PSY 3002-1 Evolutionary Psychology and Medicine
Bruce G Charlton
Important Note – The lecture contents define the syllabus – exam questions are based upon THIS YEAR’S SYLLABUS (which is not exactly the same as previous years)
PSY 3002 completed syllabus 9 December 2016
1. Evolutionary psychology – framework, assumptions etc. – Anxiety as example
2. Mismatch. Anxiety and Fear – six defences
3. Six defences continued. Causes of disease
4. Phobias, Hypo-phobia, Panic
5. OCD & PTSD
7. Schizophrenia and psychosis
8. Emotions, theory of mind
9. Delusional jealousy (and delusional disorders)
10. Neuroticism, depression and anxiety
11. Personality disorders – Borderline. Anorexia nervosa
12. Malaise theory of depression
13. Seasonal Affective Disorder
14. Life History, Lifespan and natural selection
15. Recent human evolution, effects of agricultural & industrial revolutions
16. Ageing and psychology
17. Ageing and memory, intelligence, personality
18. Evolution and Dementia – Vascular & Lewy body
19. Psychoactive drugs in modern life – pros and cons
20. Happiness and natural selection
Those don’t understand evolution by natural selection will need to learn ASAP.
Dylan Evans and Oscar Zarazate - Introducing Evolutionary Psychology. Icon Books (less than 2 quid on Amazon)
Other reading as we go – web available papers and other material.
That human nature was shaped, in some way, by natural selection.
Certain types of heritable behaviour (traits) led to greater reproductive success (more viable offspring) than other types of behaviour. And because these reproductively successful behaviors were heritable, these traits got more common with each generation.
This course – about the application of evolutionary biology to understanding human behavior with a focus on health and ‘medical’ aspects of psychology – such as psychiatry, and how evolved psychology effects health and lifespan.
That is, how human evolutionary history affects modern behaviour in ways relevant to health and illness.
Sources of evidence for Evolutionary theories – Include:
1. animal studies,
2. human observation and experiment,
3. brain correlates,
4. biochemical (eg hormonal) and genetic correlates,
5. human diseases (eg specific brain lesions)
6. history of human cultures and selection pressures
Philosophy – potential value of evolutionary explanations – cause/ prevention/ heredity/ treatment/ prognosis
How does natural selection affect human health?
- Robustness – how well made eg immune, systems
- Defence mechanisms activated too strongly
- Risky lifestyle leading to disease when excessive (eg anxiety, fatigue) or in inappropriate conditions, or differentials by age, or sex.
Context of Evolutionary Psychology
Natural selection is not really a scientific theory – it is too large scale an idea. Properly speaking it is a metaphysical assumption (i.e. an assumption about the fundamental nature of reality) which frames scientific knowledge. (See my paper.)
Charlton, BG “Reconceptualizing the metaphysical basis of biology” The Winnower
Natural selection is at most a partial explanation of human behavior, and evolved traits can be overridden by other factors – new environments may create maladaptive behaviour, disease – by definition – produces maladaptive behaviour. Eg parasites – fatigue; toxins change behaviour.
Not everything has evolved, not everything is an adaptation – many/ most things are just accidents. E.g. whiteness of bones
There are other things going-on as well as biology – e.g. ideology and religion.
Controversy: Religious, Political.
PSY 3002-2 Evolutionary Psychology and medicine
Bruce G Charlton
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
The effects of modern culture can overwhelm and hide the effects of evolved psychology – eg fashion in hair style, colour etc. often stronger than evolved psychology of attractiveness – eg fashions for grey hair, artificial colours in young women, short hair.
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.
Two big questions for Evolutionary Psychology
1. Could this specific trait be a product of natural selection?
2. (Even if it could be caused by NS); Is natural selection the main cause of this specific behaviour, in this specific animal, in this specific situation.
May be evidence to support or refute that this is a real and important trait; but typically it cannot be known for sure – so mostly we are dealing with hypotheses.
Evolution of Anxiety and Fear
Two papers for the first lectures
IM Marks, RM Nesse. Fear and Fitness. Ethology and Sociobiology. 1994; 15: 247-261.
Chris Cantor. Post-traumatic stress disorder: evolutionary perspectives. Australian and New Zealand Journal of Psychiatry. 2009; 43: 1038-1048
Theoretical background for evolutionary theory for those with a deep interest in fundamental issues - Charlton, BG. Reconceptualizing the metaphysical basis of biology (2016) The Winnower.
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)
Anxiety is an adaptation, a defence mechanism - but too much anxiety/ wrong situation is maladaptive.
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 is a defence mechanism: against predators, conspecifics (same species) and the environment.
Sometimes divided into Fight or Flight – we will use Cantor’s seven categories of fear
Many fears are non-associative – i.e spontaneous and innate. Evolved eg. fear of snakes, spiders, heights, the dark, of being alone, of strangers – 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.
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).
A hierarchy of 6 key defences to fear-provoking threats
2. Attentive immobility
3. Withdrawal (‘flight’)
4. Aggressive defence (‘fight’)
5. Appeasement (mainly for conspecifics/ same species)
6. Tonic Immobility (frozen, unresponsive)
PSY 3002- 3 Anxiety in an evolutionary context, and potential causes of disease
Refs – Cantor ref six key defences of Anxiety/ Fear already given
Charlton BG. Endogenous parasitism: a biological process with implications for senescence, Evolutionary Theory, 1996; 11: 119-124.
A hierarchy of 6 key defences to fear-provoking threats
8. Attentive immobility
9. Withdrawal (‘flight’)
10. Aggressive defence (‘fight’)
11. Appeasement (mainly for conspecifics/ same species)
12. Tonic Immobility (frozen, unresponsive)
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)
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)
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’):
4. Infectious (pathogens and parasites)
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 3002-4 – Evolut Psychol & Medicine 2016-17
Bruce G Charlton
Evolution of Phobias 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)
Anxiety and Fear related to some specific stimulus
Simple – Spiders, snakes, blood, heights
General – Agoraphobia, Social Phobia/ anxiety
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. May be mismatch, 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 – but this this is easy to miss unless looked-for.
First shown in relation to fear of heights in children.
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.
Fear of heights in children emerges when they begin to crawl – which make sense biologically.
‘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.
But - Against this is that adult panic may be silent – freezing, shaking, collapsing – which would not be an effective signal.
Panic doesn’t seem to fit closely with any of Cantor’s six categories.
A hybrid form of anxiety?
PSY 3002-5 Evolutionary Psychology and Medicine 2016-17
Evolution of OCD & PTSD
Brune M. The Evolutionary Psychology of Obsessive-Compulsive Disorder. Perspectives in biology and medicine, 2006; 49: 317-29.
Two common causes of disorder are 1. Mismatch; and
2. Hyper/ hypo/ inappropriate activation of evolved 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).
Behavioural: Ritualised, repetitive behaviours
OCD probably an exaggeration of an evolved, adaptive mechanism to ‘model’ cognitively the future consequences of present action.
All healthy humans have a harm-avoidance, risk-minimizing 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:
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 future 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 3002-6 Evolutionary Psychology and Medicine 2016-17
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
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.
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 3002-7 Evolutionary Psychology and Med 2016-17
Bruce G Charlton
Schizophrenia – did it evolve?
Brune M. Schiziphrenia – an evolutionary enigma? Neuroscience and biobehavioural reviews. 2004; 28: 41-53.
Probably more written about the evolution of schizophrenia than any other psychiatric disorder.
On the other hand, it may not have evolved – that is, in fact, what I think.
1. Definition of schizophrenia – sometimes very broad, and changing.
2. Prevalence of schizophrenia – the same everywhere and through history? Or a recent disease arising c 1800, and widely varied prevalence in modern times?
3. A genetic disorder/s – or disease/s caused by something like infection or a toxin?
What evolved? What is schizophrenia
Kahlbaum – Hebephrenia (‘Disorganised’ schizophrenia) characterised by thought disorder, disorganised speech, flat or ‘silly’ affect (mood), poor prognosis (decline).
Kraepelein – Dementia Praecox - Any chronic, deteriorating psychotic disorder – often dominated by hallucinations and paranoid (self-referential) delusions.
Bleuler – Schizophrenia ‘splitting’ of mind from reality.
Modern – >6 months; various subtypes including Disorganised
/ Paranoid/ Catatonic. Variable prognosis, but worse prospect than manic-depressive/ bipolar. .
Another factor was the separation of schizophrenia from cerebral syphilis – both mixed together in mental hospitals of 1800s, especially among men.
But syphilis first became diagnosable by microscope – then treatable by chemotherapy (salvarsan) then antibiotics (penicillin).
Depends on definition - most studies use broadish but chronic modern definition. Officially about threefold incidence from 0.2-0.6 percent. But evidence that schiz is becoming rarer in West over past decade or two; and probably no historical evidence of schiz before c1800.
Approx. 50% concordance in MZ twins, 15% in DZ twins, 10% siblings.
But most schiz have near zero fertility (30-70% reduced fertility on average) – so how could a relatively common disease have evolved if it reduces fertility?
? Mild schiz traits a reproductive advantage – no real evidence for this.
Failure to establish brain normal lateralisation – the usual differences between L and R hemispheres is diminished or absent in some schiz patients.
Could the emergence of schiz therefore be a necessary side effect of the genetic evolution of language/ lateralization? (Tim Crow)
Changes in fatty acid metabolism cause body changes, language lateralisation and schiz? (David L Horrobin).
Situation is confused.
Should we return to hebephrenia as the core diagnosis?
If schiz, is a recent disease, arising in Western nations c1800 and now becoming rare… implies did not evolve but has some cause related to the industrial revolution – a cause that is now disappearing. ?Lead
Compared with Catatonia
1. Schiz how not always possible to generate good hypotheses in evolutionary psychology.
2. Cata hypotheses are concerned with explaining the nature of a symptom, and its psychological and physical causes.
3. Schiz hypotheses are mainly concerned with the long-term rise of a common disease – with various symptoms.
In Ev Psych may be better to be more specific; and the most obvious questions are not always the best ones.
PSY 3002-8 Evol Psychol & Med 2016-17
Emotion – ideas of Damasio
Lecture is a general model of an important psychological mechanism of psychiatric symptoms which links to evolution - and a way of conceptualizing drug actions
– Ideas of Antonio Damasio
– Theory of mind delusions…
Problem of psychiatry for me – understanding how drugs interact with behavior. How can eating chemicals make you feel better, function better?
Basic model of cognitive psychology
Brain as information processing device – sensory input -> cognitive process -> behavioural output.
But 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 in viscera & muscles, and this is a quantitative dependence.
What about spinal cord transaction – can people still experience emotions? Spinal cord transaction impairs emotion – the higher the section, the more impairment.
How? Only a part of the body input of emotional states travels in spinal cord, others are in cranial nerves which enter brain stem above spinal cord. These provide inputs from upper body viscera and muscles of face; also from skull, mouth, tongue, throat. Also there are inputs from brain stem nuclei feeding back to higher levels of brain eg cortex.
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 and 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 are characteristic body states that occur in response to cognition, in other words they are body states enacted by cognitive modelling.
- 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.
- Secondary emotions probably only occur in humans and other animals capable of conscious thought - such as chimpanzees.
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 can occur even in the absence of stimulus.
Secondary emotions enable us to do effective cognitive modeling with the appropriate emotional response to what we are thinking about, which enables planning and good judgment. Probably evolved for strategic social intelligence.
1. Links the social behavior and emotions - because we use emotions to judge social situations. Emotion and social symptoms are probably the commonest problems in psychiatric illnesses.
2. Impairment of primary emotions - damage to amygdala may prevent appropriate fear in dangerous situations
3. Impairment of secondary emotions
People who cannot enact secondary emotions in response to cognitive modeling have poor judgment and planning, impaired social competence.
Examples include people with damage to the ventro-medial pre-frontal cortex who have a general inability to enact secondary emotions.
4. A model for psychiatric drugs
Anything 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, then body state change will be monitored by the brain and reduce the perception of anxiety.
If a drug such as chlorpromazine reduces the bodily state of terror, then the brain interprets this in terms of feeling calmer.
Explains why we enjoy reading novels – emotional responses to cognitive modelling. Predicts that those who cannot experience secondary emotions will not enjoy novels.
PSY 3002-9 Evolutionary Psychology and medicine – 2016-17
Bruce G Charlton
Delusional jealousy and delusional disorders
Chapter 4 - Psychiatry and the Human Condition – by Bruce Charlton
Delusional disorder is a psychiatric syndrome:
1. Delusions – false beliefs, strongly held
2. Non-bizarre/ plausible
In context of generally normal mood, speech, general behaviour; no hallucinations, catatonia, normal state of consciousness.
Ie. A normal person with a single delusional system that has a major effect on their behaviour, enough to come to psychiatric attention.
Secondary emotions, social intelligence, theory of mind
Social intelligence evolved in humans because social life is a major factor in reproductive success – understanding, predicting and manipulating the behaviour of others. But how?
By ‘theory of mind’ ie. by having accurate theories of what is in the minds of other people. We use our own emotional responses to model the emotions of others – eg their motivations, intentions, personality etc.
Eg (To simplify) If a person makes you feel afraid, then the inference may be that they are aggressive; if they sexually attract you then you may infer that they are being seductive etc.
Subject matter eg Persecution (man being persecuted by hostile group/ gang); Erotomania (women attracted to high status man, may never have met - and believes this is reciprocated); Morbid Jealousy (man believes his wife/ partner is being sexually unfaithful).
So, false beliefs about the minds of other people.
Jealousy as an adaptation
Jealousy found in animals where males contribute resources to offspring after birth. Adaptive to ensure that the offspring are his own and that he is not investing resources in raising offspring of other males.
Jealousy is intended to reduce the chance of sexual infidelity in a partner. If sexual infidelity was tolerated, if a man had the heritable trait of non-jealousy and his wife was unfaithful – he may have a double strike against his reproductive success:
1. Fail himself to reproduce – tend to eliminate his own genes
2. Actively assist the reproduction of another male – amplify the contribution of other genes
3. Context is that a woman may only have about six children, most of which will die without reproducing
Therefore, men are mainly concerned by sexual infidelity in wives.
Women may be less concerned about sexual infidelity than resources for the offspring – because the husband’s potential number of offspring is very high, but his resources are limited. May be more worried about the husband spending resources (time, money etc) on another woman, eg ‘falling in love’ - rather than the actual sexual infidelity.
(Although sex may lead to infatuation, or disease - competition.)
This reproductive difference may be some basis for the ‘double standard’ wrt. sexual fidelity – more tolerated in men than women.
Morbid jealousy syndrome
Jealousy may be adaptive under ancestral conditions on average and when in normal degree.
Excessive and or inappropriate jealousy of sexual partner – delusional when it includes a false belief in the sexual infidelity. An extreme of a normal mechanism.
Commoner in men, as expected.
Commoner in men of low self-esteem – their own low self-esteem, when used in cognitive modelling, tends to imply that the wife would also feel low esteem for them.
Commoner when men are less attractive than partner – eg after loss of status – eg loss of money, job, disgrace - or when wife is much younger and relatively more attractive. Cognitive modelling suggests that the wife would feel she ‘could do better’ then her current partner.
Extreme morbid jealousy may lead to violence to partner, or even homicide for sexual infidelity of wife. (Found in most tribal societies.)
Homicide would not be adaptive – but the threat or possibility of homicide may be, if it was to prevent infidelity.
Delusion may be immune to evidence because 1. Cannot prove a negative. 2. Can only infer what is in another person’s mind, eg their intentions – never be sure. 3. Gets suspicious if anyone else tries to persuade them of wife’s innocence – may be colluding with wife.
In general – we assume the intentions of others, and interpret their behaviour in the light of intentions. But intentions are inferred. And we use our own emotions to understand the intentions of others.
Therefore theory of mind, including errors in inference, is based on our ability to experience and model emotions.
Judging by inferred motivation is a general psychological mechanism – found in many fundamental beliefs e.g. about politics or religion.
PSY 3002-10 Personality Disorders – Borderline. Anorexia – 2016-17
Bruce G Charlton
Personality disorders – e.g Borderline; Anorexia and evolution
Martin Brune et al. Does borderline personality disorder reflect the pathological extreme of an adaptive reproductive strategy? Clinical Neuropsychiatry 2010; 7: 3-9.
Daniel Walsh, Bruce G Charlton. The association between the development of weighing technology, possession and use of weighing scales, and self-reported severity of disordered eating. Irish Journal of Medical Science 2014; 183: 471-5
About 50-80% heritability – for explanation see my book The Genius Famine (free online)
Borderline personality disorder
Concept derives from psychoanalysis – but has changed more than once over the past forty years:
Originally assumed to be patients on the borderline between Neurotic (psycho-analysable) and Psychotic (non-analysable – analysis makes them worse).
Became used as a shorthand for extremely troublesome and unstable patients who got worse with treatment, multiple parasuicides and threats of suicide, and created much work for mental health professionals and facilities.
Nowadays, a type of personality disorder that is characterised by e.g.
Overlaps with psychopathy/ sociopathy/ antisocial personality disorder especially in men; and hysteria/ histrionic/ narcissistic personality disorder especially in women.
Abnormal personalities rather than diseases. Present from teens, usually improve with age
Two oldest recognized types: Psychopathy (antisocial personality, Sociopathy) in men Hysteria/ Histrionic Personality Disorder in women
Psychopathy – (Cruel cold-hearted murderer). Lack of empathy, do not feel distress at pain and misfortune of others. Behaviours may include violence, crime, impulsivity, dishonest manipulation. Does not learn from experience - recidivist.
Histrionic – (Actress-like, Prima Donna) Attention seeking, seductive-provocative, creates emotional scenes, hot and cold towards people, manipulative.
Tend to respond to firm rules and limits, whereas psychotic patients usually respond to coaxing and distraction.
Perhaps: PSs may be result of some kind of heritable brain damage with multiple causes that used to be fitness-reducing in ancestral societies (when average fertility was high RS was mainly due to low child mortality)
– but now may be fitness enhancing under modern conditions (when RS is mainly due to higher than average fertility because child mortality rates are so low). E.g. psychopathic murderers seem to have enhanced fertility including rape; chaotic impulsive women may have high accidental fertility.
A syndrome mainly of women including food rejection – reduced food intake, reduced calories, induced vomiting and laxatives -> drastic weight loss.
Typically amenorrhea, anovulation – i.e. abolishes reproduction
In severe form has high mortality rate – probably about 5-10%
Clearly – the combination of abolished reproduction and high death rates make it very unlikely that anorexia is adaptive under modern
? Mismatch – the idea that the invention, improvement and spread of the technology of weighing machines may have been the trigger for anorexia (in a personality type that in the past would not have developed anorexia).
Hypothesis: Frequent accurate weighing leads to a focus on achieving ideal, or reducing, numbers – and emotional reinforcement - rather like a runner trying to minimise his timing, more and more.
So anorexia may be mostly a fitness-reducing artefact of modern technology.
(Compare with modern sub-fertility related t technologies of contraception and abortion, in absence of traditional-type religion.)
PSY 3002-11 Neuroticism,
Depression and Anxiety – 2016-17
Bruce G Charlton
Aka: same as Neurotic/ Reactive Depression, Dysthymia, David Watson - ‘negative emotionality’ – the tendency to experience strong negative emotions. David Nutt - ‘depression with anxiety’.
Extreme Neurotic/ Reactive Depression can be a type of ‘Clinical Depression’ ie. Severe enough depressive symptoms to seek or require specialist attention/ psychiatrist/ hospital.
Daniel Nettle. The evolution of personality variation… American Psychologist. 20016 61: 622-31
Major group of outpatient/ community psychopathology – people who suffer from psychiatric symptoms and often seek treatment.
Approx 15% of population at any one time.
Not an illness – much too common – implies a Mismatch i.e. what we call high N probably used to be adaptive under ancestral conditions.
1. An anxiety problem – treated with anxiolytics – ‘Valium’/ diazepam
2. A problem of depression: treated with antidepressants –‘Prozac’. (Mid 20th century psychostimulants such as amphetamine.)
3. Bipolar disorder – mood swings/ emotional instability – treated with ‘mood stabilizer’ cocktails.Same group as are the main focus for psychoanalysis, psychotherapy, counselling.
Roughly top 15 % population = approx 1 SD above average for Neuroticism.
High Neuroticism/ Neurotic depression is probably the commonest type of ‘depressive’ syndrome; but more like a personality type than an illness.
High Trait Neuroticism – N = ‘Big Five’ personality trait, derived from Hans Eysenck (1916-1997).
Neuroticism is an underlying personality trait/disposition which is; :
1. normally-distributed in severity;
2. substantially (not entirely) hereditary and genetic –
3. tends to peak in adolescence and decline in later life.
High/ Low Neuroticism:
1. Emotional, moody/ Stable, calm serene
2. Low-self esteem/ High self-esteem
3. Shy/ Confident
People high in Neuroticism often score mildly to moderately highly on depression and anxiety rating scales, and low on happiness rating scales. May suffer from panic, phobias and other specific disorders.
What is Neuroticism?
Eysenck conceptualised Neuroticism as a measure of limbic system (emotional) brain arousal.
Some people have a low-threshold of arousal – emotions trigger too easily – too moody; other have too high an arousal peak – chronic anxiety or depressive system.
But appropriate arousal is valuable – and low N may lack vigilance and wariness – exposed to greater dangers. Physical hazards may not be evident in modern societies but N may protect from e.g. predators, or excessive risk taking – Everest climbers low N. – c. 20 died last year.
Evolutionary aspects of Neuroticism
Disadvantages of excess N are obvious – would probably also apply in ancestral societies. But mismatch may increase the average level of N do to the new aspects of modern life – e.g. dense population, psychological stresses of planning and organisation, loneliness...
Daniel Nettle suggests that optimal Neuroticism trait may vary between societies and circumstances.
When excessive, N may be associated with psychiatric illness, poorer health, and impaired social interaction.
But Neuroticism may – in combination with other traits (intelligence, conscientiousness) – increase competiveness. Women with high N may have higher fertility/ birth rate.
Hypothesis: because optimal N varies according to circumstance, this maintains the characteristic ‘normal distribution’ of this trait; and as society changes over time, the average level of N optimal for R.S. may also change (and such change be inherited).
Also suggests that reducing anxiety with drugs – e.g. reducing emotional stability with Prozac, may be maladaptive.
1. Neuroticism is a personality trait
2. Anxiety/ Fear is an emotion
3. High trait Neuroticism is associated with higher levels of anxiety/ fear, and more sensitive triggering of anxiety/ fear.
PSY 3002-12 Malaise theory of depression 2016-17
Bruce G Charlton
Reference - hedweb.com/bgcharlton –
“Malaise theory of depression”
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 the general behaviour characteristic of a sick mammal.
Described by vet called Hart 1988 – fatigue, somnolence (sleepiness), slowing (psychomotor retardation), anhedonia (esp eating and reproduction), pyrexia, cognitive impairment.
I call this group of sickness behaviours ‘malaise’ = ‘feeling ill’ (like after flu or during glandular fever).
Sickness behaviour/ malaise is 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.
Sickness behaviour is therefore an evolved adaptation to acute infectious disease – a behavioural state that is energy-conserving, risk-minimizing and immune-enhancing. Temporary all-out attack on invading micro-organism.
So, malaise is beneficial to survival/ reproduction when present on average and in the environment in which it evolved – ie. for humans probably beneficial in HG conditions where the causes of malaise were mostly short term infections.
How malaise may cause depressed mood
Low mood is the 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.
Link this to Damasio’s conception of emotions – brain representation of body state. Malaise is the brain’s representation of the body state of malaise caused by immune activation. Results in sickness behaviour..
Treatment of malaise
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 will flu, or after flu, then painkillers may make you feel better although not completely well – different painkillers probably treat the effect of some cytokines but not others, and effectiveness will depend on the specific nature of cytokine changes.)
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.)
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.
Analgesics/ pain killers
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) suggest aspirin, other anti-inflammatories may be effective in depression.
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 3002-13 – Evol Psychol Medicine - 2016-2017
Seasonal Affective Disorder (SAD)
Seasonal Affective Disorder: a vestigial evolutionary advantage - Eagles JM, Medical Hypotheses. 2004; 63: 762-72
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).
Typical clinical picture varies in severity in a continuum, with symptoms such as:
1. Fatigue & Reduced motivation
2. Excessive sleeping (hypersomnia)
3. Increased appetite (carbohydrate) - weight gain
4. Reduced sociability
5. Some are somewhat hypomanic in spring-summer
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.
Texas 30 degrees N
Naples 40 N
Canada (most of population) 40-50 N
Newcastle 54 N
Iceland 65 N
Arctic Circle 66.5 N
Prevalence varies from 0-10 percent, according to extremity of latitude (how far north or south).
Commoner in women, especially in childbearing years
SAD seems to be caused by the shorter day in winter – maybe also reduced intensity of light/ cloudy weather.
Winter blues also perhaps caused by worsened or increased prevalence of malaise due to colds and flu.
Or SAD might itself be a cause of malaise? – however, increased appetite and weight gain in SAD are a distinguishing feature.
Acclimatization in individuals, worse recent migrants.
Longer-term adaptation of populations who have been at extreme latitude for many generations (eg Iceland) – seem to have lower prevalence than otherwise expected for latitude (eg Icelandic Winnepegians versus non-Icelandic. ie. SAD seems to vary by ‘ethnicity’.
This implies some heritable genetic element – so SAD (or resistance to SAD) probably heritable.
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.
In other words, extreme latitude causes reduced Reproductive Success in those who are not resistant to SAD.
1. Hibernation. Similarity between SAD and mammalian hibernation; e.g. in bears.
2. Cycle of fertility. Humans typically have maximum births in spring – may be reproductive advantage, in terms of reduced infant mortality (increasing food).
SAD sufferers tend to be hypomanic at time of conception (if this is a factor? – but probably not).
3. Pregnancy. SAD may be helpful to pregnant women – rest, safety, eating.
PSY 3002–14 Evolut. Psychology & Medicine 2016-17
Bruce G Charlton
Life History, health and lifespan
AJ Figueredo et al. The measurement of human life history strategy. Personality and Individual Differences 2013; 55: 251-255
Early example of work in 1982 on ‘Father absence and reproductive strategy…’ from P Draper and H Harpending.
Anthropological examination of different traditional and modern societies.
Whether the father was present or absent during a sensitive period in early (pre-pubertal) child development then led to different average mating and reproductive strategies in adolescence and adult life.
Males tend to be more aggressive and verbal; focused on winning male-versus-male status competitions, invest in mating effort and give little or no resource or time investment to their own (presumed) offspring (which may not be known, since such societies tend to be promiscuous among both men and women).
Females do not seek stable marriages, but usually a series of sexual relationships with males chosen on the basis of status, looks, dominance, charm (‘good genes’); and raise children with little or no help from father.
Therefore – Personality seems to be affected by childhood experiences during sensitive periods.
Life history theory describes the way in which organisms:
1. respond to differences in their perceived environment;
2. in order to allocate limited resources
3. between different possible ways of increasing fitness.
Life history has a range between:
Fast (r-selected): maximizing reproduction – numbers of offspring. Happens when environment is unpredictable.
Slow (K-selected): maximizing parental care, and longevity. Happens when environment is predictable and saturated with competitors from the same species – so only the most perfect organisms, with the best possible development, can survive to reproduce.
Fast maturing, quickly independent, early sexual activity
e.g. bacteria, many insects, many fish, frogs.
Slow maturing, need parental care, later sexual activity
Slower reproduction (longer generation time)
Longer lifespan, better health
e.g. humans and most primates, elephants, parrots
Humans are K selected species, but among humans there are differences in K-selection – faster and slower K life strategies. As with Father absence – switched to faster K.
Average health and lifespan affected by K
Higher K: longer healthier life, later sex and later first child, fewer sexual partners, later more stable marriages, fewer offspring, focus on investing in increasing quality rather than quantity of offspring.
In developed countries, modern humans are sub-fertile by choice – using contraception and abortion to prevent births. Many feature of ultra-high K.
But also increased early sex, promiscuity.
Suggests LH now applies to sex rather than reproduction.
But world population continues to grow mainly among those with lower K traits; so humans as a whole species are currently being selected for lower K.
Probably implies that average human lifespan will already or soon decline, child mortality will increase etc.
PSY 3002-15 Evolutionary Psychology & Medicine 2016-17
Bruce G Charlton
Recent human evolution - Effects of the agricultural and industrial revolutions on human psychology
Greg Cochran & Henry Harpending - http://the10000yearexplosion.com/
Ed Dutton and Bruce G Charlton – The Genius Famine (free online)
Bigger population means that beneficial mutations are more frequent.
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
Transition from hunting and gathering to agriculture; Perhaps the biggest change in human life in the history of the world.
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. 10-100x more calories per unit area (eg. acre or hectare) than HG. Led to denser populations, larger populations – also hierarchical/ unequal, specialized and co-ordinated populations.
Agriculture then became a new selection pressure on heritable psychological traits such as intelligence and personality. e.g. changes in diet, diseases and social structure. More planning needed. New technologies. Longer hours of work – repetitive, more gruelling.
Effects of Agricultural Revolution, probably:
Higher in intelligence
Higher in Conscientiousness and Agreeableness/ Empathising
More submissive and obedient
Less aggressive and violent
(More intelligent and ‘tamer’)
By 1800, first in England, signs of a new kind of society; further change in selection pressure.
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; greatly reduced child mortality rates all-round but especially among the poorest where child mortality had been close-to total - leading to rapid increase in English, then world population:
1300 – 4 million
1400 – 2 million (after Black Death)
1800 - 8 million
1850 - 16 million
1900 - 32 million
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.
Child mortality dropped from more than fifty percent to one percent in developed world – almost all babies born survive to adulthood, even when carrying damaging (but non-fatal) mutations.
Fertility rates (not mortality rates) drive population growth
Effects of Industrial Revolution
Poorer, less educated, lower in social status, less developed technology, more religious - expand as % population
Reduce average intelligence
Reduce average Conscientiousness
Conclusion: This is an era of very rapid evolutionary changes; natural selection mainly driven by differences in birth rates; and the heritable psychological traits of the most fertile replacing the heritable traits of the less fertile.
PSY 3002-16 Evol Psychology and Medicine 2016-17
Ageing and memory, intelligence, personality
Bruce G Charlton
TBL Kirkwood, RL Holliday. The evolution of ageing and longevity. Proc Roy Society Lond B 1979; 205: 531-46
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.
But repair mechanisms first need to evolve, and require resources to develop and run – and are themselves subject to accumulation of damage and ageing
2. Reproductive Success: Natural selection operates to optimize reproductive success, not life span – and beyond a point, 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.
3. Longevity: Humans are among longest lived animals because children take such a long time to reach independence and sexual maturity. (And this is probably due to K selection.)
To have about six children, and rear them to independence; women (and to a lesser extent men) need to be built to survive to about fifty years old (i.e. human have to be built to last up to about 70 years so that most will last until about fifty).
PSY 3002-17 Evol Psychology and Medicine 2016-17
Memory, intelligence, personality
Bruce G Charlton
Michael A Woodley et al. Possible dysgenic trends in simple visual reaction time … Mankind Quarterly 2014; 55: 110-124
To find this paper, search ‘Ageing and intelligence’ Link at Baron of Jesmond’s Aphorisms blog
Psychology of ageing
Memory – gets worse, in normal people
Intelligence – as measured by IQ tests, and by reaction time
Personality – as measured by self-rating questionnaire
Plus increasing numbers of people with dementia – cumulative, progressive degenerative generalized brain diseases increasing in incidence with age: tomorrow’s lecture
Brain effects of physical diseases (heart, lung, cancers etc.)
Increase prevalence of psychological disease esp depression
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.
4278, 53824 – 9536 – 85713 - 968241
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.
So a person at the top 15 percent for intelligence aged 20 (like many people in this room) might decline to the average intelligence of a 20 year old by age 63.
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)
Memory – gets worse, in normal people
Intelligence – gets lower as measured by IQ tests, and by reaction time
Personality – changes as measured by self-rating questionnaire
PSY 3002-18 Evolut Psychology and Medicine 2016-17
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
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%).
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 a extra decades (e.g. building a Rolls Royce costs ten times as much as a basic car).
‘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.
May 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 3002–19 Ev. Psychology and Medicine 2016-2017
Psychoactive drugs in modern life
Nesse, R.M, Berridge KC. Psychoactive drug use in evolutionary perspective. Science 1997; 278: 63-6.
Charlton BG – Palliative Psychopharmacology. Quarterly Journal of Medicine. 2013; 96: 375-8. Also at hedweb.com/bgcharlton
Contemporary human life is very different from the ecological and social environment in which humans evolved.
What is the role of psychopharmacology?
Negative: As a factor in generating mismatch – such that evolved behaviours become maladaptive?
Positive: In improving human health, happiness or R.S – eg. by treating mismatch, or treating diseases (especially the new diseases of modernity)
Negative effects of psychopharmacology
Drugs may mimic adaptive behaviour – e.g some types of drug addiction. Drugs that stimulate the meso-limbic dopaminergic system for drive, motivation (psychostimulants) or the opiate ‘pleasure’ system (euphoria, pain relief)
“Block negative emotions”
Drug may blog negative emotions such as fear or pain – but these emotions may be adaptive. Hence blocking negative but adaptive emotions may be maladaptive
e.g. alcohol of diazepam (valium) may reduce natural fear and encourage risky behaviours such as violence or bad driving.
SSRIs may reduce emotional reactions and reduce pleasure, or enable a person to continue in a job or a relationship when they would be better stopping – or fall out of love.
Pain – fatigue/ malaise may be designed to promote rest and recuperation – treating it may allow people to be active – but activity may delay or prevent recovery – exhaustion (similar to mania).
Therefore drugs may disrupt adaptive mechanisms – if symptoms are for a reason, then abolishing them would probably do harm overall.
But psychoactive drugs may also yield benefits e.g.:
Symptom worse than the disease – non-dangerous (non-fatal) disease like colds and flu. Relief of symptoms like high temperature, aches and pains.
Post-lunch sleepiness or long distance driving fatigue may be helped by caffeine.
Trade-off in chicken pox – antipyretics make patient feel better,, but lengthen illness by a day or two on average (because a high temperature inhibits the causative virus’s replication).
Symptoms due to mismatch with modern environment (eg. pain caused by surgery, panic when driving a car, extreme shyness)
Effects only adaptive on average - some defences set at very sensitive level with many false positives (excessive anxiety) – between individual variation.
Endemic illness in modern societies?
Presumably, under natural conditions a simple chemical would not be able to improve all round adaptive human behaviour – discuss why….
But our conditions are very far from natural; and what seems normal may be sick.
Large number of common illnesses which profoundly affect psychological variables such as mood, motivation and concentration . Examples would include upper respiratory tract infections; tension headaches; tiredness due to poor sleep; side-effects of prescribed drugs; hangovers from alcohol, drugs and tobacco; indigestion; hayfever and allergic rhinitis; backache, muscle and joint pain
If normal human condition is significantly sub-optimal, may be scope for psychopharmacology to improve the human condition.
What can psychopharmacology do to improve human condition?
Cure illness, alleviate symptoms and enhance function. E.g. Analgesia. Smart Drugs.
Drugs to treat mismatch – so people fit themselves to the rhythms and demands of industrial society – anti-anxiety, stimulants and sedatives.
Balance of risks and benefits?
Effective drugs always have side effects, and there is always a risk involved - as well as expense.
PSY 3002 – 20 Evol Psychology and Medicine 2016-2017
Evolution and Happiness
Bruce G Charlton
Nesse, RM. Natural selection and the elusiveness of happiness. Proc R Soc London B. 2004; 359: 1333-1347
NOTE – Natural selection cannot be the ‘bottom line’ explanation for human behaviour – because if the human mind is ‘merely’ a device to enhance reproductive success, then the products of the human mind (such as the theory of natural selection) would have no reason to be true.
Humans are not ‘designed’ (by evolution) to maximize happiness, but instead tend to maximize reproductive success.
Happiness is an emotional reward and incentive to perform behaviours that are adaptive and increase reproductive success on average in ancestral societies over many generations (eating, hunting, sex, caring for children etc.).
Happiness is temporary - we are designed to keep striving for happiness – it would reduce reproductive success if humans were able to attain a permanent state of bliss without doing anything, because then they would do nothing.
Therefore instinctive behaviours do not lead to increased happiness – and happiness has only approximate relationship to adaptive behaviours even in ancestral society. In ancestral societies seeking happiness was a reliable guide to reproductive success, and not much short-term versus long-term conflict; modern time short-and long term happiness are often in conflict.
The nature of ‘happiness’?
HG > Modern > Peasant
Most anthropologists seem to agree that Hunter Gatherer societies are the happiest overall. Corresponds to patterns of resistance, migration, child care etc.
H-Gs do not need to plan, they don’t usually work very many hours, usually get enough food of high quality (unlikely to suffer famines or starvation), they are usually fit and strong, there are not many infectious diseases, they have a light touch in bringing-up children, and usually they have enough to eat and can keep comfortable most of the time. People die of violence, predation, accidents, and diseases. Spiritual but no formal religion.
Agricultural societies are the most miserable, because most of the people are peasants. They are filthy (may never wash, may have fleas and lice etc.) and semi-starving nearly all of the time, with periodic actual famines – they are stunted by malnutrition and lack of protein. Suffer a lot from infectious diseases (caught from their animals, mostly) which may cause death and/ or chronic illness. Peasants sometimes work almost all of the time, backbreaking work – so they have endurance rather than fitness. Shelter may be very uncomfortable - cold, damp, draughty etc. Disease tends to be endemic, and in some societies people feel continually ill from chronic parasite infestation. Usually much less violence (per capita) than in HG societies. But such societies may be very religious with purpose and meaning to life, and their fulfilment may be religious and perhaps other-worldly.
Modern societies (post industrial revolution) based on growth - are probably somewhere in the middle. Nowadays - People work a middling amount of time (many do not work, but survive and can reproduce), usually have enough to eat, clean clothes, and comfortable shelter. Perhaps the most characteristic problem of modernity is ‘alienation’ feeling cut-off from life and alone. Spirituality/ Religion are feeble or absent. Life is perceived as meaningless and purposeless; people seek material goods, pleasure, distraction and unconsciousness (eg intoxication).
Modern reproductive success
Most striking feature of modernity is the disconnection of reproductive success from 1. Survival, 2. Health, 3. Happiness
This is because modern child mortality rates are low everywhere (now about 1% in developed countries, but used to be approaching 100 percent for the children of peasants, and probably about 60 percent for hunter gatherers) – so modern RS differences are almost entirely due to fertility differences.
Modern higher RS is increased by low intelligence, impulsivity, perhaps even psychopathy and criminality of some types – and the happiest and healthiest people have sub-replacement RS (considerably below 2 children per woman).
Therefore, modern RS may be increased by some types of genetic damage, and modern RS may cumulatively damage individual and social adaptations; maybe we can expect reduced happiness, health, longevity?
Value of evolutionary psychology
Helps us ask the right questions.
The usual media-type questions often make wrong assumptions.
So ‘why are we miserable’? is the wrong question, because it tries to explain the default state.
We are not designed to be happy all or most of the time.
Happiness is a specific motivation, so there need to be a reason to be happy, not a reason for not being happy.
And happiness is meant to keep us striving – so is designed to be temporary.
To ask what makes us happy and why, are better questions.
END OF COURSE - No More Lectures!