Biography of Dr. John Scott Price

My flirtation with evolutionary psychiatry began in a prefabricated building in the south west corner of the plot which contained the old Maudsley Hospital and the new Institute of Psychiatry. We were the MRC Genetics Research Unit. Our director was Eliot Slater, who was not only famed for his work on twins, but also for his follow-up study of patients diagnosed as hysterical, and as co-author of the then main textbook of psychiatry Clinical Psychiatry. We were a small group. James Shields worked on the twins, and Valerie Cowie on mental handicap, with cytological help from Jacob Kahn. We also had a visiting scholar from Japan, Kazumoto Abe, and another from the USA, Leonard Heston. My own work was mainly in pharmacogenetics, but I also did some twin work. Having trained at the Maudsley Hospital, I was given an honourary senior registrarship at the hospital, and worked mainly in the Emergency Clinic, which saw urgent referral from GPs, and also saw patients off the street.

Eliot Slater was asked to write a chapter on genetics for a publication to be called Recent Developments in Affective Disorders, and he passed this duty on to me. I duly reviewed all the evidence I could find, but the conclusion was rather boring, in that there was a genetic component to most affective disorders, but no evidence as to its mode of action. I had been interested in evolution since my time at Oxford (reading PPP), and also I had heard Eliot Slater wondering whether the experience of auditory hallucinations might be adaptive for, say, Eskimos who needed to sit over a hole in the ice for hours at a time, waiting for a seal to appear, and I had heard him talking to Swedish colleagues about the incidence of schizophrenia in the far north, including, I think, the island of Bornholm. It seemed to me that affective disorders were so common, and so similar across cultures, that maybe they had some adaptive value, in spite of the fact that the depressed patients I saw in the Emergency Clinic did not look the picture of fitness. In that publication I explored several possibilities, such as the formation and dissolution of pair bonds, the periodic migrations of nomadic tribes, and the meeting of scattered communities at a central place at regular intervals, usually at the full moon. But the most likely candidate was the management of social hierarchies. These speculations were not well received, and lost me more than one post at consultant level, but I persevered, first of all updating my chapter for the newly formed International Journal of Mental Health. Then I noticed that the Lancet had a series entitled “Hypothesis”, and I wrote them an article on the social hierarchy theory.

Social hierarchy

Unfortunately, social hierarchy was not the flavour of the month, to put it mildly. In particular, human hierarchies, to the extent that they were recognised, were thought to be the result of civilisation, and bore no relation to animal hierarchies, which themselves were not well studied, and were even thought to be artefacts of captivity. So it seemed politic to express the theory, not in terms of hierarchy, but in terms of the behavior which led to hierarchies. Comparative ethologists had studied this well, and it was clear that in most species it was one-to-one fighting (agonistic behaviour) which achieved social rank. An even more striking discovery by ethologists was that this fighting behavior had been ritualised in most species, so that a fight was decided, not by an exchange of blows or bites, but by an exchange of signals. So, if the fighting was ritualised, so must the losing of the fight be ritualised, and there must be some ritual equivalent of the death or physical incapacity which the loser in a fight suffers. What could this incapacity be but depression? This explained why my depressed patients looked so unfit. They had a high correlation with fitness, but the correlation was negative. Would calling depressed patients losers add yet another stigma to their condition? We preferred to use the term “yielding” and called depression the yielding subroutine of ritual agonistic behaviour.

Depression in vervet monkeys and birds

As a result of my paper in the Lancet, Humphrey Knipe (co-author of The Dominant Man) drew my attention to some work on vervet monkeys who not only had hierarchies but appeared to get depressed when they fell in rank, and they also exhibited a conspicuous colour change, about which more anon. Also at this time I came across the work of Thorleif Schjelderup-Ebbe who studied social hierarchy in chickens and, amazingly, he described two types of depression in these birds, a mild depression in birds of low rank, and a severe depression in birds falling in rank. This was at a time when human depression was being classified into mild neurotic depression and severe psychotic depression. Of course it was impossible that a division into two types of depression could have evolved in the common ancestor of humans and birds, but it seemed quite possible that the nature of social hierarchies encouraged the development of two types of depression, one to keep the lower rankers down, and one to get the individual falling in rank to accept their reduced status. These findings of Thorleif Schjelderup-Ebbe had been published in German in 1922, but not in English until 1935. They were not well known, possibly because the observations were made by a lonely schoolboy in his holidays on his parents’ country place near Oslo, where he not only got to know the chickens individually, but realised that they knew each other individually, and behaved towards another chicken in a manner which depended on their relative social rank.

Around this time Eliot Slater retired and the Genetics Unit closed down, and I needed another job. Eliot Slater arranged for me to work as Senior Lecturer in the Department of Psychological Medicine in Newcastle upon Tyne, where his co-author of Clinical Psychiatry, Martin Roth, was professor. Shortly after I arrived in Newcastle Martin Roth was elected President of the newly formed Royal College of Psychiatrists (he was later knighted and became professor in Cambridge).

Blue skin

Vervet monkeys have a lot of blue skin, but most of it is covered by fur, However, the male scrotum is hairless and the bright blue colour is visible from almost every angle, and is interesting to other males who come to examine it. Brain and Gartlan reported that when a male vervet falls in rank, the bright blue fades to a powdery blue or sometimes turns completely white. This colour change takes about two weeks. I enquired what the colour is due to, and was told there was a blue pigment in the skin. This seemed interesting as it might reflect a reaction of melanophores, possibly mediated by some hormonal change in the blood supply.

So, with an MRC grant, I bought a vervet monkey and housed it in the only animal facility in Newcastle which was in the department of Professor Field, who was working on Jacob-Kreutzfeld disease in chimpanzees. The cage of my vervet monkey was housed in a corner of the chimpanzee cage, and to get to it I had to go in with the chimpanzees (fortunately in a lab coat, which saved my suit from being smeared with banana). With the Professor of Dermatology (Sam Shuster) we studied the scrotal skin, and also had electron microscopy by a colleague in Vienna. It turned out that there was no blue pigment (blue pigments occur in invertebrates but, so far, have not been found in vertebrates). The blue was a structural blue, which meant that the blue light was refracted by a large number of elements around the wavelength of blue light. These elements in the vervet were collagen fibrils (in the green frog it is guanine crystals seen through a yellow layer, in blue feathers it is tiny air sacs). The dermis had rows and rows of these fibrils, and in the deep dermis there was a layer of melanophores which absorbed most of the red light, so that, looked at from underneath, the skin was red rather than blue. Increasing the water content of the skin turned the colour from blue to white.

This was an exciting finding, because hydration of the genital skin is a common occurrence in primates, but it normally occurs in females in relation to their sexual cycle (those females do not have blue skin, at least in the genital area). A female vervet we studied did not have blue skin in the genital area, nor did she show any swelling in relation to her cycle. It seemed possible that two primate adaptations (blue skin and hydration of the sex skin) had come together in the male vervet, not in relation to sex, but to signal changes in power in the group.

The vervet skin turned out to be a versatile organ. Placed in a bath of saline solution, it could be turned from bright blue to white and then back again by altering the pH or the salt content of the solution. It could also be turned to black, a colour which does not occur in nature; in this case the dermis was transparent, and one was looking right through it to the layer of melanin in the deeper layers.

It was possible that there might be a residual, vestigial sensitivity to female sex hormones in the male vervet, but in spite of trying a range of female hormones in a range of doses, we could not detect any effect, not was the skin affected by cortisone. We were about to start investigating oxytocin and other polypeptides when our funding was stopped by the MRC on the grounds that our work was “out of line with current thinking”, meaning that depression was thought to be due to separation and not to changes in hierarchy. At this stage I decided to devote myself to the development of theory and to do more clinical work, so I left the CRC and went to work for the Oxford Regional Health Authority in setting up a psychiatric service for the new city of Milton Keynes.

Encouraged by my Canadian colleague Leon Sloman, I went to Milan to learn about the Milan style of family therapy, and realised that the family therapists were the only clinicians who were interested in hierarchy, particularly Jay Haley, who was interested in cross generational coalitions. Shortly after, a child and adolescent psychiatrist was appointed in Milton Keynes (Mary Ellis) and she too had studied in Milan. We then ran a joint clinic in which we would alternately see her adolescents with their parents and my patients with their adolescent children. This appeared to be very effective, but of course we had no control group. We continued this joint clinic for five years, and it was not only the most informative, but also the most enjoyable, part of my clinical work.

Clinical work

Most of my work was in the out-patient clinic, seeing patients referred by GPs, or in the patient’s home on “domiciliary visits”. Two things struck me about these patients. One was that many of them thought they were going mad, and the other was that their physical symptoms, usually due to stress of some sort, had been dismissed as unimportant by their doctors. I therefore told all my patients that they were not going mad, but rather suffering the effects of stress, and that these physical symptoms were real and severe. I tried to make sure that no patient left my consulting room thinking that I thought he or she was less ill than they thought they were. This was because the signal given by the depressed patient was of two sorts: one to rivals, saying “I am a sick person and no threat to you!” and the other to friends and allies (including their doctors), saying, ”I am out of action, do not send me into the arena to fight on your behalf”, and this latter message could be given with some force. To tell the patient that they were really ill made sure that they knew the message had been received, with the additional positive possibility that they would no longer need to send the message.

Writing to the patient

It was customary to write a letter to the referring doctor after an out-patient consultation, and it was my wife who said to me, “Why write to the doctor, why not write to the patient and send a copy to the doctor?” This seemed a good idea, so I got a grant from the Health Authority research fund, and employed a psychologist to visit the patients at home a week or two after the consultation. After doing a small pilot study, I randomised 50 new referrals to either a letter to the GP or a letter to the patient, only opening the randomising envelope after interviewing the patient, before the patient left the room. Two things might be of interest. One was that, knowing I had a fifty-fifty chance of writing to the patient, the interviews became more patient-oriented, and I was moved to see things more from the patient’s point of view. The second was that I was quite unable to be honest with the patient, and say, “We are studying the difference between writing to you and writing to the doctor, and you have been randomised into the group which does not receive a letter from me.” Instead, I told the patient that we were randomising patients into a follow up visit from a psychologist and no follow up, and so I was able to say to each patient that they had been chosen into the group to receive a visit. Otherwise it meant offering the possibility of a personal letter from me, and then denying it to them.

The psychologist reported that the patients liked getting the letter, and often showed it to spouses or family members, and some brought the letter to their follow-up visit to say that I had got something wrong. The only patients that did not appreciate the letter were the small number who were psychotic and those with somatising disorder (who were convinced they had a physical illness). There was one rather chastening result of this procedure: I had a whippet with me most of the time (who sat in the patient’s chair when it was empty) and, when asked what they liked most about the consultation, many patients said they liked having the dog there. The GPs I spoke to said they did not mind getting the copy of the letter to the patient – there were a few cases in which I wanted to tell the GP something that I did not want the patient to see, and then I wrote a covering letter to the GP, but this was only rarely necessary. Now in the UK it is standard practice to offer the patient a copy of the letter to the GP.

Liaison with colleagues

On the whole I think it would be true to say that my ideas on the relation of depression to hierarchical behaviour did not appeal to colleagues. My own fellow consultants thought I was crazy. Primatologists were not interested, although I gave a talk to the Primate Society. Others felt that evolutionary ideas were untestable, and people were recovering from the popularity of psychoanalytic ideas which were also largely untestable. Psychiatry moved in the direction of description and diagnosis (and the elaboration of Diagnostic and Statistical Manuals). Then attention was held by the new range of drugs, and now the move is towards sophisticated brain imagining and genomics. So there has been little enthusiasm for speculations about how or why these syndromes evolved.

My first evolutionary psychiatric colleague was Leon Sloman, who was a child and adolescent psychiatrist at the Clarke Institute in Toronto. He had the idea that depression magnified small differences in ability, and had therefore been important in the rapid expansion of the human brain. His idea was that when two people competed over some skilful action, the winner became enhanced and had an “adaptive cycle” while the loser became depressed, and entered a maladaptive cycle, and the features of depression made him more likely to lose the next contest and so he became less attractive to the opposite sex, less able to support a family, and so the minor difference in skill which had led him to lose the first contest had a large effect on his fitness. These adaptive and maladaptive cycles may have made a major contributing to the rapid expansion of the human brain

Then Russ Gardner wrote a paper for the Archives of General Psychiatry suggesting that hypomanic patients had the features necessary for leadership, such as energy, optimism, sociability, quick decision making and reduced need for sleep – so that the problem was not in their symptoms, but that they were not actually in a leadership role. Leon and I wrote a joint letter commenting favourably on his paper, and thence the ASCAP Society was formed (Across Species Comparisons and Psychopathology) and led to regular meetings and the publication of the monthly ASCAP newsletter which expressed our ideas informally and ran for 11 years, followed by the quarterly ASCAP Bulletin which ran for a further four years. Russ was Editor in Chief, and I was the European Editor, but the bulk of the work, and the creation of a friendly ethos, was due to Russ.

In the UK Michael Chance, an ethopharmacologist at Birmingham University, created a hedonic forum for the exchange of ideas, and Paul Gilbert, Professor of Psychology in Derby, got down to testing our ideas on patients and wrote important books on the evolution of depression. Dan Wilson came over from the US to take a PhD in anthropology at Cambridge; he told me, gratifyingly, that his father read my Lancet paper at breakfast and commented, “Here at last is a psychiatrist talking some sense!” Later we were joined by Peter Rhode, who in addition to his work as a Consultant Psychiatrist, had a practice in Harley Street, and by Mark Erickson, who was interested in the Westermarck effect, whereby children brought up in the same family at an early age develop an inability to form a romantic relationship, but instead have a bond of strong altruism. This applied to Mary Shelley and her creation of Frankenstein. With these colleagues I wrote several papers, one in the British Journal of Psychiatry and one in the Archives of General Psychiatry, and a historical review of our efforts for the free-access “Evolutionary Psychology”.

Revenge killing

It was brought to my attention that revenge killing was a major source of both death and conflict in present day hunter-gatherers and similar groups which did not have law courts to enforce justice. When a death occurred, the perpetrator was punished by the family and friends of the victim, which often led to feuds lasting years or even generations. How much more efficient it would be if feuds were settled by ritual agonistic behaviour, and the yielder became depressed. Imagine a group which has two powerful members who disagree about an important issue. If one kills the other, a feud is started. But if one makes the other depressed (perhaps by ridicule in the council chamber) the depressed person will be seen as physically ill by the group, and the cause of the illness is not likely to be attributed to the successful rival. This could not happen in animals, whose brains cannot conceptualise the idea of revenge, so that the capacity for depression would increase fitness in man more than in our animal relatives.

Redirected aggression

The redirection of aggression is common, even normal, in animals, and the aggression is always redirected down the hierarchy. So also, in humans, the sergeant “bollocks” the corporal, the corporal bollocks the private, and the private, if he is lucky, is able to take it out on the regimental cat. You do not bollock the sergeant who has bollocked you, if you do, you have magnified your trouble many times over. Likewise, the husband is reprimanded at work by his boss, and goes home and takes it out on his wife. These facts are well known, but not the general proposition that aggression is more likely to be redirected than other attitudes such as love. I can recall cases in which redirection has confused explorations of family life, for instance a son redirected his aggression against his father on to his fiancée, a mother who redirected her aggression against her own mother onto her daughter, and a father who redirected his aggression against his daughter to women pushing prams in the street.


The World Psychiatric Association recently established a Section on Evolutionary Psychiatry (Chairman Daniel R Wilson). With Dan Wilson I wrote a paper on critical learning periods for self-esteem and another on sex differences in the incidence of depression. Recently there was a meeting of evolutionary psychiatrists in Delmenhorst (Germany) organised by Martin Bruene, who has written a good textbook on our subject, and a report of our meeting. The fifteen speakers were each asked to nominate a promising younger psychiatrist who was then invited, so the meeting was a stimulating one. Hopefully these younger men and women will continue to stress the importance of an evolutionary perspective in contemplating human behaviour and its pathologies.