reproduction), pyrexia, cognitive impairment.
    Aches and other unpleasant physical sensations, caused by reduced pain threshold.
    I call this group of sickness behaviours ‘malaise’ = ‘feeling ill’ (like after flu or during glandular fever).
    Sickness behaviour is therefore an evolved adaptation to acute infectious disease – a behavioural state that is energy-conserving, risk-minimizing and immune-enhancing. Allowing short-term (few days) all-out immune attack on invading micro-organism.
    So, malaise is adaptive when present on average and in the environment in which it evolved – ie. beneficial in HG conditions where the causes of malaise were mostly short term infections.
    Sickness behaviour/ malaise is mainly caused by activation of the immune system, and increased blood levels of immune chemicals called cytokines. eg interferons, interleukins, TNFs etc – dozens of types and classification.
    Signalling molecules, secreted by cells involved in immune response e.g. white blood cells. .
    Much evidence of raised levels of cytokines in depression e.g work of Michael Maes over many years
    Cytokines also increase in autoimmune diseases (such as rheumatoid arthritis), and disseminated cancer, in which sickness behaviour may be sustained, and where depressive symptoms are common.
    How malaise may cause depressed mood
    Damasio model of emotions. Malaise is an emotion (rep of body state). Malaise is the brain’s representation of the body state of malaise caused by immune activation. Results in sickness behaviour. 
    Depressed mood is a mental response to this bodily state of malaise.
    Malaise depression is primarily a problem of the body, not necessarily the brain. ie. body change is primary, brain change is secondary.
    Treatment of malaise with analgesics
    Treatment of malaise is mainly with analgesics/ pain killers – since malaise is like the sense of feeling ill in flu or other infections.
    If ill with flu, or after flu, then various types of painkillers may make you feel better although not completely well. Alleviate not just pain, but unpleasant physical sensations such as aches, physical exhaustion.
    Tricyclic antidepressants (TCAs) are analgesics, especially amitriptyline. Used in cancer pain, palliative care, migraine etc.
    (Also studies suggest that some antidepressants may suppress immune activation.)
    Malaise and mood
    But improving malaise would not necessarily improve mood, because mood improvement might take days or weeks or not improve.
    Like recovering from flu or glandular fever.
    And mood may not recover – so treatment could be effective, malaise could be treated but a person could still fell depressed for other reasons.
    So drugs may relieve malaise, but not always mood.
    Antidepressants are analgesic/ analgesics antidepressant
    If TCAs are analgesic and potentially able to treat malaise then other analgesics should be also antidepressant in malaise states.
    Also anecdotal evidence that analgesics are effective in some types of depression – eg opium in melancholia, other opiates in studies in 1980s.
    Old and recent studies (in mainstream press, eg from Prof Bullman’s group at Cambridge) suggest aspirin and other anti-inflammatories may be antidepressant. 
    Some types of depression, may be an inappropriate or excessively-sustained type of malaise (malaise is the evolved and adaptive behavioural and psychological response to immune system activation).
PSY 3002-14 – Evol Psychol Medicine - 2017-2018
Bruce Charlton
Neurotic Depression and Seasonal Affective Disorder (SAD)
Daniel Nettle. Evolutionary Origins of Depression. Journal of Affective Disorders; 2004; 81: 91-102
Eagles JM, Seasonal Affective Disorder: a vestigial evolutionary advantage. Medical Hypotheses. 2004; 63: 762-72
Neurotic Depression
Nettle’s paper reviews several evolutionary theories of depression, considered mostly as the commoner (99%?), milder, non-hospital ‘depression’ that is characterised by anxiety and unstable emotions. (Not endogenous/ melancholic depression – hospitalised several months.)
Nettle’s theory is that the personality trait Neuroticism has a normal distribution in the population. Neuroticism is considered as in essence the degree of reactivity/ sensitivity of emotions to environment: high N is excess emotional reactivity, low N is insufficient.
Natural selection favours a middling level of N as most adaptive – but there are always people on each side of ideal, due to variations in heredity and environment.
Those people with a too-high levels of N may be diagnosed with a range of affective (mood) disorders, including depression and bipolar disorder type 2. (But not melancholia or bipolar type 1.) 
SAD - Winter depression/ blues, linked with treatment with artificial bright light therapy given in the mornings.
Increased incidence of depressive symptoms/ major depressive disorder during winter months (although ‘seasonal’ does allow for other times of the year – unlikely to be the same thing).
Pathology – Lack of early morning light in winter.  Humans evolved Africa +/-30 degrees latitude – similar day length in summer and winter. At extreme latitude day length varies widely between summer and winter.
Prevalence SAD varies from 0-10 percent, according to extremity of latitude (how far north or south). SAD seems to be caused by the shorter daylight period in winter – maybe also reduced intensity of light/ cloudy weather.
Natural selection for resistance to SAD
Acclimatization in individuals, worse recent migrants.
Longer-term adaptation of populations who have been at extreme latitude for many generations. Iceland) has lower prevalence of SAD than expected for latitude. Icelandic-descended Canadian/ Winnepegians lower prevalence of SAD than non-Icelandic Winnepegians
This implies some heritable/ genetic element – so SAD (or resistance to SAD) probably heritable.
In other words, extreme latitude causes reduced Reproductive Success in those who are not resistant to SAD. 
This theory says SAD is maladaptive; and implies susceptibility to SAD is gradually being selected-out of high latitude populations, but the process is still ongoing, has not finished.
Overall; Sensitivity to seasons is natural to original humans – extreme shortness of daily photoperiod may naturally cause pathology; but resistance to this has evolved in some populations present at extreme latitude for many generations.
Evolutionary theories…
Some, like the above, suggest SAD is maladaptive – a pathology – some find possible adaptive reasons for SAD in extreme latitudes.
  1. Hibernation. Similarity between SAD and mammalian hibernation; e.g. in bears. Increased appetite and weight gain, reduced sociability, demotivation and sleepiness. This theory suggests SAD susceptibility may have been adaptive – i.e. an advantage.
  2. Other SAD- advantage theories focus upon women and reproduction. SAD is commoner in women, especially in childbearing years
  3. Cycle of fertility. Humans typically have maximum births in spring – may be reproductive advantage, in terms of reduced infant mortality (increasing food).
SAD sufferers may tend to be hypomanic, hyper-sexual at time of conception (if this is a factor? – but probably not).
  1. Pregnancy. SAD may be helpful to pregnant women – rest, safety, eating.
    Some Other SAD maladaptive theories.
  2. Some cases of SAD may be malaise – due to higher winter incidence of viral infections such as colds and flu. Doesn’t fit with increased appetite and weight gain.
  3. In turn, there may be increased susceptibility to viral infections in winter due to insufficient levels of Vitamin D impairing the immune system. (How pale skin evolved for extreme latitudes to make vitamin D). Could be the cause of increased rate of winter infections.