Evolutionary Psychopathology PDF - Textbook

12 Evolutionary Psychopathology and Darwinian Medicine Key Concepts evolutionary psychopathology Darwinian medicine pathogen aetiology pathogenesis trait variation immune system verification module smoke detector principle affective disorder...

12 Evolutionary Psychopathology and Darwinian Medicine Key Concepts evolutionary psychopathology Darwinian medicine pathogen aetiology pathogenesis trait variation immune system verification module smoke detector principle affective disorders social competition hypothesis schizophrenia personality disorders seasonal affective disorder FSD model Life on earth has existed in some form for well over 3 billion years. Given this lengthy period of evolutionary change, why is it that modern-day humans still suffer from colds, fever, morning sickness, personality disorders, anxiety and depression and the most serious of psychiatric illnesses – schizophrenia? Surely natural selection has had time to rid us of such problems? One of the ma- jor contributions that evolutionary psychologists have made in the last quarter of a century lies in reconsidering the symptoms of mental and physical illnesses in one of three ways based on a knowl- edge of evolutionary theory. They suggest that symptoms may be adaptations, they may be due to constraints on evolutionary processes or they may be due to a mismatch between our evolutionary heritage and our current environment. Our susceptibility to infectious diseases, for example, is now seen as a pathogen–host arms race that, due to the vast asymmetry in life cycle time and in sheer numbers, humans can never win. Darwinian medicine leads to the counter-intuitive conclusion that perhaps sometimes unpleasant symptoms should be left to continue because they are good for you. It is in the field of psychiatry, however, that evolutionary psychology may have its greatest impact as, for the first time, psychologists are asking why the propensity for mental illness is so widespread in our species. What Are Evolutionary Psychopathology and Darwinian Medicine? Evolutionary psychopathology and Darwinian medicine are overlapping but slightly different concepts. Psychopathology is the study of mental illness – so we can think of evolutionary psy- chopathology as the Darwinian approach to the study of mental illness (Baron-Cohen, 1997). Dar- winian medicine is also concerned with improving our understanding of mental illness by applying evolutionary principles but is somewhat broader since it also encompasses non-psychiatric health problems (Nesse and Williams, 1995). In recent years the terms ‘evolutionary medicine’ and ‘evo- lutionary psychiatry’ have also come into common parlance (Brüne, 2016; Gluckman et al., 2016; Nesse, 2019). In this chapter we will generally use the term ‘Darwinian medicine’ as shorthand for  316 Evolutionary Psychopathology and Darwinian Medicine Figure 12.1 Is there a mismatch between the lifestyle of our ancient ancestors and the lifestyle we have developed recently? evolutionary psychopathology, evolutionary medicine, evolutionary psychiatry and Darwinian med- icine. In addition to being concerned with improving our understanding of health-related problems, as we’ll see, proponents of Darwinian medicine have also considered how we might improve their treatment. We might ask how Darwinian medicine differs from conventional medicine. In essence, it differs in the same way that evolutionary psychology differs from the traditional social sciences – that is, whereas conventional medicine deals with the proximate questions of ‘how’ and ‘what’, Darwin- ian medicine is concerned with ultimate ‘why’ questions (Nesse and Dawkins, 2010). This means that evolutionists are interested more in why each health-related problem continues to exist today rather than in the mechanism of causation. The best way to understand this difference in approach is by example. In this chapter we will consider the evolutionary approach to understanding and treating illnesses – both mental and physical. In order to illustrate how evolutionary principles may be brought to bear in this area we begin with infectious diseases and genetic disorders before con- sidering serious mental health issues and personality disorders (Brüne, 2016; Nesse, 2012; 2019). Infectious Diseases and the Evolutionary Arms Race When we complain that we are ill with an infectious disease we are really saying that our body has become host to a pathogen which is causing us a number of unpleasant symptoms. Such pathogens include viruses, bacteria and other microbial parasites such as protozoa and fungi. Conventional medicine seeks to understand the aetiology (cause) and the pathogenesis (mechanism) of each  Infectious Diseases and the Evolutionary Arms Race 317 illness (McGuire et al., 1992; Troisi, 2020). Note that these are proximate levels of explanation – that is those that deal with how illnesses happen rather than why illnesses happen. From such a proximate level of understanding clinicians aim to develop treatments to help alleviate the symp- toms and destroy the pathogen. Darwinian medicine, however, seeks ultimate explanations for the symptoms of disease in order to aid treatment. The evolutionary approach asks why such symptoms exist – what function, if any, might they serve? At this point it is important to realise that the propo- nents of Darwinian medicine are not attempting to replace conventional medicine but rather that an evolutionary approach might be used to provide an overarching framework for understanding health and illness (Gluckman et al., 2016; Nesse, 2005; 2012). Recall from Chapter 2 that the evolutionary approach views the host–parasite relationship as an arms race conducted on an evolutionary time scale where each side struggles to gain the upper hand. Adaptations by one side lead to counter-adaptations on the other. One of the advantages of this approach is that symptoms may often be seen as adaptations. But therein lies a problem. Adapta- tions for which side of the equation – host or parasite? This question is not merely an academic one. Adaptations by the host are designed to destroy or expel the pathogen. Adaptations by the pathogen are designed to spread copies of itself to other bodies. Traditional medical practitioners tend to view all symptoms as pathological, that is, as problems which should be relieved (Nesse, 2012; 2019). Evolutionists, however, have suggested that many of our symptoms may well be defence mecha- nisms which have evolved to protect us (Martin, 1997; Gluckman et al., 2016). Perhaps we should concentrate on alleviating the symptoms which are designed to benefit the pathogen but allow the symptoms which are designed to kill it off to persist for a little longer. By allowing the latter symp- toms to persist we might, in the long run, speed up recovery. Specific examples of viral and bacterial infections will help to illustrate this point. Bacterial Infections Bacteria are single-celled microbial organisms. Many of them are free-living but others can only survive on or in the bodies of other organisms where they frequently cause debilitating symptoms. Bacterial infections lead the body to release a chemical called leucocyte endogenous mediator or LEM. This substance, in turn, leads to both a raising of the body temperature and to iron withdraw- al from the bloodstream (and into the liver – leading to a reduction of up to 80 per cent of blood iron). These events may sound like bad news for us – and in a sense they are – we tend to feel both listless and feverish. However, since bacteria require iron to develop and multiply and since higher body temperatures help to kill them off, these uncomfortable changes are exactly what the doctor ordered to dispel the invader. Unfortunately for the sufferer, what the doctor frequently does order is antipyretic (fever suppressant) drugs and iron supplements. In fact, most doctors and pharmacists don’t even realise that such treatments can help to maintain the illness (Nesse and Williams, 1995; Nesse, 2012). Although many of the unpleasant symptoms that we exhibit may have evolved to dispel the pathogen, there are others that are clearly adaptations of the pathogen to aid its transmission. In the case of cholera (Vibrio cholerae), for example, the severe diarrhoea that develops within hours of contagion helps to pass the parasite on to others (see Figure 12.2). The dehydration that stems from the diarrhoea can be fatal. The fact that cholera kills so many of its hosts might be viewed as a poor adaptation for the bacterium. It is passed on so quickly, however, that death of a host may not matter from the point of view of the pathogen. 318 Evolutionary Psychopathology and Darwinian Medicine Figure 12.2 Computer-generated illustration of the cholera bacterium (Vibrio cholerae). Box 12.1 Is Morning Sickness an Adaptation? Until quite recently, most clinicians have considered the early proneness to nausea and vomiting in pregnancy (NVP) as a non-functional by-product of a woman’s physical state at that point. In 1992, however, the medical researcher and evolutionist Margie Profit provided evidence that this ‘morning sickness’ may be an adaptation to protect the embryo from toxins and micro-organisms in food that might otherwise lead to deformities. Potential toxins are found in a wide range of plant foods such as cabbage, celery, oranges and bananas and micro-organisms can be common in meat. Such foods normally pose no problems to adults since the liver uses enzymes to convert the poisons in them into harmless substances which are excreted. Although the adult human is able to deal with these toxins, during its early stages of development the foetus is susceptible to them. Moreover, the mother’s own immune system is ‘down-regulated’ in order to stop her body attacking the perceived foreign tissue of the foetus. Profit has suggested that the problem is re- solved by the release of pregnancy hormones that lower the nausea threshold which is controlled by an area of the brain stem (the chemoreceptor trigger zone). This, in turn, makes women less likely to consume such foods and when they do so makes them more likely to vomit following their consumption. Profit’s theory is supported by the finding that women who show little or no sign of morn- ing sickness are far more likely to spontaneously abort their foetus than those who suffer from it (Profit, 1992). It is also supported by that fact that women are most likely to become aversive to meat during the early stages of pregnancy (Bjorklund et al., 2016; Sherman and Flaxman, 2001; 2002; Flaxman and Sherman, 2008). Rather than being merely an unpleasant side effect of pregnancy, NVP might in reality be a well-developed adaptation to protect the developing foetus.  Fighting Back – the Immune System 319 Bacteria may be uninvited microscopic guests but some pathogens are even smaller and decidedly simpler. As we’ll see when we consider viruses it is not always the case that symptoms aid only one side of the equation. Viral Infections If bacteria are microscopic then viruses are sub-microscopic, consisting only of a short strand of nucleic acid surrounded by a protein coat. Broadly speaking these pathogens may be subdivided into DNA and RNA viruses. The illness that we refer to as the ‘common cold’ is a rhinovirus which exists throughout the world in around 100 rapidly changing forms. This 20-sided (icosahedral) RNA virus enters the cells of the nasal passages where it rapidly reproduces asexually. New copies of the virus are then shed and released into nasal secretions from which they spread to others in their millions each time we sneeze. Clearly, the sneeze both expels the virus (which is good for us) and helps it to spread (which is good for the virus). We might ask who benefits from the behaviour of the host? The cold virus thus illustrates that in some cases symptoms might arise which benefit both host and par- asite even though such symptoms may damage others in the population (Clamp, 2001; Goldsmith and Zimmerman, 2001; Gluckman et al., 2016). Fighting Back – the Immune System If we have been locked in an evolutionary arms race with viruses and other pathogens for millions of years, we might ask what sort of long-term counter-measures have we developed? At some stage in our evolutionary history we came up with a master-stroke – we invented the immune system. To be more precise, our reptilian ancestors invented it and passed it on to all of their descendants. The part of the immune system that is found in the blood consists of an army of specially adapted white cells or lymphocytes. There are two main categories of these cells: B-lymphocytes, which are formed in the bone marrow, and T-lymphocytes, which develop in the thymus at the base of the neck. The immune system is activated by the entry of large foreign molecules known as antigens into the body. Antigens may be any large molecule such as a protein or a sugar. Given that pathogens have such antigens on their surface, their appearance in the body causes B-lymphocytes to secrete proteins called antibodies (antigen is short for antibody generator). These antibodies then circulate in the blood and bind (attach) to the antigens, marking them for destruction. When the surface of, say, a virus or bacterium has thus been ‘marked out’ by antibodies, it is then engulfed by other white blood cells called macrophages (‘eaters of large things’). The T-lymphocytes also aid the process in a number of ways. When a pathogen is detected T-lymphocytes begin to proliferate and form various sub-classes that both help in the attack of the antigen and aid the B-lymphocytes in their production of antibodies. Because antibodies can occur in millions of different forms, we each have millions of different types of antigens. This variability is maintained, in part, by sexual reproduction. Since sex increases the level of variability in the immune system (and, in particular, different types of anti- gens) as we saw in Chapter 3, such parasites have been used to explain the very existence of sexual reproduction (see the ‘Red Queen’ hypothesis in Chapter 3). The problem with developing a complex anti-parasite adaptation such as the immune sys- tem is that, of course, the parasites have hit back with their own adaptations. Some, like the bilharzia parasite, cloak themselves by attaching host cells to their surface so that they are ignored by the 320 Evolutionary Psychopathology and Darwinian Medicine immune system. Others, such as influenza viruses, are so virulent that they are passed on by the time the immune system kicks in. Such counter-adaptations illustrate once more that evolution is more of a treadmill than a ladder. HIV and AIDS – the Virus That Cheats the System? Since the 1980s we have seen the evolution of one virus which has cheated the system. This patho- gen does not attempt to avoid the attentions of the immune system, nor does it cloak itself, it simply attacks the immune system itself. The human immunodeficiency virus, or HIV, binds to the sur- face of the helper T-cells, gains entry and then destroys them. Since the helper T-cells coordinate the activity of the immune system, by taking out the T-cells HIV has played an ace card. Following contraction of HIV an individual may remain healthy for some time as new T-cells are produced to compensate for the death of others. Once T-cells are killed off at a greater rate than they are produced, however, the sufferer becomes progressively more susceptible to other pathogens such as bacteria, fungi and protozoa. Many of these pathogens are mild infections to healthy people but in the advanced HIV sufferer they are now able to multiply, causing serious symptoms. It is these secondary symptoms that medical experts call acquired immune deficiency syndrome or AIDS (see Figure 12.3). HIV and AIDS illustrate two important points with regard to host–parasite relationships. First, they show how our own behaviour can alter the evolution of pathogens – increased promis- cuity and intravenous drug use have favoured the development of this highly virulent virus. And second, they illustrate that we cannot win the host–parasite arms race outright but only gain a tem- porary respite with each bug. One final question that we might ask about infectious diseases is why is it that some path- ogens are so virulent and debilitating and others far less so? Evolutionist Paul Ewald (1994; 2002) has proposed that the virulence of a pathogen is strongly influenced by its method of transmission. Figure 12.3 HIV virus in the blood- stream.  HIV and AIDS – the Virus That Cheats the System? 321 Those that are passed on directly by personal contact, he suggests, should be less debilitating than those that are passed on by a vector (an organism that acts as an unwitting go-between). The rhino- virus, for example, is more easily passed on if it allows the host to remain active, thereby making contact with others more likely. In contrast, the protozoan that causes malaria (Plasmodium) is transmitted by the anopheles mosquito and can lead to a chronically debilitating state which there- by decreases the sufferers’ ability to ward off the attentions of these unpleasant insects. To put it crudely, killing the host may not matter as long as there are plenty of opportunities for the vector to take copies of the pathogen onto other hosts (Nesse and Dawkins, 2010). Each year up to 3 million people die of malaria, whereas the common cold is merely a mild inconvenience to most sufferers. Hence, an evolutionary approach may help to provide surprising insights into infectious diseases. Box 12.2 Genetic Diseases It seems inconceivable that our own genes can cause us to be ill. Surely selection pressures will have removed mutant genes that cause illness from the human genome? Such a conclusion may make intuitive sense – there is, however, clear evidence that certain genes which cause illness are maintained in our species because, on balance, they are beneficial. The first of these was dis- covered at Oxford University in the late 1940s and has subsequently become the classic biology textbook example – sickle-cell anaemia (Ridley, 1999). Sickle-cell anaemia causes the sufferer to have an abnormality of the red blood cells (they become sickle-shaped rather than round), leading to problems in oxygen transportation and a whole series of unpleasant symptoms such as general weakness, impaired mental abilities and kidney damage. The disease only occurs in individuals who have two copies of the sickle-cell gene – one from each parent. Sickle-cell anaemia is found in people who live in areas where malaria is common and a single dose of the sickle-cell gene conveys a degree of resistance to this disease. Since most individuals have only a single dose of the sickle-cell gene, then it is maintained in the population due to this advantage of resistance to malaria. Sickle-cell anaemia reminds us that the effects of a gene are always contingent on not only the environment, but also the existence of other genes in the organism. This argument is known to geneticists as heterozygous advantage. That is, when the condition of having two different alleles which confer an advantage is found in a population, then the pos- sibility of the homozygous condition will occur every so often (see Chapter 2). This homozygous condition may be either neutral or harmful. We can think of heterozygous advantage as a special case of the pleiotropy argument presented below. Today, some evolutionists consider that many of the mutations which are maintained in the population and cause problems (either in a single or a double dose) may be the price we pay for the beneficial effects of such genes on ourselves or our relatives (Martin, 1997; Ridley, 1999; Gluckman et al., 2016). In addition to the heterozygous advantage argument there is a second, probably more com- mon, way in which genes that cause damage to our health may be maintained in our species. If a harmful gene normally has its effects after the age of reproduction, then natural selection is un- able to remove it from a population. In this way inherited diseases such as Huntington’s chorea, which does not emerge until middle age, may be kept in the population. In Huntington’s chorea there is a progressive loss of motor control and eventual death. Huntington’s chorea is fortunately quite a rare condition, but it may be only the tip of the iceberg, as many other degenerative con- ditions such as Alzheimer’s and osteoarthritis might also be maintained in our species owing to 322 Evolutionary Psychopathology and Darwinian Medicine Box 12.2 (cont.) their late onset. It might even be the case that these late-acting diseases are so common because the genes which help to cause them may confer advantages early on in life. Perhaps people with the ‘genes for’ Alzheimer’s are particularly quick-witted in early adulthood – or perhaps they are more athletic than their peers. We really have not, as yet, even begun to look for such advantages. Figure 12.4 Microscopic view of sickle cells causing anaemia disease. Psychiatric Problems Although parasites may have played a very important role in human evolution, it is psychological rather than physical problems which have been of greatest interest to evolutionary psychologists. During its short history, researchers into Darwinian medicine have already considered a wide range of mental health problems including depression and anxiety, schizophrenia and serious personality disorders (including psychopathy; Brüne, 2016; Del Giudice, 2018). In short, all of the psychiatric problems that clinical psychologists and psychiatrists consider. We will consider each of these in turn. But first we need to consider, if natural and sexual selection promote positive changes, why ha- ven’t psychiatric disorders been removed from our species? An understanding of evolutionary theo- ry helps us to understand that we still contract colds because we are in an unwinnable arms race with pathogens – but surely the existence of psychiatric disorders cannot be explained away so easily? Why Can’t Evolution Rid Us of Psychiatric Problems? One of the pioneers of the Darwinian approach to medicine, American evolutionist Randolph Nesse (2019), has suggested six ultimate reasons as to why many modern-day humans have psychiatric problems:  Why Can’t Evolution Rid Us of Psychiatric Problems? 323 1. Adaptations have ‘trade-offs’ – that is some advantages can also have consequential disadvantages. 2. Environmental factors that cause psychiatric disorders may be novel when compared to our an- cestral past – that is there is a mismatch between current and ancestral environments (the mis- match hypothesis). 3. There are constraints to what natural selection can do. Among other factors this includes the fact that traits occur along a normal distribution curve, hence, those at either ends of the extreme will have too much or too little of a trait (e.g. anxiety). 4. Natural selection maximises reproduction not health. 5. Unpleasant responses such as pain and anxiety are useful in the face of challenges. 6. Pathogens evolve faster than we are able to in response to them (think of COVID-19). The last of these has already been flagged up and is not normally considered as a mental health prob- lem (although there are circumstances where it can lead to mental health problems such as when pathogens cause brain damage). Hence, here we restrict our discussion to the first five. We might label the first of these (‘trades-offs’) as the pleiotropy argument – that is, many genes have more than one phenotypic effect, so the negative effects of a gene may be maintained in a gene pool because the positive ones outweigh them. A variation of this argument is that the harmful genes provide a benefit when combined with other genes, but that sometimes such genes are found in bodies that lack the necessary ‘good’ genes. The second argument we could call the mismatch hypothesis – that is, humans have developed a lifestyle that did not exist in our ancestral past too rapidly for selection pressures to have led to appropriate changes (as we have seen, this is also known as the time lag; Gluckman and Hanson, 2008). The third point we might call the trait variation argument. This is based on the notion of a normal distribution curve. This means that within a given population, individuals may be plotted along various dimensions for physical traits such as height, weight and hair colour and for psychological traits such as level of intelligence and personality factors (e.g. extraversion and neuroticism). A large number of factors determine an individual’s position in the normal distribution of each characteristic measured. These include the combination of genes they inherit from their parents (sexual reproduction leads to unavoidable var- iation) and their life experiences. When such measurements are plotted for a population they gener- ally produce a bell-shaped graph – the normal distribution – with most people in the middle of the range and progressively fewer individuals as we move to the extremes. There are, for example, very few Einsteins and very few seven-foot men. Thus if, say, an emotional trait like anger has evolved in a species such as our own, then there will be some individuals who are found at the extremes of the distribution who have too much or too little of it for their own good (Triosi, 2020). Finally, we might group the fourth and fifth ones together and label them the compromise argument – that is, selection pressures act on inclusive fitness, not on perfecting psychological (and physical) devices. Hence, having children can be very telling on a woman’s health and having high levels of testosterone is useful in young men, but it also puts a strain on a man’s body which is one reason why women, on average, live longer than men. The pleiotropy, mismatch, compromise and trait variation arguments are having a growing impact on the early development of Darwinian medicine and should be borne in mind when consid- ering each of the topics discussed below. We considered moment-by-moment internal states which we call emotions in Chapter 11. In our discussion of psychiatric problems below, however, we are more concerned with pervasive and enduring emotional and mental states. 324 Evolutionary Psychopathology and Darwinian Medicine Anxiety – Why Worry? We all recognise anxiety – it’s a general feeling of apprehension about what might happen to our- selves or our loved ones. In colloquial terms we call it ‘worrying’. In some ways anxiety is one of the easiest psychological problems to explain within an evolutionary framework. Imagine the selective advantages that might accrue to the first individual to be born with a mutant allele which endowed him with the propensity to feel anxious in a population that previously lacked it. Right from birth he would want to attract his mother’s attention if she left him alone. Throughout life he would be wary of eating unfamiliar foods or approaching strange animals. He would surely fare much better than his conspecifics who, even in the jaws of a predator, remained perfectly calm. Clearly this is a simplification of how anxiety originally arose. It probably predates hom- inin evolution (Nettle and Bateson, 2012) and there are likely be a whole series of genes involved in endowing us with the ability to experience this state. But the point remains the same. As Nesse (2019) put it: [I]ndividuals with a capacity for anxiety are more likely to escape from dangerous situa- tions now and avoid them in the future. (71) When threatened, anxiety focuses our attention and prepares us for action in a way that would have been advantageous to our ancestors. The problem that needs to be explained, however, is why do so many of us have so much of it? One in seven American citizens will develop a clinical level of anxiety and even those of us who are not in this league on the anxiety scale have quite astonishing propensities to worry about all sorts of things. We worry about how good the weather will be on vacation; we worry about how well our soccer team is performing; we worry about what we should wear to a social engagement. Surely such trivial things cannot have fitness consequences? The Smoke Detector Principle Nesse and Williams suggest that in order to understand just why we worry so much we need to consider how the mechanisms that regulate anxiety are likely to have been shaped by selection pressures. They point out that there is a cost–benefit asymmetry associated with being over- or un- der-anxious. If you compare the fitness consequences of not feeling anxious when we should with the consequences of feeling anxious when we shouldn’t then it immediately becomes clear that we should err on the anxious side of the equation. Nesse and Williams call this the ‘smoke detector’ principle, where false alarms are cheap but ignoring a real warning might be deadly. In their words, ‘[T]he cost of getting killed even once is enormously higher than the cost of responding to a hundred false alarms’ (Nesse and Williams, 1995; see also Nesse, 2019). Interestingly, the smoke detector principle is supported by recent research which demonstrates that for people with a low level of anx- iety proneness long-term survival is reduced when compared with their more anxiety-prone peers (Mykletun et al., 2009; Bateson et al., 2011). Turning the question on its head, we might ask: if anxiety is so useful to us then why hav- en’t we evolved to be in a constant state of anxiety? The problem with this argument is that anxiety uses up time and energy, both of which might better be spent elsewhere. So, given a Pleistocene past teeming with predators, pathogens and competitive conspecifics, and where we had little control over climatic conditions, it may have made sense for our ancestors to have passed on a well-devel- oped ability to worry – but only up to a point. The fact that many of these pressures currently exist at a lower level in the West does not mean that our propensity to feel anxious can simply ‘unevolve’. Note that the smoke detector hypothesis is an example of a mismatch explanation.  Anxiety – Why Worry? 325 Even if we accept this line of reasoning, however, there are still those for whom anxiety is not just well developed – it is a debilitating illness or, as clinicians label it, a disorder. Can Darwini- an medicine explain this widespread phenomenon? Perhaps the trait variation argument can help us here. This is certainly the view of some evolutionists. In the words of two proponents of Darwinian medicine ‘Anxiety disorders, like disorders of other defence systems, are mainly disorders of regu- lation that entail excessive or deficient responses’ (Marks and Nesse, 1994, 69–70). In addition to this trait variation explanation we might also resort to the mismatch argument. One possibility is that some features of an anxiety disorder, for example, in agoraphobia (fear of leaving the home), the highly anxious feelings about leaving the home would have had a rational basis in our ancient past (Nesse, 2019). If, for example, an unpleasant close encounter with people from another tribe had caused you to retreat to a safe home base such as a cave, and if this was followed by a period of anx- iety that kept you there for some time, then this might, arguably, have been an adaptive response. Even- tually, it would have been necessary to leave such a base to forage for food, thereby breaking the cycle. Box 12.3 Obsessive–Compulsive Disorder – an Overactive Verification Module? Obsessive–compulsive disorder (OCD) is an example of a disorder, which according to Stevens and Price may be evidence of a verification module in our species, and one that can become overactive. Sufferers of OCD have two related problems (Berle and Phillips, 2006). First, they have obsessions – that is, recurrent thoughts and urges that cause anxiety. These may vary from being rather concerned that they haven’t locked the front door to, in severe cases, feeling that they might have knocked someone over in the car. Second, they have compulsions to carry out repetitive acts – for example, in the first instance going back to check the front door is locked two or three times or, in the second example, driving back five miles to check that there isn’t an injured person lying by the roadside. Other examples of obsessions include recurrent thoughts about health and hygiene – sufferers may consider other people to be unclean or have a conta- gious disease (and interestingly OCD sufferers who have a health and hygiene problem often also have an overdeveloped sense of disgust; Berle and Phillips, 2006). In this case the compulsion may involve a great deal of hand washing. Hence the obsessive thoughts lead directly to the compulsive acts, which then reduce them (e.g. hand washing reduces fear of contamination). Un- fortunately in the case of severe sufferers, the reduction in anxiety that is gained by performing the compulsive act is often short-lived and the obsessive thoughts frequently return. Official figures suggest that around 2.5 per cent of the population suffer from OCD, which makes it a very common disorder (Kring and Johnson, 2019). One way to think about OCD is that it may be an exaggerated form of a normal internal state and behaviour of our species (i.e. we might explain it via the trait variation argument). This means that it may pay all of us to have some concern about hygiene, especially when it comes to preparing food, which might other- wise contain pathogens. A person who had no sense of food hygiene would be unlikely to leave descendants. It may also pay us to show some concern about how we treat others – for example feeling guilt at times may stop us behaving in ways that might exclude us from future reciproca- tion (see reciprocal altruism; Chapter 8). Stevens and Price (2000) suggest that OCD may be traced back to maintaining healthy resources and to the preparation of weapons that might be used in warfare or hunting. Clear- ly, if you get these wrong it might have inclusive fitness consequences, but for some anxious 326 Evolutionary Psychopathology and Darwinian Medicine Box 12.3 (cont.) individuals such ritualised practices might become exaggerated. But how might we test this idea? Stevens and Price suggest that we can use a comparative method both by making comparisons with other species and with present-living forager societies (as described in Chapter 4). With regard to other species, Stevens and Price suggest that repetitive, stereotyped behaviour patterns are common including continuous grooming and cleaning when placed under stress or given little stimulation. In such cases obsessive (or at least excessive) preening in birds, hair pulling in cats and compulsive paw licking in dogs are well-documented behaviours when these animals are put under stress. Perhaps the existence of these ritualised patterns in other species suggests that the roots of OCD are quite ancient. As our species evolved we developed more complex ways of being anxious (as we are able to conceive of future events and worry about them). On balance these more complex forms of anxiety may have given our ancestors a selective advantage by developing into a ‘verification module’ (i.e. one that looks for things to worry about in order to avoid problems before they occur). But they may also have opened the door to the disorder in individuals that have this module at ‘the wrong setting’ (see ‘The smoke detector principle’). When considering present-living forager societies, in support of Stevens and Price, anthropolo- gists have recorded how hunter-gatherers take enormous care over their weapons and how they frequently have complex rituals before setting off on a hunt or to engage in warfare. This to Stevens and Price is evidence that we do have a verification module that prompts us to check and double check. If we add in the trait variation argument then some individuals who are prone to anxiety and have stressful life events may be led down the path to OCD and help to explain why 1 in 40 of our species currently suffers from this debilitating problem. Figure 12.5  Depression – an Epidemic of Modern Times? 327 If we still have such responses within our repertoire today then, perhaps, highly socially anxious encounters might lead some people to retreat to their homes for an extended period. The difference of course is that this might become extremely extended as other people can bring to us the things we need to survive today. Perhaps the novel environment of today does not allow us to break such a rewarding cycle of withdrawal due to social anxiety. Such explanations for prolonged anxiety (i.e. anxiety disorders) are rather presumptive. Since, however, our environment has changed so rapidly over the short period of cultural history, it is not unreasonable to suggest that our anxiety responses may well manifest themselves in enduring ways which may not have occurred in our past. To put it another way there may be a mismatch between the environment in which our anxiety responses evolved and our current post-industrial environment (Bateson et al., 2011; Nesse, 2019). Serious long-term anxiety is rarely an isolated psychiatric problem. In the words of clini- cians it shows comorbidity with another possibly more serious and debilitating problem – depression. Depression – an Epidemic of Modern Times? Depression is a very common mood problem which has been growing at an alarming rate since the middle of the twentieth century. Recent World Health Organization reports suggest that it affects 350 million people worldwide and that it is currently the world’s third most common cause of morbidity (WHO, 2008; 2012). Psychiatrists and clinical psychologists distinguish between endogenous/clin- ical depression and reactive depression. Reactive depression can be very severe but is considered to be a normal response to life events that would make anybody unhappy, such as bereavement or disappointment. Clinical or endogenous depression, however, is either considered to be unrelated to life’s events or is seen as an overreaction to them in its depth or longevity. Psychologists lump all clinical levels of depression together with serious mood disturbances as ‘affective disorders’ (Kring and Johnson, 2019). The two main sub-categories are unipolar disorder and bipolar disorder. In uni- polar (sometimes called major) depression there are generally alternating periods of depression and of relatively normal mood, whereas in bipolar disorder (sometimes called ‘manic depression’) there may be alternate bouts of mania and depression which may be separated by periods of normal mood. Around 1 person in 100 is diagnosed as having bipolar depression (Dawson and Tylee, 2001; Ustun and Chatterji, 2001) and onset is usually during their late twenties. During the manic phase there are periods of euphoria and high energy where grandiose plans may be conceived. A slightly less extreme form of mania known as hypomania may also occur. Money may be squan- dered, sex drive is often very high and sleep may become rare. At its extreme, mania may lead to delusions and hallucinations. Frequently, following a period of mania or hypomania the sufferer be- comes exhausted. This exhaustion is frequently followed by a brief period of relatively normal mood before depression sets in. When depression does set in, however, it is usually severe. Rare indeed is the individual who has never experienced some form of depression as a reaction to disappointment or bereavement. But for the bipolar depressive the sense of bleak hopelessness is so severe that one in eight succeeds in suicide. Unipolar depression is far more common with at least 5 per cent of the population suffer- ing from it at some stage (Kring and Johnson, 2019). Average age for onset is around 40 and it is far more frequently diagnosed for women than for men. Unipolar depression is frequently associ- ated with feelings of sadness, lethargy and social withdrawal. Sufferers may be preoccupied with thoughts of death and suicide, but are statistically much less likely to kill themselves than sufferers of bipolar depression. Again, like anxiety, depression is such a frequent problem for our species that the possibili-  328 Evolutionary Psychopathology and Darwinian Medicine most researched area by proponents of Darwinian medicine. Given that a depressed person appears to be acting in such a maladaptive way, how might evolutionists explain this problem? Although evolutionists have argued for some time now that depression serves a function, it is only in quite recent years that a number of specific models have begun to emerge as to what that function might be. In their review of evolutionary explanations for this debilitating problem, Michael McGuire and Michael Raleigh of UCLA and Alfonso Troisi of the University of Vergata in Rome have identified three types of model which have been developed by evolutionists to explain depression. These are represented in Table 12.1. Given the sheer amount of theoretical work that has taken place into the relationship be- tween evolution and depression, it is beyond the scope of this text to discuss all of the models Table 12.1 Evolutionary models of depression Models emphasising ultimate Models emphasising Models emphasising ultimate– causes developmental disruption proximate cause interactions (1) Depression is an adaptive Infants have normal genetic (1) Decline in social status model. trait. Views depression as an information for development but Depression is due to a fall in adaptive response to adverse some form of disruption leads status or inability to rise in social conditions. It has, for example, to depression or an increased hierarchy. Note that this model been considered as a response to vulnerability for depression. overlaps with the depression as an the intolerability of low social adaptive trait model. status which then prevents a person from challenging high- status individuals. (2) Pleiotropy explanation. Examples include effects of toxins (2) Failure to resolve interpersonal Genes that increase inclusive on the developing foetus such as conflict model. Depression fitness (for example, genes alcohol intake by the mother. results from a failure to resolve for attractiveness or creative conflict with regard to dominance thinking) may also lead to a state relationships. Depressive state of depression as an epiphenom- enables individual to accept defeat. enon. (3) Trait variation explanation. Adverse social effects may also (3) Response to loss model. Depression may be due to the be included in this model such as Depressive state is a reaction to chance effects of genetic mixing rejection by mother at an early interpersonal loss. Again fits in well that occurs at conception. age. This model is similar to with other psychological models more traditional psychological but includes a consideration of the explanations for depression such evolved neural hardware. as behavioural or psychoanalytic in that abnormal upbringing may be a key feature in increasing the likelihood of a disorder developing. Source: McGuire et al. (1997).  Depression – an Epidemic of Modern Times? 329 presented in Table 12.1 in detail. However, there are a number of points that can be explored in relation to these models. In particular a number of the arguments presented in Table 12.1 draw on an influential evolutionary theory of depression that has been around since the 1960s (see below). The first point to consider is that these explanations are by no means mutually exclusive – an individual, for example, might have developmental disruption and problems due to a loss and low social status. In this case then it would be surprising if they did not develop some form of depression. Also, since the form and intensity of depressive symptoms vary greatly between indi- viduals, it is possible that different sub-types of depression (such as uni- and bipolar depression) are related to different explanations. It is also worth pointing out that a number of these separate models of the ultimate cause of depression overlap to a large extent. The ‘depression as an adaptive trait’, the ‘failure to resolve interpersonal conflict’ and the ‘decline in social status’ models are all related to a lack of social standing. In fact all three of these models draw on the long-term work of British psychiatrist John Price. The Social Competition Hypothesis Long before the advent of Darwinian medicine, John Price argued that mood, in general, plays an important role in human status hierarchies and that this may be related to the social conditions of our early ancestors. More specifically, he suggested that depression is often observed in individuals who are unable to win a hierarchy struggle and yet refuse to yield (Price, 1967; Price et al., 1994). Price calls this the social competition hypothesis of depression. This hypothesis is based on the notion that we share with our ‘more primitive ancestors a mechanism for yielding in competitive situations’ (Price et al., 1994). According to Price, this is an involuntary subordinate strategy which serves to inhibit aggression, provides a signal that there is no threat and thereby expresses ‘volun- tary yielding’. Such an internal state and overt behaviour may serve to terminate conflict and allow for reconciliation. Price and his co-workers consider that when the voluntary yielding fails to occur then the state of depression, which would otherwise be transient, develops into prolonged depressive illness. Perhaps in today’s society we are unable to express such voluntary yielding and the normally transient state of depression often develops into a long-term problem which may have been rare or non-existent in our ancient ancestors. This is another example of a mismatch explanation. As we will see below there may be other reasons why long-term and more frequent states of depression are so common in today’s society. Price’s model certainly fits in with the notion discussed in Chapter 11 that feeling sad cre- ates the urge to withdraw from action (Fredrickson, 1998; 2013). But is there evidence to back it up? Depressed Monkeys? If the social competition hypothesis is correct and depression arose some time ago in our evolu- tionary past then we can predict that other extant primates will exhibit homologous responses. We might also predict that they are likely to share with us common proximate mechanisms for this state. McGuire, Raleigh and Troisi have uncovered evidence of a relationship between mood and status in vervet monkeys, which is mediated by the neurotransmitter serotonin. They discovered that alpha (highest-ranking) males in each group had levels of serotonin which were twice as high as in low-ranking subordinate males (Raleigh and McGuire, 1991). Such males can easily be identified 330 Evolutionary Psychopathology and Darwinian Medicine Figure 12.6 Three vervet monkeys (Cercopithecus aethiops), including a dominant male with blue testes. as they have remarkable bright blue testicles (see Figure 12.6). When such males lost their position, however, their serotonin levels fell dramatically (McGuire et al., 1997). At the same time their be- haviour altered. Whereas they had previously appeared ‘confident’ within their groups, they now huddled up and rocked back and forth refusing to eat (and their testicles lose their lustrous blue and become grey). In fact their behaviour was remarkably similar to that of a seriously depressed human (bar the change in testicle hue). Interestingly, these behaviours were removed when the monkeys were given the antidepressant Prozac (a selective serotonin reuptake inhibitor or SSRI) which boosts serotonin levels (McGuire et al., 1997; McGuire and Troisi, 1998). And, incredibly, they also discov- ered that when the alpha male was removed from a group and another randomly chosen male was given Prozac, the latter became the new alpha male in every case! The fact that in one of our primate relatives, the vervet monkey, there is a relationship be- tween status, a neurotransmitter known to be involved in depression and an apparent depressive state adds weight to Price’s social competition hypothesis in humans. Arguments about human internal states based on other species (even primates) are frequently criticised on the grounds that we are fundamentally different. In this case, however, there is also supporting evidence from human studies of the relationship between status and serotonin and mood. Machiavellians and Moralists Some studies of human social behaviour label males as either ‘Machiavellians’ who are relatively aggressive and competitive individuals or as ‘moralists’ who, in contrast, are more deferential. For Machiavellians social rank and serotonin levels are positively correlated, but for moralists there is a negative relationship between social rank and serotonin (Madsen, 1985; Madsen and McGuire,  Depression – an Epidemic of Modern Times? 331 1984). Put simply, in our own species, as in vervet monkeys, there is evidence that pushy high-status males have high levels of serotonin. Given that low levels of serotonin are known to be related to many cases of depression (Ray, 2018) then this finding might be taken as further support for Price’s social competition hypothesis. We need to bear in mind, however, that this evidence is indirect since the findings for Machiavellians and moralists were not concerned with levels of depression. Currently the social competition hypothesis appears to have some experimental support and may help to explain many cases of depression in an evolutionary context. Perhaps one of the functions of serotonin is to mediate status hierarchies with low mood being an adaptive response to failure to gain status. The social competition hypothesis is unlikely to explain all cases of depression of course. It might even be criticised on the grounds that, with its emphasis on competition and sta- tus, it is a male-centred view of depression. Women do, however, also compete for status, albeit in a less overt way than men (Cashdan, 1996; Campbell, 2002; 2006; 2020). If the social competition hypothesis does help to provide insight into the ultimate cause of some forms of this debilitating illness then Darwinian medicine might help clinicians to identify potential cases of depression. Is Depression Becoming More Common? It is a commonly held belief that depression is on the increase (see earlier). But does this notion stand up to scrutiny? In fact a number of longitudinal studies suggest rates of depression have been rising with each subsequent generation since the 1930s (Hidaka, 2012; Twenge, 2015). Furthermore, and perhaps counter-intuitively, rates of depression were found to be higher in the richer societies than in the poorer ones (WHO, 2008; Hidaka, 2012; Twenge, 2015). So why is it that more of us, in the relatively comfortable and materially successful West, are becoming depressed? One way that evolutionary psychologists have explained this problem is by proposing that certain novel aspects of modern life, which would not have occurred in our ancestral past, currently increase the likelihood of depression. Back in 1995 Nesse and Williams suggested that two particular novel aspects of our environment might help to explain this – mass communication and disintegration of communities. One result of mass communication, according to Nesse and Williams, is that it effectively makes ‘us all one competitive group’. This is particularly true of television and films, they argue, since, whereas in our ancestral past we would have compared ourselves with others in our relatively small forager group, today we constantly compare ourselves with images of the most successful on earth. If we are consistently bombarded with images of the rich, the beautiful and the talented then in comparison our own abilities pale into insignificance – so the argument goes. If our perceived status is based, as the social competition hypothesis would suggest, on how we view ourselves in comparison to others around us then this could lead to depression. Furthermore, we may also feel that our partners are less attractive when we compare them to such glamorous images, which may also make people feel dissatisfied and more prone to depression. This may be rather a speculative explanation for the rise in rates of depression over the last century but there is some empirical support for it. Evolutionary psychologist Douglas Kenrick found that if you expose individuals to photos of, or stories about, desirable potential mates they will thereafter decrease both their com- mitment to, and ratings of, their current partners (cited in Nesse and Williams, 1995). Perhaps mass communication helps to emphasise our lack of perfection and that of our partner when compared with the unrealistic images brought into our lives on a daily basis and this, in turn, leads to an in- crease in rates of depression. With regard to disintegration of communities, Nesse and Williams suggest that in recent years ‘[e]xtended families disintegrate as individuals scatter to pursue their economic goals’ (Nesse 332 Evolutionary Psychopathology and Darwinian Medicine and Williams, 1995, 12). According to them the worst punishment that can be meted out to a human is to live in solitary confinement. And yet, because of the disintegration of the extended family (and even the nuclear family, often breaking down due to increased divorce rates), this is virtually what life is like for a growing number of people in the West. Again this idea is quite speculative – but it is certainly the case that marriage and close family ties can militate against depression (Kring and Johnson, 2019). However, the correlation between increased rates of depression and the increased break-up of the family unit does not prove that the latter has caused the former. One might argue the reverse or that other independent factors play a causal role in both. Both of these ideas are attractive but both are a long way from being fully accepted as playing an important role in the recent rise in rates of depression. We should also bear in mind that at least part of the rise in reported rates of depression might be due to a rise in the awareness of the problem (Kring and Johnson, 2019). It will be necessary for evolutionary psychologists to develop a means of testing such hypotheses more fully. Box 12.4 Do Women Drive Other Women into a State of Anorexia Nervosa? Given that both natural and sexual selection are considered to boost inclusive fitness, the fact that an estimated 10 per cent of young women in the developed world currently starve themselves into a state of emaciation (Steiger et al., 2003) may appear to be quite a challenge for evolution- ary psychology. The eating disorder known as anorexia nervosa is characterised by measures that control weight at a level at least 15 per cent below the healthy norm through dieting, use of laxatives and excessive exercise to burn off calories. It is also associated with a disturbed body image that leads to anxiety and depression over potential weight gain. This sounds an unlikely complaint for evolutionary psychology to address? Over the last 30 years, however, evolutionists have suggested a number of ways in which this behaviour might have arisen. Such explanations include the reproduction suppression hypothesis (Lozano, 2008) where females reduce their weight to avoid becoming pregnant (the menstrual cycle ceases when women lose substantial weight – a state known as amenorrhea) and the parental manipulation hypothesis where parents manipulate a female offspring in order that she shifts her reproductive investment from herself towards other siblings (i.e. it is maintained by kin selection; Voland and Voland, 1989). These explanations place the sufferer or her parents in a central causal role. Recently, however, evi- dence has accumulated that places a female’s peers centre stage in the development of anorexia nervosa. First proposed by Abed in 1998, the sexual competition hypothesis is based on sexual selection and suggests that eating disorders are driven by high levels of female–female competi- tion for the attention of potential partners. You may recall that sexual selection is concerned with gaining access to mates (see Chapters 3 and 4). Given that fertility in females is associated with youthfulness and, given that youthfulness is associated with slimness, the sexual competition hypothesis suggests young women compete with each other for attention of potential mates by appearing to be youthfully slim. Put simply the sexual competition hypothesis suggests that body dissatisfaction and anorexia arise from intrasexual competition. Although, at the time that it was proposed it was largely a theoretical explanation, a number of subsequent studies have provided support for it. For example, a study by Abed and co-workers demonstrated that in a sample of 206 young women those that displayed high levels of female–female competition were indeed also most likely to exhibit disordered eating behaviour (Abed et al., 2012). Also consistent with  The Downside of Treatment 333 Box 12.4 (cont.) this hypothesis, Faer et al. (2005) uncovered links between body dissatisfaction, female-female rivalry and anorexia in a student sample. This fits in with the well-established finding that indi- rect aggression (non-physical acts of meanness, offence and cruelty such as reputational damage) is significantly more common in young women than in young men (Vaillancourt, 2013). Inter- estingly, this means that eating disorders might be driven by competition between females (i.e. by intrasexual selection) over males, a position that is in direct contrast to the commonly held feminist view that pressure from men leads to anorexia in women (Chernin, 1994). Creativity – the Function of Mania? The evolutionary models which suggest that low mood serves the general function of altering so- cial behaviour in ways that may be adaptive (or would have been in the ancestral past) might help to explain unipolar depression but can they help to explain bipolar depression? Perhaps we need a different explanation for people who suffer from alternate periods of depression and mania. One intriguing argument that has been proposed for manic depression suggests that there may be advantages associated with this illness. Psychiatrist Kay Redfield Jamison of Johns Hopkins University has proposed that manic depressive illness may have a genetic basis and that the genes predisposing a person to the illness also endow the sufferer with a compensatory advantage. This is a form of the pleiotropy argument that we outlined earlier. Jamison (1989; 1993; 1995; 2011) noticed that many famous artists, writers and musicians had a tendency to suffer from depression and mania, including William Blake, Lord Byron, Alfred Lord Tennyson, Sylvia Plath, Vincent van Gogh, Tennessee Williams and Robert Schumann. This led her to make a retrospective study of 47 distinguished British writers, painters and sculptors. In comparison to the 1 per cent of the general population that suffer from bipolar depression, Jamison found that an astonishing 38 per cent of her sample had been treated for bipolar depression. Jamison is not alone in this finding – other studies have confirmed this relationship between creativity and bipolar depression and have demonstrated that this problem runs in families (Ludwig, 1992; Jamison, 1995). Jamison uses an evolutionary argument to suggest that the energy, creativity and focus that accompany a manic state may have been of sufficient advantage that the individuals with the genes for such states were kept in a popu- lation because of the advantages they conferred on their ancestors. In support of her argument she was able to demonstrate that these famously talented people were most productive during manic or hypomanic states (Jamison, 1995). The depressive state that accompanies such creative periods may be seen as a pleiotropic effect of the gene (or genes) for this state. This argument may be thought of as the old ‘mad genius’ idea of exceptionally talented people also having psychiatric problems. This is rather a speculative argument and requires further testing. But if it does stand up to scrutiny then it could lead to a large practical dilemma for many talented people. That is, if bipolar artists are treated with drug therapy for their illness, might such treatment also tone down their creativity? The Downside of Treatment Darwinian medicine may help us to understand the ultimate causes of depression and anxiety but can it provide us with any guidelines so as to improve their treatment? 334 Evolutionary Psychopathology and Darwinian Medicine There may be one unforeseen problem associated with a common practice in modern med- icine. That is the widespread use of drugs such as Prozac to alleviate depression and anxiety. As health researcher Paul Martin, who is also a trained ethologist, has pointed out, if unpleasant states serve adaptive functions then suppressing these might be akin to suppressing coughs and fevers. In other words the immediate alleviation of the symptoms might lead to the problems ultimately lasting longer (Martin, 1997). Nesse and Williams have also considered this problem and further suggest that, if serotonin does play an important role in both status and depression, there might be problems in large hierarchical corporations if so many of their employees were taking antidepres- sants that boosted serotonin. It might be argued that, if lithium and antidepressants do help to even out the mood of bipolar people, such sufferers should also be made aware of the possible damping down of creative processes. Proponents of Darwinian medicine are not suggesting that, as with fever suppressants, antidepressants should never be prescribed but that we should be more aware of the potential drawbacks to their indiscriminate use (Andrews et al., 2012; Nesse, 2019). In the long run some sufferers might be better off if they allow these problems to run their natural course. However, in the case of suicidally depressed cases, then there is an argument for their short-term use. Box 12.5 Did Blue Eye Colouration Evolve to Provide Resistance to Seasonal Affective Disorder? Do you find that as the seasons change so does your mood? If so you are not alone. A large proportion of the world’s population has a noticeable change in mood with the seasons such that they are of lower mood in winter than summer. When severe this seasonal variability in mood is known as seasonal affective disorder or ‘SAD’ (Rosenthal et al., 1984). SAD is a form of recur- rent depression which has a seasonal pattern. In the common form, winter SAD, periods of low mood occur during the winter months, accompanied by an increase in sleepiness and social with- drawal. In contrast, during the summer, such sufferers are frequently described as up-beat and ‘life and soul of the party’ but also often have periods of insomnia. Whilst rare near the equator, SAD becomes increasingly common as we move away from equatorial latitudes (Mersch et al., 1999). This is believed to be related to the greater seasonal variation in photoperiod increasingly associated with latitudes away from the equator. The finding that rates of SAD increase as does seasonal variation in levels of sunshine raises the question of what is the causal mechanism for such mood variability? Currently it is believed that this is related to seasonal variation in the amount of light that manages to make it through the eyeball and on, via specialised cells in the retina, to an area of the hypothalamus (the suprachiasmatic nucleus or SCN). Stimulation of the SCN leads to an increase in production of serotonin which, in turn, elevates mood. Hence if too little light reaches this sensitive part of the brain then, for those who, for as yet unknown reasons, are more susceptible to SAD then the winter can be very bad news. Interestingly it is well known that variability of iris pigmentation leads to variation in how much light manages to make it to the retina, with lighter irises allowing for more light to pass to the back of the eye. Recently, we reasoned that, if more light reaches the retina in blue eyed indi- viduals than in brown eyed ones, then it is feasible that the former might be less prone to SAD. So we decided to test this hypothesis by use of a self-report questionnaire requesting information about both eye colouration and seasonal mood variability. (Note that participants were unaware  The Downside of Treatment 335 Box 12.5 (cont.) of our hypothesis). We measured seasonal mood variation by the Seasonal Pattern Assessment Questionnaire (SPAQ) which provides a Global Seasonality Scale (GSS) to assess the extent of the problem (Rosenthal et al., 1984). The GSS can range from 0 (no seasonal change) to 24 (ex- treme changes in mood and behaviour with the seasons). The proposed cut-off point to diagnose SAD has been established as a GSS score of 11 or higher. But scores a little below this may be taken as evidence of moderate but noticeable mood changes with the seasons (‘winter blues’). This has led to the notion of a general population continuum in seasonal mood variability. Eye colouration was established using the well-established Martin-Schultz Scale (Sturm and Lars- son, 2009). The scale comprises 16 hues, but allows for broad classification into dark/brown and light/blue. Using a sample of 175 individuals from Wales and Cyprus we found that those with blue eye colouration did indeed have a significantly lower GSS score than those with brown eyes (Workman et al., 2018; Workman, 2019). In other words, at least in our study, people with blue eyes were substantially less likely to suffer from seasonal affective disorder. Is it possible that, as humans moved away from the equator and into northern land masses where they encountered low light luminosity in the winter months the blue eye mutation was selected as a counter-meas- ure to this debilitating condition? Conducive with this hypothesis is the fact that as we move to more northerly latitudes, even today, the proportion of people with blue eyes increases pro- gressively. Clearly, in order for blue eye colouration to be maintained within northern European populations, the resilience to SAD that it endows would have to have led to higher reproductive success rates at these latitudes than for brown eyed individuals. This suggests that SAD can be so debilitating as to reduce offspring production when compared with those who have resistance. Is this feasible? Interestingly, Norman Rosenthal, the researcher who coined the term SAD, has described how in severe cases social withdrawal is commonly seen. Moreover, in such extreme cases there can be suicidal ideation during the winter. Hence it’s possible that resistance to SAD may have had notable selective advantages for those living in northern Europe. Mean GSS scores and Standard Error of Mean for blue/light and brown/dark-eyed partici- pants. Note those with blue eyes have significantly lower GSS scores. 16 Figure 12.7 Mean GSS scores and standard error of 14 the mean for blue/light- and 12 brown/dark-eyed participants. Mean GSS Score Note that those with blue eyes 10 have significantly lower GSS scores. 8 6 12.31 8.79 4 2 0 blue eyes brown eyes Eye Colour 336 Evolutionary Psychopathology and Darwinian Medicine Figure 12.8 Would you be happier if you lived a lifestyle similar to that of our ancient ancestors? Some studies suggest this might be the case. Evolution-Based Therapy for Depression: Can Knowledge of the EEA Help Us to Solve the Problem of Depression? Currently there is debate among evolutionary psychologists as to the degree to which depression is an adaptation (Andrews and Thomson, 2009; Nettle, 2004; Troisi, 2020). Whether it is adaptive or maladaptive we may still ask the question can evolutionary psychology help in treatment of this highly disabling problem? There is now evidence that it can. Evolutionist Stephen Ilardi and his co- workers have developed a 14-week 6-step treatment regime for depression that is designed partially to mimic the conditions under which our Pleistocene ancestors lived. The regime includes increasing the amount of sunlight a sufferer receives each day while also boosting the amount of omega-3 fatty acid in the diet and adopting other measures such as spending more time with friends and family and in outdoor pursuits. Sleep patterns are also altered to be more in tune with ancestral habits. Re- markably, Ilardi et al. (2007) were able to report a 75.3 per cent success rate for those undertaking the regime (compared with 22 per cent for a control sample). Such a success rate may be taken as evidence that one of the current causes of depression is the current mismatch between our lifestyle today and that under which our ancestors evolved (Ilardi, 2010; see also Jiaqing et al., 2019). The Schizophrenia Spectrum Schizophrenia is arguably the most severe psychiatric illness and unfortunately is not uncommon. Today it is known that worldwide around 1 per cent of the population will succumb to this condition (Del Guidence, 2018; Ray, 2018). Most people will have met someone with schizophrenia; many will have a relative with the illness.  The Schizophrenia Spectrum 337 Table 12.2 Changes to the classification of schizophrenia under DSM-5 The Diagnostic and Statistical Manual of Mental Health, or DSM (produced by the American Psychiatric Association), is an international manual which is used by clinicians around the world to diagnose and classify mental disorders. In previous editions of the DSM, schizophrenia was subdivided into five sub-types – ‘disorganised’ (incoherent speech), ‘catatonic’ (immobility and periods of excitement), ‘paranoid’ (suspicious and grandiose), ‘undifferentiated’ (a little of each of the others) and ‘residual’ (a lesser degree of symptoms). With the publication of the DSM-5 in May 2013 these sub-types were dropped due to the fact that there is a huge degree of overlap in symptoms between patients. Another problem is that sufferers of bipolar affective disorder can demonstrate many of these symptoms during manic periods. Today clinicians still look for these symptoms, and many sufferers (but by no means all) may in theory be primarily associated with one of these categories. DSM-5 defines schizophrenia as part of a broad category known as ‘schizophrenia spectrum and other psychotic disorders’. Technically, to be diagnosed as having schizophrenia, a sufferer must have one or more of the following symptoms for at least six months (including at least one month of active symptoms): delusions, hallucinations, disorganised speech and behaviour and other symptoms that cause social or occupational dysfunction. Schizophrenia literally means ‘split-mind’. This split refers to a split in connections be- tween cognitive, emotional and motivational processes and should not be confused with ‘multi- ple personality disorder’ – a rare problem where the sufferer behaves as if they have two or more separate personalities. People suffering from schizophrenia have a number of psychotic symptoms including hallucinations (usually auditory but also visual in some cases); delusions and disorders of affect (that is inappropriate emotional responses), and of thought (Ray, 2018). The auditory hallu- cinations are usually voices which typically tell the sufferer to do things, or make comments about them. Frequently they hold bizarre beliefs, for example, that they are really another person such as a member of a royal family or even God, or that they are the centre of a sophisticated conspiracy. Many people with the illness are socially withdrawn and find it difficult to maintain relationships. In a sense the ‘split’ in schizophrenia is a split from reality. Schizophrenia is what many people colloquially refer to as ‘insanity’ or ‘madness’ – but such terms have no place in the language of modern-day psychiatry and clinical psychology. Schizophrenia Runs in Families – So Is It Transmitted Genetically? It has long been recognised that schizophrenia tends to cluster in families. As Table 12.3 demon- strates, genetic relatives of persons with schizophrenia are more likely to develop the illness than the general population. Furthermore, the closer the relationship (i.e. in terms of number of genes shared by common descent), the greater the likelihood of developing schizophrenia. The term proband refers to individuals in a genetics study who have the trait under investigation. Also remember that the coefficient of relatedness (r) refers to the proportion of genes shared between two individuals by common descent (see Chapter 2). When considering Table 12.3 notice in particular that the spouse (not genetically related to the proband) is no more likely to develop schizophrenia than the rest of the general population. As the proportion of genes shared increases, however, so too does the probability of developing schizophrenia. Given the pattern uncovered here, it appears as if schizophrenia is largely genetically determined. There are, however, two problems with the ‘all in the genes’ argument. First, relatives who share the most genes are also likely to share much of their environment; and second, although 338 Evolutionary Psychopathology and Darwinian Medicine Table 12.3 Summary of hereditary studies of schizophrenia Relation to proband Percentage schizophrenic Coefficient of relatedness (r) Spouse 1.00 0.00 Grandchildren 2.84 0.25 Nieces/nephews 2.65 0.25 Children 9.35 0.50 Siblings 7.30 0.50 Dizygotic twins 12.08 0.50 Monozygotic twins 44.30 1.00 Source: Based on Gottesman et al. (1987). the concordance rate is very high for monozygotic twins (who share 100 per cent of their genes), if it is purely hereditary then the rate should be 100 per cent. These findings demonstrate the importance of environmental risk factors and epigenetic mechanisms in the aetiology of schizophrenia (Plomin, 2018; see Chapter 2). It is, however, clear that genes play a central role in schizophrenia (the three- to four-fold increase in monozygotic when compared to dizygotic twins is the acid test here). The Diathesis–Stress Model A diathesis means a predisposition towards developing an illness or abnormality (Kring and John- son, 2019). The fact that schizophrenia runs in families but not in a perfect Mendelian manner has led many experts in the field to propose that some people may have a diathesis for the illness but Figure 12.9 All four of the identical girls known as the Genain quadruplets developed schizophrenia. The likelihood of this occurring due to chance alone is 1 in 2 billion. Such cases provide strong support for the argument that there is a genetic component in schizophrenia.  The Schizophrenia Spectrum 339 that it will only be phenotypically expressed following stressful life events. This is known as the diathesis–stress model of schizophrenia (Kring and Johnson, 2019). It is certainly the case that the psychotic symptoms of schizophrenia tend to occur following stressful events in life. If we accept the diathesis–stress model then we can still use the term ‘genes for schizophrenia’ provided we make it clear that such genes create a predisposition for the illness but that epigenetic factors are also in- volved. This means that having the ‘genes for schizophrenia’ does not make it inevitable. This might help to explain why many close relatives of sufferers (including identical twins) do not develop the illness themselves. Are Brain Changes Associated with Schizophrenia? Some clinicians who study the pathology of schizophrenia suggest that the illness is related to abnormalities of neurotransmitters such as dopamine or glutamate (Moghaddam and Javitt, 2012). Others propose that a loss of grey matter or other forms of brain atrophy are implicated (Thompson et al., 2001; Ray, 2018). One well-replicated finding is that individuals with schizophrenia lose grey matter (neuronal cell bodies that make up much of the cortex) at a greater rate than non- schizophrenic controls. This is an important finding because it is well established that a great deal of processing occurs in the grey matter of the cortex including decision-making and the creation of self-awareness. Perhaps the symptoms of schizophrenia are directly related to this loss of grey matter? One counter-argument to this suggestion is the fact that people with schizophrenia are gen- erally prescribed antipsychotic medication. Hence the reduction in grey matter might, arguably, be the result of such long-term medication? One way of resolving this debate is to study young people who have only recently begun to show the symptoms of the illness, that is adolescents. In fact there is now ample evidence that this loss of grey matter precedes the use of antipsychotic medication (Ray, 2018). One particular study by Californian neuroscientist Paul Thompson and his co-workers involved the use of a high-resolution MRI scanner to compare the brains of sets of adolescent twins where only one of the pair had developed schizophrenia. They found significantly greater grey mat- ter loss in the afflicted twin than in the non-impaired one (around 1 to 2 per cent compared with 4 to 5 per cent in the impaired twin; see Figure 12.10). In this study it is important to note that twins acted as control subjects for each other. This provides strong evidence that the development of schiz- ophrenia is associated with loss of cortical tissue. It does, however, also raise the question of why, in these cases, did one twin in each pair develop the illness while the other remained unimpaired. Clearly, as we outlined earlier on, having the ‘genes for schizophrenia’ is necessary but not sufficient for development of the illness. Neurological findings such as the one above are important in helping us to understand the aetiology and the pathogenesis of schizophrenia. They do not however, tell us why the disorder is so common in our species. In recent years evolutionists have begun to propose ultimate explanations for the illness. How Do Evolutionists Explain Schizophrenia? Schizophrenia is a difficult psychiatric problem for evolutionists to explain. Unlike anxiety and depression, the symptoms are not simply exaggerations of normal internal states, nor is there a straightforward relationship between the illness and positive traits such as creativity. In fact, due to their social problems, individuals with schizophrenia are at a procreative disadvantage which makes it all the more difficult to explain how there can be a genetic component to the illness (Ray, 340 Evolutionary Psychopathology and Darwinian Medicine Figure 12.10 Average rates of grey matter loss in normal adolescents and in schizophrenia (24 participants in each group, aged 13–18). The image consists of three-dimensional maps of brain changes, derived from high-resolution MRI scans. The scans reveal profound, progressive grey matter loss in the participants with schizophrenia (right- hand images). 2018). A number of hypotheses have been suggested by evolutionists to explain why schizophrenia is maintained in the population. Three that have been proposed are the ‘abnormal lateralisation of language’, ‘group-splitting’ and the ‘social brain’ hypotheses. All three hypotheses suggest there may be compensatory advantages to having schizophrenia when viewed within an evolutionary framework. ABNORMAL LATERALISATION OF LANGUAGE HYPOTHESIS Tim Crow, a psychiatrist from Oxford who has an interest both in neurology and in evolutionary theory, has suggested that schizophrenia is related to the evolution of lateralised language in our species. Lateralisation, you might recall, is the differential functioning of the left and right cerebral hemispheres (see Chapter 11). Normal lan- guage lateralisation involves left hemisphere specialism during development (Hsiao and Man Lam,  The Schizophrenia Spectrum 341 2013; Del Guidice, 2018). According to Crow (2005), while this lateralisation is maintained in our species because there are advantages to having an asymmetrically functioning brain, given just how complex this is in terms of neurodevelopment, for some people the pattern develops abnormally. For such people this leads to an inability to dissociate external voices from internal language. All of the symptoms of schizophrenia including paranoia and disordered thought then stem from this prob- lem of language lateralisation. Hence for Crow schizophrenia is maintained in our species because the genes that lead to language development and functional brain asymmetry work well for the vast majority of us. Crow also suggests that the gene combinations implicated in schizophrenia when found in slightly different combinations (i.e. in the relatives of the sufferer) may then lead to high achievement in, for example, the arts. In this way the genes for schizophrenia may be maintained in our species. Crow’s hypothesis is supported indirectly by the finding that people with schizophrenia fre- quently have an atypical leftward shift in handedness distribution, that is, there are more left-handers than in the rest of the population (a sign of abnormal development of lateralisation). It should be borne in mind, however, that the vast majority of left-handed people do not develop schizophrenia. GROUP-SPLITTING HYPOTHESIS Stevens and Price (2000) have suggested a novel evolutionary explanation for schizophrenia that they call the ‘group-splitting’ hypothesis. They propose that throughout recorded history many charismatic leaders from Adolf Hitler to David Koresh (leader of the Waco cult) may well have had schizophrenia. They claim that what we see today as a mental illness may be related to leadership which arises when members of a society become disaffected and look for a new leader who is going to suggest radical change. The group then splits off from society and follows the new radical leader. This means that in Stevens and Price’s model the bizarre way of thinking and talking which reflects a very different world view might be attractive to disaffected peo- ple looking to form a new society. In this way schizophrenia may be related to leadership which, with the associated raised status, might lead to increased mating opportunities and hence fitness benefits. The group-splitting hypothesis is quite a radical notion but again, does it stand up to exam- ination? It is certainly true that leaders such as Hitler, Stalin and, more recently, David Koresh did rise to positions of prominence among groups of disaffected people. Also Koresh, in particular, used his position to have sex with a large number of women – and thereby perhaps pass on genes related to his condition. If such circumstances happened regularly in our past then perhaps such a strategy might be adaptive. There are, however, three problems with this theory. The first is that only rarely in recorded history have disillusioned people followed a ‘mad’ charismatic leader like Hitler or Koresh making it unlikely that it is an adaptive strategy. Second, most people suffering from schizophrenia are not organised and coherent to the point of being able to form a cohesive group-splitting plan. Third and finally, we can’t even be certain that any of these world leaders was suffering from schiz- ophrenia – they may have been, but it would be very difficult to prove this. Stevens and Price might argue that in our ancient past group-splitting may have occurred on a more regular and local basis, which means that the state may have been adaptive during the EEA. It might also be argued that seriously disaffected people might not be in an ideal state of mind to make such decisions. Certainly, the writings and speeches of Hitler (or Koresh for that matter) are thoroughly unconvincing (and immoral) when examined today by anyone who is in a balanced state of mind. But their followers literally laid their lives down for such ramblings. SOCIAL BRAIN HYPOTHESIS A third evolutionary argument of the existence of schizophrenia was proposed by Darwin-influenced South African psychologist Jonathan Burns in 2007. In The Descent 342 Evolutionary Psychopathology and Darwinian Medicine of Madness: Evolutionary Origins of Psychosis and the Social Brain Burns proposed that, due to the intricacies of human social life where we constantly attribute internal meaning to the actions of others, we have evolved a brain of such complexity that in some cases neurodevelopment that under- lies social cognition does not proceed properly. This has the knock-on effect of over-interpretation by some and, this in turn, leads to psychotic symptoms. In common with Crow, Burns sees schiz- ophrenia as a secondary consequence of having a very complex brain but his argument differs in that it relates the illness not specifically to language lateralisation but to interpreting complex social behaviour. Burns’ proposal, like Crow’s, is both speculative but, up to a point, compelling. Given that the human brain is the most complex entity that we are aware of in the universe, perhaps the neural circuitry underlying social cognition has pushed the mammalian brain to a point where for some people having the wrong combination of genes can lead them down the path of mental illness. As with Crow’s proposal, however, the social brain hypothesis is not without problems. One problem is that, since sufferers often report hearing voices when alone, schizophrenia affects people outside of social settings. A potentially larger problem with this (and the other two evolu- tionary hypotheses outlined above) is that today, as we have seen, many experts see schizophrenia as a cluster of different mental illnesses that have been grouped together due to some degree of overlap in symptomology rather than a single illness with a single cause (Ray, 2018). In fact one extreme, yet quite commonly held view is that the ‘illness’ we label ‘schizophrenia’ does not exist at all, but that the symptoms are an extreme example of normal human internal experiences (Bentall, 2003). Genes Underlying Schizophrenia? If schizophrenia has been maintained in Homo sapiens by Darwinian natural selection, then it has to be related to the genes we carry that code for brain development (see Table 12.3). In 2007 an international team of Crespi, Summers and Dorus, after analysing the DNA from a series of human populations, identified 28 genes that make individuals susceptible to the disorder. Since then the number of genes identified which are associated with this illness has grown exponentially (Ray, 2018). Today a number of experts consider that there may be more than 1000 different genes in- volved in the development of schizophrenia (Cannon, 2015; Plomin, 2018). Some researchers, such as Crespi, suggest that having various combinations of these genes may well promote linguistic skill and creativity, but that having most or all of them leads to schizophrenia. Hence these genes might be maintained in the population because they provide people with advantages such as high levels of creativity but having too many of them might make a person susceptible to schizophrenia. Inter- estingly, this explanation fits in quite well with both the social brain and the abnormal lateralisation hypotheses (and perhaps even the group-splitting hypothesis). Perhaps these ideas for the evolution of schizophrenia are not mutually exclusive explanations but rather approaches that address the problem from different angles. Evolutionary explanations that either view schizophrenia as an adaptation to a previous age or that suggest the genes associated with it may currently provide compensatory advantages either to the sufferer or to their relatives are not entirely convincing or well accepted at present (Brüne, 2004; 2016). As a problem that shows remarkable uniformity of both incidence rates and symptomology around the globe, however, explanations that ignore ultimate causation may well miss an opportunity to develop a unifying theory of the existence and maintenance of this most serious psychological illness.  The Schizophrenia Spectrum 343 Personality Disorders A personality disorder does not normally involve psychotic symptoms such as hearing voices or believing that you are a deity. Rather, personality disorders are ‘long-standing, pervasive, and in- flexible patterns of behaviour and inner experience that deviate from the expectations of a person’s culture and that impair social and occupational functioning’ (Kring and Johnson, 2019). To use a rather outdated term, people with personality disorders are neurotic rather than psychotic. In contrast to schizophrenia, personality disorders may be more easily explained when viewed from an evolutionary standpoint, in part because they may be thought of as forms of thought and behaviour which many of us frequently exhibit, but taken to an extreme. DSM-5 recognises ten personality disorders which form three clusters – odd/eccentric, dramatic/erratic and anxious/ fearful (see Table 12.4). Can Evolutionary Psychology Explain Personality Disorders? Looking at Table 12.4, it is clear that people with personality disorders have certain features in com- mon. They are frequently self-absorbed, and highly anxious. They may be unreliable and difficult. In short they do not make for ideal partners. Psychiatry today considers personality disorders as enduring abnormalities that people have in their dealings with others and with life in general. Such a view would suggest that people who have personality disorders are behaving in a maladaptive way. But are they? Psychologists trained in evolutionary theory are beginning to question this assumption Table 12.4 Personality disorder clusters according to DSM-5 Cluster Specific personality disorder Odd/eccentric paranoid – intense suspicion of others, frequently hostile, often a high level of sexual jealousy schizoid – lack of warm feelings to others, indifferent, socially withdrawn, similar to residual schizophrenia schizotypal – serious interpersonal difficulties, odd beliefs including e.g. belief in magical events Dramatic/erratic borderline – impulsive, particularly in relationships, erratic emotions, argumentative and unpredictable histrionic – great show of emotions, but in reality emotionally shallow narcissistic – overblown view of own abilities, highly self-centred, lack of empathy, opinionated antisocial – highly dishonest, destructive, manipulative, irresponsible and in many cases aggressive Anxious/fearful avoidant – oversensitive to criticism, highly anxious in social circumstances dependent – lacks both a sense of self-confidence and of autonomy, highly dependent on partner obsessive–compulsive – preoccupied with rules and details, tend to be work orientated but poor at completing projects due to drive for perfection; often called a ‘control freak’ due to inability to give up control 344 Evolutionary Psychopathology and Darwinian Medicine – perhaps some forms of ‘personality disorder’ would have been adaptive in our ancestral past. Perhaps others would not have been adaptive but are an outcome of the mismatch between genes adapted for earlier conditions and today’s environment. It may also be the case that genes associat- ed with such disorders code for other, fitness-enhancing, features. Note that these are forms of the mismatch, compromise and pleiotropy arguments introduced earlier on in this chapter. As in the case of t