First EPSiG symposium on evolution and psychiatry

It was only a small meeting – by the standards of scientific symposia – barely 50 participants in one of the smaller lecture rooms donated for the purpose by the Royal College of Psychiatrists in London. But, as Randy Nesse pointed out, it was a miracle that it was there at all and, to his knowledge, there was nothing else like it in the international world of psychiatry. It was the inaugural symposium of the Evolution and Psychiatry Special Interest Group of the RCP, EPSiG for short, and it was held on October 4th. EPSiG’s leading lights, Riadh Abed and Paul St. John-Smith were supplemented by three heavy-hitting guest speakers: Robin Dunbar, Simon Baron-Cohen, and Randolph Nesse as the case for putting evolution at the foundation of all psychiatry was forcefully made. A recurring theme was the complexity of the social environment and how this interfaces with psychiatry and psychiatric conditions. All presentations were videotaped and hyperlinks that follow will lead to them on Youtube. And for those of you who would like to know more about what EPSiG thinks evolution has to offer to psychiatry, here is an excellent paper, co-authored by Abed and St. John-Smith.

Paul St. John-Smith kicked us off with a useful backgrounder for the un-initiated as to what thinking in evolutionary terms wasn’t (eugenics) and what it was – a meta-theory of psychiatry that provides a framework that helps define the role of various proximate factors in the causation of mental disorder. Hence, accepting the assumption that the human mind/brain has been shaped by selection over thousands of generations to solve the recurring problems of survival and reproduction can in itself provide a plausibility index that renders a whole range of hypotheses unlikely while pointing towards the possibility of others.

The challenge for evolutionary psychiatry, he said, is to move from general facts to evidentially well-supported specifics about the adaptive processes that shaped the mind and thus created the vulnerability to illness. It may be that there are many things about the evolution of the human mind that we will never know and about which we can only hypothesise. At its very best, however, it can aid the discovery of knowledge of why all our complex human psychological characteristics evolved, why we have vulnerabilities to illness and ultimately, what we might do about that in terms of prevention and treatment.

Since much anxiety, depression and general emotional disorder is rooted in our social lives we need to understand the complexities of social life in more detail – enter Robin Dunbar. Dunbar disarmingly reminded us that he can scarcely call himself a scientist at all, being a lapsed philosopher who got embroiled in psychology, and thence evolutionary biology. This is typical British false modesty because Dunbar’s enduring motif is the evolution of social behaviour and the social brain, a subject in which he has made many valuable contributions. Big brains equate with behavioural flexibility and the computation of social complexity. So when you plot brain size across the primates against social group size you get a nice linear relationship which predicts that the optimum group size for humans should be 150 individuals. This figure, thanks to Facebook, has become known as Dunbar’s number. And that 150 figure crops up wherever Dunbar has looked for it: from Neolithic village size to Domesday Book village census size and even to the operational divisions of the Goretex company and to Facebook friends. Even Christmas card networks tend to average 150 strong.

Social networks are really important for our health and happiness. Survival to 12 months following a heart attack correlates with social network strength as does stopping smoking. Within your social network there are concentric circles of influence and 60% of your contact effort is spent on only 15 people – it falls off as you approach 150 and outwards. Outside a network of 150, feelings of altruism to others plummet. There’s also a dynamic between friends and family – our networks tend to be 50:50 but people in big families tend to number fewer friends and vice versa. Women rely far more on talking to members of their social networks to prevent relationships dying – men rely much more heavily on joint activity. The average length of a woman’s phone call with a woman friend – even if she has just recently physically seen her – is one hour. The average length of a male-male phone call is 7.5 seconds! The time it takes to say “See you down the pub in 20 minutes!”

Light stroking triggers endorphins in the brain via dedicated un-myelinated neurons. PET-scanning human males (if you can show it in a man you can show it in anything) while they were subjected to light torso stroking from a partner causes huge endorphin release. It turns out that the size of your social network correlates with the density of endorphin receptors. Intensity of your social network also correlates with the area of your body it is permissible to touch. Humans should have to spend 45% of our time grooming – we clearly don’t – so we have invented powerful social mechanisms to stand in for it: laughter, ritual, music, dance and language which trigger the endorphin system just as well. Eating and alcohol increase endorphins so when you think you are an alcoholic it may be endorphins that you are addicted to! Social drinking leads to wellbeing and larger social networks and the same is true of social eating. And the arrow of causation goes from social eating and drinking, not that people with larger social networks eat and drink more together.

Are there limits to sociality? It is known, in humans, that theory of mind can extend to 5th order understanding of intentionality: Jack thought that X thought that Y thought that Z thought that A was a liar. Extroverts have bigger social networks but they are far less intense, while introverts are the opposite, but the social capital remains the same. Interestingly, psychiatry affects mind-reading. Higher order mentalizing is reduced from 5th order to 4 and 3 in bipolar and schizophrenic individuals. Mentalizing also relates to neuro-anatomy. Network size and mentalizing performance is predicted by the size of the orbito-frontal cortex, which is the last part of the brain to myelinate. Developmental experience is crucial here, these parts of the brain, because they evolve late, develop late, and mature late, may be very plastic in response to the social environment of upbringing.

Riadh Abed continued the theme of the social dimension of much psychiatric illness by showing how it is a fundamental part of an over-arching theory to explain schizophrenia. He set out out what he called the out-group intolerance hypothesis. 99% of our hominid history, he said, has been spent in close-knit groups, and, as per Robin Dunbar, this has sped the evolution of brain size and the “social brain”.

This led, over evolutionary time, to a distinction between in-groups and out-groups that has been blurred by the towns and cities in which much of the world’s population now congregates. This in turn has led to a crucial mismatch and the stress of this ambiguity is felt most by vulnerable individuals and where a genetic factor is evident, as in schizophrenia. The stress is imposed on cortical neurons in the social brain and manifests itself as an oversensitivity to the existence of strangers. Because of in-group solidarity, out-group paranoia is common and males are more likely to be ethnocentric and xenophobic and more likely to dehumanize an out-group.

It was once thought that schizophrenia was a universal trait, appearing at more or less the same frequency wherever you looked. But we now know, says Abed, that this is not so – variation in schizophrenia rates across the world can vary 55-fold. There is a lower incidence in traditional societies and an increased risk is associated with immigration which becomes elevated between the first and second generation immigrants. The urban environment is 30% of the risk and it seems that high levels of your own group density within an envelope of resident population are protective. Conversely, the larger the numbers of the majority host population living in the neighbourhood with a high density of immigrants, the greater the risk of schizophrenia among them. Poorly assimilated immigrants show increased risk and step-parentage may also be a risk factor, especially when it is short-term and early on in one’s life.

In schizophrenia the evaluation of social threats becomes overreactive and schizophrenia involves dys-regulation of systems that govern our relationship with out-groups. The “socialisation” hormone oxytocin has anti-psychotic effects and can correct these social deficits in schizophrenia patients. Oxytocin increases empathy to perceived pain in control subjects but not in schizophrenics but it does increase the accuracy of your recognition of kinship. Thus, oxytocin treatment may be of some value if given early on. The toxic element in the environment is the existence of perceived strangers – so it is a threat response. In conclusion, Abed theorizes that schizophrenia, therefore, is a disease of mismatch and recognizing this gets around the old arguments like “If it is genetic, and dysgenic, why hasn’t it died out?”

Simon Baron-Cohen has done a vast amount of research into “theory of mind”, the mentalizing deficits in altruism, the autism spectrum, and is the author of the “male brain hypothesis” which suggests that autism spectrum disorder lies at the extreme end of how the male brain works.

The prevalence of autism, he reminded us, has been increasing year on year and a diagnosis of ASD is currently given to 1 in 48 boys and 1 in 189 girls. This is not due to some unexplored etiological factor but by more professional eyes looking for it and better diagnosis. Autism runs right through the population and is massively polygenic and the fact that MZ twins can be discordant for it suggests epigenetic factors are involved. There are anatomical features: The size of the amygdala is increased in autistics; in autism the brain grows larger; and there is early brain overgrowth (reduced neural pruning during development) such that there are 65% more neurons in the frontal cortex of autistics while they tend to have a smaller corpus callosum. Diffusion tensor imaging reveals that autistics have more short range connections, therefore more connectivity.

There is a pretty much fool-proof test for ASD. If you estimate the length of time a subject spends looking at coloured balls versus a human face, if the eyes rest more than 70% of the time on the ball, the diagnosis of autism is 100% accurate. People with autism are much better than controls on the embedded figures test – recognising a cube in a complex geometrical diagram. And they tend to search for detail in a picture rather than concentrate on the big picture. So, while they have social deficits, high functioning autistics, or people on the autism spectrum, often have enhanced spatial faculties and a rapid understanding of fine (mechanical) detail.

Simon reminded us of the book NeuroTribes, by journalist Steve Silberman, which celebrates what he calls neurodiversity. There is no single way to become normal — we all have strengths and weaknesses and autism may be one example of such neurodiversity within the population. The term neurodiversity is attributed to an Australian social scientist Judy Singer who has autism. And it was Asperger himself who said that for success in science a dash of autism was essential! Math students are overwhelmingly autistic compared with controls, while scientists weren’t overtly autistic but did have a higher frequency of autistic traits. This association between math, science and engineering clearly has a genetic component, ASD kids are more likely to have engineering fathers and grandfathers. Simon’s team predicted that conurbations that disproportionately specialized in computing, engineering and IT would show a high rate of autism and so they compared Eindhoven (a major IT city and the HQ of the Philips electronic group) with control towns Haarlem and Utrecht. Sure enough, the rate of autism in Eindhoven was over 2 times that of the controls.

Baron-Cohen’s team developed a questionnaire which they administered to over 1,000 individuals, male and female, to examine where individuals sat on a grid measuring low to high for empathising ability versus systematising ability .The data he obtained showed that women were overwhelmingly represented in a quadrant of the grid which plotted high values for empathizing and low values for systematizing. Conversely, there were more men distributed where systematizing was better than empathizing. Male and female autistics plotted at an extreme quadrant of the plot, where values for empathizing were the lowest and systematizing the highest, representing an extreme of the male condition. This is the data that supports Baron-Cohen’s idea of the extreme male brain. So what may have been selected for by natural selection is not autism per se but a brain that is better at systematizing the world. We might imagine, from data like this, says Baron-Cohen, that evolution has favored one brain type over another for any number of evolutionary niches over millions of years. The autism spectrum with its abilities in spotting patterns, being better at innovation, but at the cost of understanding of social world, may be one of those niches.

Why do we get sad and what has that to do with the role of emotions in directing social interactions and expectations? This is the subject of Randy Nesse’s next book, and was the subject of his talk to EPSiG. He began with a forceful critique of modern psychiatry. There are deep problems with modern psychiatry, he said: Diagnosis is in disarray, diagnostic categories are not trusted, and they are frequently accused of being non-scientific. There is huge comorbidity among psychiatric disorders and huge and growing prevalence. Meanwhile the genetics that researchers expected to find is proving elusive, as are the brain lesions hypothesized to relate to various conditions. And the field is short of genuine breakthroughs in understanding causes and treating conditions. We’re muddling along – our foundations are shaky. In the words of one critical psychiatrist, George Engel, as long ago as 1961: “Psychiatry has become a hodgepodge of unscientific opinions, assorted philosophies and schools of thought, mixed metaphors, role diffusion, propaganda, and politicking for ‘mental health’ and other esoteric goals.” It’s just as true today, said Nesse, we still need a proper biopsychosocial model. Enter evolution.

Randy took the understanding of emotional disorders as his example. Here the world-wide problem is immense – ⅓ of all medical problems among women are down to unipolar depression, for instance, and a total of ⅔ can be put down to psychological problems – mainly emotional in origin. He reminded us that evolution does not shape diseases – there is no point looking for the adaptive value of schizophrenia for instance – it shapes vulnerabilities.

What is an emotion? Is it a point in a matrix of mildness to intensity, pleasantness to unpleasantness, or does it correspond to a basic list – every expert who has ever pontificated on emotion has a different one. Even reading Darwin, McLean or numerous authors in evolutionary psychology only added to the confusion. We cannot successfully explain emotion by relying on clean boundary definitions. We have to accept that evolution is messy even while it gets the job done. Emotions have nothing to do with happiness, per se, but are mechanisms refined by natural selection to pass on genes. So an evolutionary approach best lends itself to explaining how emotions increase fitness, how different emotions evolved, how were regulation mechanisms shaped, why are negative emotions excessive, and why can emotions be so irrational? Thinking about the long evolutionary trajectory of what we, today, call emotions can take you back to even interpreting sporulation or avoidance taxis in bacteria as being some kind of precursor to an emotional reaction and teaches you that emotions correspond to situations, not functions or brain loci; they have fuzzy, overlapping boundaries; and there is no distinct set of basic emotions.

Bringing in the social dimension, Randy reminded us that the vast majority of the emotions that greet us are not caused by hunger or injury but are social – such as loss, jealousy, and loneliness. That hope or anxiety can give rise to happiness or relief at a positive social outcome, or disappointment and sadness after failure, has been known since Plato and Cicero, there’s nothing new in the world, but old wisdom has become lost in a welter of neuroscience. You have to consider motivation – reading of Charnov’s marginal value theorem is essential for psychiatry. Mood affects motivation – causes it to fluctuate – and can prevent you wasting time against mounting odds and encourage moving on. But, when costs are greater than benefits for all available actions, it is best to do nothing, because getting trapped pursuing an unreachable goal leads to depression. Equally, although in 50% of the patients Randy has seen over the years, being unable to detach from an unattainable goal is at the root of their depression, in the other 50% genes, drugs, or inflammation may be the cause. And you have to take an inventory of a patient’s life circumstances because they can dictate whether or not they can function despite any particular psychological deficit, or whether that deficit overcomes them. Do they have social support, a job, children and/or family, a decent income, some ability, and love in their lives? The social context. Finally, negative emotions are so common because they are useful, either as examples of the smoke detector principle, because they are on behalf of our genes, not us, or because they are examples of mismatch with modern environments. So even if our “smoke detector” affect systems go off when they are unnecessary it does not mean that they are not normal – and we should be very careful, as psychiatrists, in switching the smoke detector off with pharmacology.

Finally, Dr. Agnes Ayton rounded off the proceedings with a detailed plea for evolution to be taken up in psychiatry training in medical schools, and a schema for how it could be developed and put increasingly in place, including incorporation in masters courses in psychiatry. Mainstream evolutionary medicine – in the form of the International Society for Evolutionary Medicine and Public Health – looks forward to developing further ties with EPSiG and to the day when it is not the only outpost in the world for the study of evolution and psychiatry.