Darwinian theory is the organising framework for all life sciences.
Evolutionary thinking can transform our understanding of causality in medicine and psychiatry through the application of Tinbergen’s four questions.
Without evolution, our understanding of the causes of disease is necessarily incomplete.
The evolutionary perspective can help us understand human vulnerability to disease and disorder.
Evolutionary psychiatry complements and augments mainstream psychiatry and does not seek to replace it.
Evolution can also help us understand human uniqueness and especially the role of cumulative culture and gene–culture co-evolution in shaping the human body and mind.
1.1 Introduction to Evolutionary Theory
Charles Darwin made two distinct and revolutionary proposals in 1859. The first was that all living organisms shared a common ancestor and the second was that natural selection was the mechanism through which all the diversity of life on Earth arose (Nesse and Stein, Reference Nesse and Stein2019).
These insights set in motion one of the greatest scientific revolutions in history. Whereas other major scientific paradigm shifts occurred in the physical sciences (e.g. those of Copernicus, Newton, Einstein and Heisenberg), they had few conspicuous implications outside their specialist fields. Darwinism, however, challenged deeply entrenched assumptions in multiple fields of enquiry and belief, ranging from biology to geology, as well as having profound meta-scientific consequences in its challenge to creationism, essentialism and anthropocentrism (Mayr, Reference Mayr1971). Yet despite being part of the life sciences, psychiatry (as well as much of medicine) has remained largely pre-Darwinian in its approach. In this book, evolutionary scholars of various disciplines, including psychiatrists, philosophers, anthropologists and psychologists, aim to rectify this, not by rejecting or replacing current mainstream psychiatry, but through the addition of the evolutionary perspective, which should provide the discipline with a more contemporary, sound scientific foundation.
Psychiatry is the branch of medicine that deals with mental disorders that manifest themselves through disturbances in cognition, emotions and behaviour. However, the failure of psychiatry to make significant progress in understanding the aetiology of mental disorders has been described as a ‘crisis’ by leading evolutionists (Brüne et al., Reference Brüne, Belsky, Fabrega, Feierman, Gilbert, Glantz, Polimeni, Price, Sanjuan, Sullivan, Troisi and Wilson2012) – a fact that has also been acknowledged in an article in Science that stated that there have been no major breakthroughs either in the treatment of schizophrenia for 50 years or in the treatment of depression for 20 years (Akil et al., Reference Akil, Brenner, Kandel, Kendler, King, Scolnick, Watson and Zoghby2010). Evolutionists would contend that this is partly because mainstream psychiatry focuses exclusively on proximate causation and favours mechanistic explanations of disease and disorder. However, unlike medicine, where human physiology provides clear reference points for normal functioning, psychiatry has attempted to identify disorder and dysfunction without a coherent theory of normal human psychology (Nesse, Reference Nesse and Buss2016). Also, even on the rare occasions when the vital questions of function and the role of evolution are considered by mainstream psychiatrists, they stop well short of exploring the full implications of such a radical shift in thinking and approach (e.g. Kendler, Reference Kendler2008). Evolutionary psychiatrists argue that Darwinian theory can serve as the essential, missing basic science for psychiatry (Nesse, Reference Nesse2019).
Psychiatry’s pre-Darwinian state may be changing very gradually with the development of evolutionary models for a number of psychiatric disorders and the publication of a number of influential evolutionary psychiatric texts over the past couple of decades (Baron-Cohen, Reference Baron-Cohen1997; Brüne, Reference Brüne2015; Del Giudice, Reference Del Giudice2018; Gilbert and Bailey, Reference Gilbert and Bailey2000; McGuire and Troisi, Reference McGuire and Troisi1998; Nesse, Reference Nesse2019; Stevens and Price, Reference Stevens and Price2000).
In its development, evolutionary psychiatry has benefited from work in two closely related fields. The first field is evolutionary medicine, which has seen a massive expansion since the publication of Nesse and Williams’ (Reference Nesse and Williams1994) foundational work (preceded by an article by Williams and Nesse (Reference Williams and Nesse1991) and an American Association for the Advancement of Science symposium on evolutionary medicine in 1993) followed by many others (e.g. Gluckman et al., Reference Gluckman, Beedle and Hanson2009; Trevathan et al., Reference Trevathan, Smith and McKenna2008). The other field is the now highly accomplished and rapidly expanding domain of evolutionary psychology. This was heralded as an academic discipline by the publication of the highly influential Adapted Mind (Barkow et al., Reference Barkow, Cosmides and Tooby1992) followed by the publication of many influential texts and specialised academic journals, as well as the voluminous scientific output of numerous university departments across the Western world. Furthermore, evolutionary anthropologists have had a significant impact on these academic strands, especially on the development of evolutionary medicine (Trevathan et al., Reference Trevathan, Smith and McKenna2008).
In this book, we provide reasons as to why evolution is ideally placed to guide psychiatrists in determining what the phenotypic end products of neurobiological systems are (these are the genetically based, behavioural and psychological traits that have been shaped by selection). Importantly, the evolutionary emphasis on function can provide the scientific basis for a non-reductionist expansion of the concept of the biological to encompass the psychological, social and cultural domains (Abed and St John-Smith, Reference Abed and De Pauw2021). Hence, in contrast with mainstream biological psychiatry’s narrow ‘decontextualized’ view of mental disorder as brain disorder (or brain circuit disorder) (Insel and Cuthbert, Reference Insel and Cuthbert2015), evolutionists consider the environmental context to be of paramount importance in determining the existence and nature of mental disorder (Nesse, Reference Nesse2019).
Thus, evolutionists consider Darwinian theory to be the fundamental organising framework or meta-theory underpinning the whole of the life sciences and not simply one perspective to be considered alongside many others. Evolutionary psychiatry is the application of modern evolutionary theory to the scientific understanding of mental health and disease. The goal of evolutionary psychiatry then is to understand why people get sick as well as how they get sick.
The remainder of this introductory chapter will provide a survey of some of the fundamentals of evolutionary science relevant to the understanding of health and disease in humans.Footnote 1
1.1.2 Evolution, Natural Selection and Adaptation
What is evolution? Evolution may be defined as any net directional change or any cumulative change in the characteristics of organisms or populations over many generations – in other words, descent with modification. When individuals in a population vary in ways that influence their genetic contribution to future populations, the average characteristics of the population will change.
It is essential to understand that biologists recognise many ways in which evolution can occur, evolution by natural selection being just one of them, although it is often held to be the most important. Other basic evolutionary processes include genetic drift, mutation, migration and sexual and social selection.
Natural selection can lead to speciation, where one species gives rise to a new and distinctly different species. This is one of the processes that drives evolution and helps to explain the diversity of life on Earth. Natural selection is the process through which populations of living organisms adapt and change. Natural selection, however, involves no foresight, planning or goal. Hence, any heritable (genetically based) phenotypic trait that confers a reproductive advantage in competition with alternatives within a population will spread, and given enough time the trait may become fixed as a species-wide characteristic. The measure of reproductive success is referred to as ‘fitness’. Repeated cycles of natural selection lead to the preservation of successful variants and the elimination of less successful ones, leading to the appearance of design and the shaping of traits that increase the organism’s fitness. These are referred to in the evolutionary literature as ‘adaptations’. Although Darwin was unaware of the existence of genes or how variation came about, we now know that variation arises as a result of mutations, which are copying errors in the DNA sequence that occur during cell division (NIH, 2020). When mutations occur in germ-line cells as opposed to somatic cells they can be transmitted to offspring.
The basic Darwinian ideas (variation, inheritance and natural selection) were enhanced in the twentieth century by what was called the ‘modern synthesis’. This involved the incorporation of the modern science of genetics, which included the concepts of genes, mutation and Mendelian inheritance, into evolutionary theory.
The modern synthesis led to the insight that while the primary mechanism that generates variation is random (mutations), the success or failure of the different variants depends on the fitness they confer and is not at all random. Thus, natural selection shapes adaptive and functional systems that aid survival and reproduction through favouring certain phenotypic traits over others and leads to the spread of the underlying genes within the population. Nevertheless, the same evolutionary processes that shape functional adaptations, paradoxically and inevitably, produce maladaptations (Brady et al., Reference Brady, Bolnick, Angert, Gonzalez, Barrett, Crispo, Derry, Eckert, Fraser, Fussmann, Guichard, Lamy, McAdam, Newman, Paccard, Rolshausen, Simons and Hendry2019) as well as vulnerabilities to disease and disorder (Nesse, Reference Nesse2019) (see Box 1.1). However, before tackling the evolutionary causes of the persistence of disease and disorder, we will first explore how evolutionary thinking can transform our understanding of causality followed by a brief discussion of a range of other important evolutionary concepts.
Life history factors
Overactive defence mechanisms
Co-evolutionary considerations: consequences of the arms race against pathogens
Constraints imposed by evolutionary history
Sexual selection and its consequences
Balancing selection and heterozygote advantage
Demographic history and its consequences
Selection favours reproductive success at the expense of health
Extremes of adaptations
One of the most significant implications of evolutionary theory is in the understanding of causality in the biological sciences. In his seminal paper on the subject, Nikolaas Tinbergen, Nobel Laureate and co-founder of the science of ethology, proposed a causal system that is now known as ‘Tinbergen’s four questions’ (Tinbergen, Reference Tinbergen1963). Building on the distinction between proximate (mechanistic) and ultimate (evolutionary) causation made by Mayr (Reference Mayr1961), Tinbergen proposed that a complete understanding of any biological system, trait or organ requires an understanding of all four categories of its causation (Table 1.1). These are the mechanisms that make it work (physiology, structure), the developmental processes that form the system during the lifetime of the organism, the phylogenetic history of the system and the function that the system served the organism in its natural environment. In Table 1.1, boxes (1) and (2) correspond to the proximate causes and boxes (3) and (4) correspond to the ultimate causes according to Mayr’s classification. It is important to note that all four causes apply simultaneously to all biological phenomena and are not alternatives to each other, and that neglecting any of these four causal elements necessarily results in an incomplete understanding of the given system or trait.
|Developmental/historical||Characteristics of the trait/system|
|Proximate causation||(2) Ontogeny: how does the trait develop during the lifetime of the organism?||(1) Mechanism: how does it work?|
|Evolutionary or ultimate causation||(3) Phylogeny: what is the phylogenetic history of the trait? (Why is the trait/system the way it is?)||(4) Adaptive function: how has the trait or system contributed to the organism’s inclusive fitness in its natural environment? (Why does the trait/system exist?)|
As diseases and disorders are phenomena affecting biological systems, they should plainly benefit from the application of Tinbergen’s system by asking ‘why’ questions that supplement the more traditional ‘how’ questions (see Chapter 2 for a detailed discussion of some clinical applications).
Focusing exclusively on the proximate (as is currently the case in mainstream psychiatry) is akin to a technician’s view of a machine, whereas considering ultimate causation as well is more like an engineer’s view (Nesse, Reference Nesse2019). Evolutionists consider that a clinician skilled in the recognition of distressing emotional states who also understands why we have such emotions and how emotional systems interact with people’s current lives is likely to have a deeper understanding of the patient’s distress and is able to take greater account of the circumstances that may be contributing to the patient’s current state (Abed and St John-Smith, Reference Abed and De Pauw2021). In addition, importantly, evolutionary considerations have the potential for influencing research agendas through testing hypotheses regarding what is the normal function of the system that is giving rise to psychopathology; questions that are seldom asked by mainstream psychiatry (Brüne, Reference Brüne2015).
Fitness is a central concept in evolutionary theory. Darwinian fitness is a measure of reproductive success and can be defined either with respect to a genotype or to a phenotype in a given environment. This is measured by the average contribution to the gene pool of the next generation that is made by an individual of the specified genotype or phenotype. Where fitness is affected by differences between various alleles of a given gene, the relative frequency of those alleles will change across generations through selection, and alleles with greater positive effects on individual fitness will become more common over time.
As alluded to earlier, the integration of modern genetics with Darwinian theory led to the ‘modern synthesis’ and the formulation of the concept of ‘inclusive fitness’ (Hamilton, Reference Hamilton1964). According to Hamilton’s formulation, fitness should be measured not only through the number of direct descendants who carry copies of one’s genes, but also through the number of non-descendant kin who also carry copies of the same genes. It follows that behaving altruistically towards kin can improve one’s overall fitness or inclusive fitness (the sum total of descendant and non-descendant kin who carry copies of one’s genes) provided that the fitness cost to the altruist is lower than the fitness gain to kin multiplied by the coefficient of relatedness (this is also known as Hamilton’s rule). This provides a basis for the understanding of the evolution of altruism and of the conditions that would give rise to competition and cooperation (Del Giudice, Reference Del Giudice2018). ‘Kin selection’ is the term that is used for the evolutionary strategy that increases inclusive fitness through the application of Hamilton’s rule.
Natural and sexual selection are the only known causal processes capable of producing complex functional mechanisms (also known as adaptations). An adaptation may be defined as an inherited characteristic that came into existence as a feature of a species through natural selection because it facilitated survival and reproduction during the period of its evolution (Tooby and Cosmides, Reference Tooby, Cosmides, Barkow, Cosmides and Tooby1992). Solving a recurrent adaptive problem is the function of any given adaptation. There must be genes for any adaptation because they are axiomatically required for the passage of the adaptation from parents to offspring. Therefore, evolutionary psychologists/psychiatrists start from the position that all brain neurobiological mechanisms/systems have been shaped through a long process of selection within a particular set of environmental conditions (see Section 1.1.8) (Buss, Reference Buss2009).
Psychological mechanisms are viewed as specialised neurobiological systems shaped by selection to solve recurrent problems of survival and reproduction faced by ancestral humans over evolutionary history (Tooby and Cosmides, Reference Tooby, Cosmides, Barkow, Cosmides and Tooby1992). An understanding of the function and phylogeny of evolved mechanisms thereby provides unique insights into both their adaptive output as well as how and why these mechanisms can misfire, leading to maladaptive responses (e.g. in novel environmental conditions; see Section 1.2.1). Examples of evolved psychological mechanisms include: fear, attachment, security, status, mating and caregiving (Del Giudice, Reference Del Giudice2018).
An illustrative example of the derailing of an evolved mechanism is the way in which the cuckoo chick exploits the innate parental feeding mechanism of certain bird species. The hatching cuckoo chick provides a supernormal stimulus that triggers a (parental) feeding response through its huge gaping beak despite being in the nest of a different species (such as a great reed warbler), which induces the warbler to feed the cuckoo chick to the detriment of its own offspring (e.g. Tanaka et al., Reference Tanaka, Morimoto, Stevens and Ueda2011). Similarly, evolved psychological mechanisms in humans can be derailed and produce maladaptive responses when exposed to novel environmental conditions, leading to mental disorder in some individuals (see Section 1.2.1).
Parental investment is the investment that parents make in an offspring that increases that offspring’s chances of surviving. By definition, such investment imposes a cost on the parents as measured by their ability to invest in other offspring, current and future. Components of fitness include the well-being of existing offspring, parents’ future reproduction and inclusive fitness through aid to kin (Hamilton, Reference Hamilton1964; Trivers, Reference Trivers and Campbell1972). Parental investment may be performed by both males and females (biparental care), females alone (exclusive maternal care) or males alone (exclusive paternal care). Care can be provided at any stage of the offspring’s life, from prenatal (e.g. egg guarding and incubation in birds and placental nourishment in mammals) to postnatal (e.g. food provisioning and protection of offspring).
Parental investment theory predicts that, on average, the sex that invests more in its offspring, including the size of gametes, gestation, lactation and child rearing, will be more selective when choosing a mate, and the less-investing sex will engage in more intra-sexual competition for access to mates. This theory has been influential in explaining sex differences in sexual selection and mate preferences throughout the animal kingdom, including humans. Trivers (Reference Trivers1974) extended parental investment theory to explain parent–offspring conflict: the conflict between optimal investment from the parent’s versus the offspring’s perspective.
A further complication in nurturing occurs with parent–offspring conflict. This is a biological process that can start from the moment of conception. This conflict, which occurs exclusively in sexually reproducing species, is based on the fact that while the mother (or father) is related to their offspring by 50%, the foetus is 100% related to itself. This is used to signify the evolutionary conflict arising from differences in optimal parental investment to an offspring from the standpoint of both the parent and the offspring (Trivers, Reference Trivers1974).
Similarly, each sibling is only 50% related to any of their full siblings, and so they have a propensity to attempt to acquire more than their fair share of parental investment and more than the parents are willing to provide. However, parent–offspring conflict is functionally and statistically counterbalanced by the processes related to inclusive fitness and thus limited by the close genetic relationship between parent and offspring as additional parental investment obtained by one offspring at the expense of its siblings can decrease the number of its surviving siblings and reduce inclusive fitness. This leads to the prediction that, all other things being equal, parent–offspring conflict will be stronger among half-siblings than among full siblings. These observations and models may have significant effects relevant to child psychiatry (see Chapters 14 and 15).
Plasticity is an evolutionary adaptation to environmental variation that is reasonably predictable and occurs within the lifespan of an individual organism as it allows individuals to ‘fit’ their phenotype to different environments. Phenotypic plasticity describes the possibility of modifying developmental trajectories in response to specific environmental cues and also the ability of an individual organism to change its phenotypic state or activity (e.g. its metabolism) in response to variations in environmental conditions (Garland and Kelly, Reference Garland and Kelly2006).
Phenotypic plasticity can evolve if Darwinian fitness is increased by changing the phenotype. However, the fitness benefits of plasticity may be limited by the trade-off of the costs of plastic responses (e.g. synthesising new proteins, adjusting expression ratios of isozyme variants, maintaining sensory machinery to detect changes) as well as the predictability and reliability of environmental cues. Canalisation is the converse of plasticity and refers to developmental stability that resists both genetic and environmental disruption or perturbation. Canalisation mechanisms are vitally important and ensure that an organism’s traits demonstrate robustness and develop reliably. However, their drawback is that they limit plasticity (Haltigan et al., Reference Haltigan, Del Giudice and Khorsand2021; Waddington, Reference Waddington1942).
Another interpretation of psychological findings that are traditionally discussed according to the diathesis–stress model is differential susceptibility (Belsky, Reference Belsky1997). Both models suggest that development can be differentially susceptible to experiences or qualities of the environment. Whereas the diathesis–stress model suggests a distinct and mostly negativity-sensitive response, Belsky describes a group that is sensitive to adverse experiences but also to positive experiences. These models may be complementary if some individuals are dually or uniquely positivity-sensitive while others are uniquely negativity-sensitive.
Bakermans-Kranenburg and van IJzendoorn (Reference Bakermans-Kranenburg and van IJzendoorn2006) were the first to test the differential susceptibility hypothesis as a function of genetic factors, examining the moderating effect of the dopamine receptor D4 seven-repeat polymorphism (DRD4–7R) on the association between maternal sensitivity and externalising behaviour problems in 47 families. Children with the DRD4–7R allele and ‘insensitive mothers’ displayed significantly more externalising behaviours than children with the same allele but with ‘sensitive’ mothers. Children with the DRD4–7R allele and sensitive mothers had the fewest externalising behaviours of all, whereas maternal sensitivity had no effect on children without the DRD4–7R allele.
Research has also demonstrated that possessing at least one s-allele of the serotonin transporter gene HTTLPR confers an increased risk of developing depression when facing adverse events. However, the same variation is linked to superior cognitive performance in several domains and increases social conformity (Homberg and Lesch, Reference Homberg and Lesch2011).
These examples serve as evidence against simple genetic determinism and also provide indications that naïvely aspiring to alter genes alone in order to treat disorders may not be in an individual’s best interest as differing circumstances alter the harmfulness or benefits of such a gene.
The concept of the environment of evolutionary adaptedness (EEA) was first proposed by John Bowlby (Reference Bowlby1969) of attachment theory fame. Broadly speaking, the EEA refers to the overall ancestral human environment during which the distinctive traits of modern humans were shaped. It is sometimes referred to incorrectly as if it were a single, uniform time and place. However, it is more appropriately conceptualised as ‘a statistical composite of the adaptation-relevant properties of the ancestral environments encountered by members of ancestral populations, weighted by their frequency and fitness consequences’ (Tooby and Cosmides, Reference Tooby and Cosmides1990: 386–387). The EEA is therefore a compound idea representing the sum of a population’s exposure, over a given time frame, to external conditions and stimuli, threats and opportunities, including nutrients, social pressures, threats from parasites, predators and competitors as well as climate and general habitat (Gluckman et al., Reference Gluckman, Beedle and Hanson2009). Thus, it may be considered as a ‘composite of environmental properties of the most recent segment of a species’ evolution that encompasses the period during which its modern collection of adaptations assumed their present form’ (Tooby and Cosmides, Reference Tooby and Cosmides1990: 388). It is important to note that ‘different adaptations will have different EEAs. Some, like language, are firmly anchored in approximately the last two million years; others, such as infant attachment, reflect a much lengthier evolutionary history’ (Durrant and Ellis, Reference Durrant, Ellis, Gallagher and Nelson2003: 10).
Critics of the concept of the EEA have argued that we do not know much about how our remote ancestors lived, and they claim that this makes the concept of the EEA a highly speculative and unscientific premise (Hagen, Reference Hagen and Buss2016). Critics such as Gould (Reference Gould1997), Buller (Reference Buller2005) and Laland and Brown (Reference Laland and Brown2011) also objected to the use of the concept of the EEA because they assumed that we are unable to specify the living conditions of our ancestors with sufficient precision. There is no doubt that some of these concerns are legitimate and should be seriously considered. However, if their assertions are true, such that we can never know anything about how our ancestors lived and will never be able to do so, then an evolutionary approach could not ascertain the exact function of any somatic or brain system. As all functions are adaptations shaped by selection in response to past environments, discovering facts about past environments remains an important part of the evolutionary endeavour and a prerequisite to understanding current function and dysfunction.
The assertion that we cannot know much about the past is nowadays no longer tenable and contradicts a wide range of academic disciplines whose focuses are entirely on investigating the past. These fields include archaeology, palaeontology, palaeoanthropology, history and cosmology, which now include not only research into fossils and artefacts, but also sequencing the DNA of ancient and extinct species (Hagen, Reference Hagen2020). This has allowed enormous progress and clearly and decisively demonstrates that scientific research aimed at discovering facts about the past is capable of producing rigorous, testable and falsifiable models of past environments (e.g. Dunbar, Reference Dunbar2014). Without knowledge of the past, evolutionary science simply cannot progress, and hence a concept of the EEA or ancestral human environment is essential. This does not mean that statements about human evolutionary history should be accepted blindly or uncritically. All such claims should be stated as hypotheses that can be supported or falsified by the evidence, and a similar level of scientific rigour should also apply to hypotheses about human psychological adaptations and their functions.
As we have seen, natural selection produces bodies and brains with assortments of adaptations shaped over thousands of generations to enhance reproductive success (fitness) but not necessarily well-being or happiness. The explanation for the conundrum of why evolution has left humans so vulnerable to disease and disorder has itself been evolving ever since it was first posed by the founders of modern evolutionary medicine (Nesse and Williams, Reference Nesse and Williams1994). Accordingly, a range of pathways have been proposed by which evolutionary processes can lead to the existence and persistence of disease or disorder, as presented in Box 1.1.
Some of these pathways are more relevant than others to psychiatry, and they are not mutually exclusive. Several may be implicated concurrently or sequentially in the origin of mental disorders. They represent a list of ultimate/evolutionary causes of our vulnerability to disease and disorder, including mental disorder.
Mismatch is arguably one of the most important insights of evolutionary medicine and is indispensable to the understanding of a range of diseases and disorders prevalent in the modern environment, such as the increased prevalence of coronary artery disease, hypertension, obesity, type 2 diabetes, depression, alcoholism and eating disorders, to name a few (Nesse and Williams, Reference Nesse and Williams1994; Pollard, Reference Pollard2008). The idea of mismatch is based on the fact that adaptations are shaped by selection within a given environment. If the environment changes rapidly and radically, some biological systems run the risk of becoming mismatched to the new environment. This is also referred to as ‘genome lag’ (Li et al., Reference Li, van Vugt and Colarelli2018). Given that the modern human environment has undergone a radical change from that of our ancestors in a number of ways, this has led to some systems becoming mismatched to this novel environment, giving rise to dysfunctional outcomes, including a range of mental disorders (see Chapter 2 for further discussion). Examples of mental disorders arising/increasing in the modern environment include eating disorders (Rantala, Reference Rantala, Luoto, Krama and Krams2019; Russell, Reference Russell, Gelder, Lopez-Ibor and Andreasen2000) and drug and alcohol addictions (Nesse, Reference Nesse2005) (see Figure 1.1 for an illustration of nutritional mismatch). However, while humans may be mismatched to certain aspects of the modern environment (e.g. the constant abundance of nutrients and especially of ultra-processed foods), we are well matched to the majority of modern conditions, as humans are clearly thriving and not becoming extinct (Hagen, Reference Hagen2020).
Life history theory (LHT) deals with species’ typical solutions to problems associated with survival and reproduction that change over an individual’s lifespan (Brüne, Reference Brüne2015). Hence, LHT provides a framework for understanding how organisms allocate time and energy in achieving core biosocial goals across their lifespan. Life history strategies involve a series of trade-offs that shape important biological developments, including the timing of sexual maturity and the number and quality of offspring, as well as the length of lifespan (Stearns, Reference Stearns1992). The application of LHT demonstrates that these trade-offs yield a spectrum of life history strategies, and the trade-offs include somatic versus reproductive effort, present versus the future and quality versus quantity of offspring. The ‘fast’ end of the spectrum is characterised by a shorter lifespan, faster growth, earlier maturation and reproduction and a larger number of offspring, while those at the ‘slow’ end of the life history spectrum show the opposite characteristics (Del Giudice, Reference Del Giudice2018). The idea of a fast–slow spectrum of life history has been proposed as a framework for understanding individual differences, including vulnerability to mental disorders (Del Giudice, Reference Del Giudice2018). Differences in life history strategies are partly under genetic control, but it appears that the nature and quality of an individual’s early environment may also be important (Belsky et al., Reference Belsky, Steinberg and Draper1991; Ellis et al., Reference Ellis, Shirtcliff, Boyce, Deardorff and Essex2011). The application of LHT to trait variations between individuals as opposed to between species has recently come under critical scrutiny (e.g. Zietsch and Sidari, Reference Zietsch and Sidari2020). As a result, this area of research is undergoing considerable revision regarding both its methodology and its theoretical assumptions (Del Giudice, Reference Del Giudice2020; Young et al., Reference Young, Frankenhuis and Ellis2020).
Defences such as the mood- and anxiety-regulating systems can become overactive or dysregulated, resulting in harmful outcomes and leading to defence activation disorders (Del Giudice, Reference Del Giudice2018; Nesse, Reference Nesse2019). Examples of defences in general medicine include pain, diarrhoea, vomiting and pyrexia, for which similar principles apply. Importantly, all defences – whether in biologically evolved or human-made systems – have a common design feature such that they are designed to allow false alarms (also known as false positives), as these are far less costly than failure to activate (false negatives) when the risk is present (usually with catastrophic results; imagine, for example, ingesting a toxin and failing to vomit). This is referred to as the ‘smoke detector principle’ and explains why all bodily defences (including aversive emotions) can activate excessively (Nesse, Reference Nesse2019). The excessive tendency for false alarms that characterises all defence systems is akin to a strategy of ‘better safe than sorry’ (Blumstein, Reference Blumstein2020) and explains why it is usually safe to block a defence once it is established that the response is not necessary or even counterproductive.
Humans as hosts have been and continue to be engaged in an unending arms race with rapidly evolving pathogens such as bacteria and viruses (Ewald, Reference Ewald1994). This means that increasingly innovative host defences (e.g. increasingly sophisticated immune responses) are matched by even more novel ways of evading such defences. Also, increasing numbers of pathogens have become resistant to antimicrobial therapy, which poses an increasingly serious hazard to human health. In this arms race, pathogens, as rapid replicators, have the advantage because of their much faster capacity to evolve (Nesse, Reference Nesse2005). The recent Covid-19 pandemic is a vivid example of a newly evolved virus jumping species and spreading globally through the human population, taking a massive toll in terms of human life and livelihoods, and there seems no doubt that there will be other such pandemics in the future. This is undoubtedly a massive problem for medicine in general, but examples in mental health appear more limited. For example, obsessive-compulsive disorder (OCD) can arise as a result of streptococcal-induced autoimmune disease (Swedo et al., Reference Swedo, Leonard and Kiessling1994), and there have been ongoing suggestions of a link between Toxoplasma gondii and schizophrenia (Fuglewicz et al., Reference Fuglewicz, Piotrowski and Stodolak2017) (see Chapter 10).
Unlike a human designer, evolution cannot go back to the drawing board and start afresh. This is called ‘path dependency’ and explains poor ‘designs’ such as why human eyes have blood vessels that occlude portions of the retina (Nesse, Reference Nesse2005), why the light receptors in the human retina face the wrong way (Lents, Reference Lents2020), the tortuous path of the recurrent laryngeal nerve and why our bipedal skeleton – a modified version of a quadrupedal design plan – creates myriad vulnerabilities from ubiquitous back problems to birth canals too narrow to admit a foetal head (Pavličev et al., Reference Pavličev, Romero and Mitteroecker2020; Taylor, Reference Taylor2015). It is also why phylogenetic history and the EEA matter so much. Evolution must work with what has gone before; complex systems are not created out of nothing. Evolution has been described as a tinkerer, shaping adaptations (from available biological systems) that work just well enough for survival and reproduction (Jacobs, Reference Jacobs1977). Hence, evolution is a process that shapes adaptations through historical constraints, multiple trade-offs and (genetic) errors (Nesse, Reference Nesse2005). Evolutionary thinking, therefore, explains the flaws, quirks and tortuous complexity that is ubiquitous in biological systems, all of which can create vulnerabilities to dysfunction and disorder.
It is necessary to appreciate that all biologically evolved adaptations, traits and systems represent trade-offs, as increasing one trait is often at the expense of worsening the performance of another. For example, increasing resistance to infections increases the risk of autoimmune diseases. Also, this explains why improving energy conservation and famine resistance increases the risk of obesity when food becomes plentiful and why the reciprocal trade-off between body size/muscle bulk and speed of movement has an optimum balance such that increasing one can lead to a decrease in the other.
1.2.7 Sexual Selection and Its Consequences
Sexual selection was described by Darwin (Reference Darwin1871) to explain the evolution of traits that do not aid survival and may even be detrimental to it. The canonical example of a sexually selected trait is the peacock’s tail, which serves no survival purpose but is an attractor of peahens. Sexually selected traits are those that improve reproductive success through increased attractiveness to the opposite sex. Sexual selection occurs in all sexually reproducing organisms, including humans, and usually involves the display of costly and extravagant traits that are difficult to fake and can therefore act as honest markers of good health and high-quality genes. Sexual selection tends to shape traits that are gender divergent and to specifically target the preferences of the opposite sex. The evolution of sexually selected traits can create particular kinds of vulnerabilities to mental disorders, which are often skewed in their sex ratios. Examples of mental disorders where sexual selection may play an important role include eating disorders (Abed, Reference Abed, St John-Smith and Shackleford1998) (see Chapter 11), sexual dysfunction and schizophrenia (Del Giudice, Reference Del Giudice2017).
In diploid species such as humans, the two alleles can be identical (homozygote) or different (heterozygote). The classical example in medicine of a heterozygote advantage is sickle cell anaemia, where the heterozygote state confers immunity to malaria (which is a major advantage in parts of the world where malaria is endemic), whereas the homozygote state causes sickle cell anaemia, a serious and debilitating disease (Gluckman et al., Reference Gluckman, Beedle and Hanson2009). In this example, the benefits of the heterozygote state are counterbalanced by the deleterious effect of the homozygote state. Other examples of heterozygote advantage in medicine are more speculative (e.g. cystic fibrosis). There are currently no examples of this process relevant to mental health.
Human migrations out of Africa took place around 70,000 years ago onwards. They took place in successive waves and in doing so human populations frequently passed through impediments or bottlenecks (due to famine, disease, etc.) that caused significantly reduced genetic diversity (Henn et al., Reference Henn, Cavalli-Sforza and Feldman2012). Such scenarios also include small populations that become isolated through chance events and continue living in small, isolated communities where otherwise-rare mutations can become unusually prevalent as a result of a ‘founder effect’ (Gluckman et al., Reference Gluckman, Beedle and Hanson2009). Such chance events are also referred to as genetic drift. Examples of rare harmful genes becoming prevalent as a result of the founder effect include Tay–Sachs disease, which exclusively affects Ashkenazi Jews, and Gaucher’s disease, which is found disproportionately in French Canadians. Interestingly, recent findings suggest that globally, human populations, in their migration out of Africa, have been subject to serial bottlenecks (and founder effects) that increased the further away they travelled from the African continent, as a result of which genetic diversity successively declined (Henn et al., Reference Henn, Cavalli-Sforza and Feldman2012). This phenomenon may also explain the high prevalence rates of Huntington’s disease in Venezuela, Colombia, Peru and Brazil (Kay et al., Reference Kay, Tirado-Hurtado, Cornejo-Olivas, Collins, Wright, Inca-Martinez, Veliz-Otani, Ketelaar, Slama, Ross, Mazzetti and Hayden2017).
The basic tenet of Darwinian theory is that selection works through reproductive success and not necessarily through good health and well-being. Therefore, a gene that reduces health and well-being but increases reproductive success will nonetheless spread within the population (Nesse, Reference Nesse2005). Hence, high levels of competitiveness, reduced cooperativeness, increased jealousy, greed and envy and unquenchable sexual desire will spread despite their potential adverse effects on the health and well-being of self and others because of their positive effects on reproductive success (Buss, Reference Buss2000).
Deleterious genes that allow survival beyond reproductive age and do not manifest themselves until later life may remain within the population, such as those responsible for Huntington’s disease. Such alleles/mutations can remain at low levels in the population as selection is limited in its ability to eliminate them. Also, non-fatal de novo mutations (mutations that arise in the germ line during the lifetime of a parent and where the parent is unaffected by the mutation) will be passed on to offspring. Such mutations are invisible to selection in the first generation and will only be subject to selection in subsequent generations if they are compatible with survival to reproductive age.
Functionally adaptive traits such as anxiety, fear or fastidiousness can become dysfunctional and maladaptive at the extreme end of the spectrum, where they present as generalised anxiety disorder, phobia or OCD (Abed and De Pauw, Reference Abed, Ayton, St John-Smith, Swanepoel and Tracy1998; Crespi, Reference Crespi, Alvergne, Jenkinson and Faurie2016). Similarly, the extreme ends of adaptive personality traits can lead to dysfunctional and maladaptive states (Trull and Widiger, Reference Trull and Widiger2013). Maladaptive extremes can be dysfunctional at both ends (i.e. where the trait is too low as well as too high). This can apply to any biologically based trait, such as mentalising (theory of mind), where both overactivity and underactivity have been implicated in mental disorders (schizophrenia and autistic spectrum disorder, respectively) (Crespi, Reference Crespi, Alvergne, Jenkinson and Faurie2016).
Hence, taking an evolutionary perspective provides a key insight that mental distress can arise from functional systems (e.g. overactive defences or mismatch) (Abed et al., Reference Abed2019). It therefore follows that undesirable conditions, which should still warrant intervention by healthcare professionals, may result from a variety of situations that may but do not necessarily involve true biological dysfunction. In addition, an evolutionary analysis provides a theoretical framework that enables us to distinguish states of mental distress and mental disorder that arise from functional or dysfunctional systems and also provides a more effective way of understanding the role of environmental context (see Chapter 2 for a discussion of harmful dysfunction).
The human brain accounts for 2% of body weight but consumes 15–20% of the total energy required by the body (Brüne, Reference Brüne2015). This striking fact requires an evolutionary explanation as such an energetically expensive organ could only evolve if its benefits outweighed its costs (Aiello and Wheeler, Reference Aiello and Wheeler1995). The most compelling and empirically supported explanation for this is that the demands of the social environment were the main drivers of the increase in brain size over the course of human evolutionary history (Dunbar, Reference Dunbar2003a; Humphrey, Reference Humphrey, Bateson and Hinde1976).
The social brain refers to a network of neurobiological systems that specialise in the processing of information relating to the social domain (Brothers, Reference Brothers1997; Dunbar, Reference Dunbar2003b). There appears to be a quantitative relationship between a species’ brain size and the average size of its social groups that holds true across species (Dunbar, Reference Dunbar2014). However, the relationship between brain size and group size (strictly speaking the volume of the neocortex) applies only to species that have bonded social relationships and form highly structured groups. These social bonds manifest in the form of friendships – intense, emotionally close relationships that are similar to pair-bonds but do not involve sex and reproduction. Such complex social arrangements contrast sharply with the fleeting and ephemeral interactions of herd animals that do not form lasting bonds (Dunbar, Reference Dunbar2014).
The social organisation of hunter-gatherers appears to have been characterised by a nested hierarchy of groups starting with bands of 30–50 people, bonded communities of 150 people, endogamous communities of 500 people and ethnolinguistic units (tribes) of 1,500 people (Dunbar, Reference Dunbar2014). Interestingly, these various levels of organisation are still evident in modern-day humans in the concentric ‘circles of acquaintanceship’ (Dunbar, Reference Dunbar2014).
Such an increase in social complexity would not have been possible without language, which is one of the most distinctive human traits (Del Giudice, Reference Del Giudice2018; Pinker, Reference Pinker1994). This has enabled unprecedented levels of information and knowledge transfer that laid the groundwork for cumulative culture (see Section 1.3.2). The scaling up of human social organisation into mega-groups comprising millions (even hundreds of millions in modern nation states) would not have been possible without the human facility for culture acquisition and transmission on a massive scale (Henrich, Reference Henrich2016). Understanding the functions and dysfunctions of the social brain may be relevant to a number of mental disorders involving impairments to sociality, including schizophrenia (Burns, Reference Burns2007) and autistic spectrum disorders (Baron-Cohen, Reference Baron-Cohen1994).
Humans, unlike other organisms, have two parallel and interacting inheritance systems, namely genes and culture. Although culture of sorts is present in a wide range of species and is not unique to humans, cumulative cultural evolution, which involves cumulative improvement over many generations that could not be achieved by any one individual alone (sometimes referred to as the cultural ratchet effect; Tomasello, Reference Tomasello, Parker and Gibson1990), is widely considered to be unique to our species (Dean et al., Reference Dean, Vale, Laland, Flynn and Kendal2014). Cumulative cultural evolution creates changes in the environment that produce selection pressures on genes. In addition, culturally evolved social environments favour the possession of an inherited psychology that is suited to such environments (Richerson and Boyd, Reference Richerson and Boyd2005). The consequences of gene–culture co-evolution for modern humans is related to the phenomenon of ‘self-domestication’ described by some authors (e.g. Brüne, Reference Brüne2007). The existence of these two evolving and interacting systems running in parallel (genes and culture) has been referred to as the ‘dual inheritance system’.
The role of culture in shaping humans both behaviourally and morphologically cannot be overestimated. For example, while we do not know what the last common ancestor (LCA) of chimpanzees and humans (who lived about 7 million years ago) looked like, one influential view suggests that the LCA was a chimpanzee-like ape (Pilbeam and Lieberman, Reference Pilbeam, Lieberman, Muller, Wrangham and Pilbeam2017). If this is so, then humans would have undergone a truly radical behavioural and morphological transformation since the LCA, whereas chimpanzees appear to have changed very little during the same period. Similarly, without cumulative culture or gene–culture co-evolution, gorillas (who resemble overgrown chimpanzees morphologically) have not altered significantly over even longer evolutionary timescales (humans shared a common ancestor with gorillas around 10 million years ago). One plausible explanation for this is that humans have been subject to sustained and prolonged gene–culture co-evolution while there is no evidence of any such effects in the chimpanzee (including bonobo) lineage or the lineages of other great apes (Henrich and Tennie, Reference Henrich, Tennie, Muller, Wrangham and Pilbeam2017). Hence, it may not be an exaggeration to suggest that gene–culture co-evolution has shaped the human mind, the human body and human social structures. It is ultimately worth considering how culture can and has influenced gene frequencies, as culture is in itself an environment and thus becomes part of selection processes.
In addition to culture’s influence on gene selection over evolutionary timescales, it appears that cultural practices can lead to the rewiring of our brains during an individual’s lifespan (Henrich, Reference Henrich2020). The example that has been studied extensively is literacy, where it has been shown that the literate have brains that differ significantly from the illiterate, with a thicker corpus callosum, the shifting of the processing of faces to the right hemisphere, an impairment in face recognition and an improvement in verbal memory (Dehaene et al., Reference Dehaene, Cohen, Morris and Kolinsky2015).
A salient example of the influence of gene–culture co-evolution on modern humans is the shaping of our digestive system. Our digestive system is unusual for an organism of our size with a small mouth, small teeth, small stomach and a short colon, all of which have evolved as a result of the cultural practices of food preparation and the use of fire in cooking in the human lineage (Wrangham, Reference Wrangham2009). Also, the culturally influenced, unique human ability to accurately use projectiles in hunting and fighting over human evolutionary timescales has been proposed as an explanation for the reduction in the physical robustness of modern humans who no longer needed to hunt or fight at close quarters (Richersen and Boyd, Reference Richerson and Boyd2005). Other more evolutionarily recent consequences of gene–culture co-evolution include the evolution of lactase persistence (lactose tolerance), which occurs in populations descended from ancestors with a dairying culture (mainly in northern Europe and parts of the Middle East and Africa). These populations carry a mutation that arose 6,000–7,000 years ago that enables individuals to digest lactose in adulthood (Cavali-Sforza et al., Reference Cavali-Sforza, Menozzi and Piazza1994). Culture has also shaped human psychology, making us ‘cultural addicts’ through weeding out norm violators and rewarding sociable, docile conformists. Humans have also evolved the capacity for accurate learning from members of our in-group so that we developed what might be called ‘collective brains’ (Henrich, Reference Henrich2016).
A recent study, taking a metabolic approach in an attempt to tease out ecological, social and cultural factors over human evolutionary history, suggests that ecological rather than social challenges played the crucial role and that the extraordinary brain growth in the human lineage was strongly promoted by culture (Gonzalez-Forero and Gardner, Reference Gonzalez-Forero and Gardner2018). This finding is consistent with the cultural hypotheses of human brain evolution (Henrich, Reference Henrich2016; Laland, Reference Laland2017).
Interestingly, a novel theory was recently proposed regarding human evolution that may have a direct bearing on the unique human phenomenon of cumulative cultural evolution. This is the proposal that sometime between 70,000 and 100,000 years ago modern humans evolved a ‘systemising mechanism’ that uniquely enables humans to detect patterns in the world that are hidden from other species (Baron-Cohen, Reference Baron-Cohen2020). The claim is made that this mechanism uniquely endowed humans with the talent for ‘generative inventiveness’, which has resulted in the extraordinary diversification in cultural/artistic/utilitarian artefacts in the archaeological record from around 50,000 years ago onwards and contrasts sharply with the long periods of cultural stasis before then (Baron-Cohen, Reference Baron-Cohen2020). It is claimed that the extreme variant of the systemising mechanism is evident in individuals with autistic spectrum disorders. The theory has clear implications for the phenomenon of cumulative cultural evolution as the systemising mechanism provides the engine for the continuous production of new inventions (cultural variants) that is present in humans and absent in other species.
However, with the exception of Baron-Cohen’s recently proposed link between autistic spectrum disorders and the systemising mechanism, the implications for mental health of the recent cultural evolution models and gene–culture co-evolution, as well as recent research findings on the developmental influences of cultural practices, remain largely unexplored and deserve further attention from evolutionary psychologists and psychiatrists.
One recently published evolutionary theory attempts to explain the emergence of mental disorders in humans as being the result of the relaxation of natural selection pressures (RNSP) (Fuchs, Reference Fuchs2019). This is an interesting and novel idea that proposes that, over thousands of generations of evolutionary history, humans have constructed around them an environment that shielded them from a wide range of hazards (e.g. predation), and this has resulted in what the author has termed ‘diversification of human instinctual drives’. The author bases his assumption on a range of sound evolutionary and ethological ideas and concepts, including the differentiation/diffusion of instinctual drives, open and closed genetic instinctual programmes (Mayr, Reference Mayr1974), active versus reactive behaviours and the consequences of frustration of instinctual drives that include vacuous behaviour, displacement, aggression and dysphoria. His ideas on the human construction of a shielding environment are closely related to both the concepts of ‘niche construction’ and gene–culture co-evolution. Interestingly, in their discussion of niche construction, Laland et al. (Reference Laland2017) placed this phenomenon somewhere between natural and artificial selection, and they considered that niche construction would lead to reduced genetic diversity but not to the extent that artificial selection does. This view seems to contradict Fuchs’ RNSP model.
Nevertheless, the relaxation of particular natural selection pressures is an observable phenomenon that has clear consequences on the traits that are freed from specific selection pressures. This is demonstrated in cavefish (Calderoni et al., Reference Calderoni, Rota-Stabelli, Frigato, Panziera, Kirchner, Foulkes, Kruckenhauser, Bertolucci and Fuselli2016), who not only lose their eyesight, as imperfect structures are no longer eliminated (as it is not disadvantageous to have no eyesight in complete darkness and maintaining eyesight is costly), but the absence of daylight leads also to the degradation of their biological clocks. The effects of RNSP are also evident in humans (and many other primates), where the loss of function of the GULO gene, due to the wide availability of vitamin C from plant sources, has resulted in the loss of the ability to synthesise vitamin C (unlike the majority of mammals) and thus has given rise to humans’ susceptibility to the risk of scurvy (Lents, Reference Lents2020).
Fuchs argues that RNSP was exploited during human evolution to shape useful human adaptations, but that the extremes of these diversified adaptations led to dysfunctional forms of behaviour and to various forms of mental disorder. The merits and implications of Fuchs’ novel theory for the understanding of mental disorder remain largely unexplored and deserve further attention from evolutionists.
When applying Fuchs’ RNSP model to present-day culture, and to medicine in particular, we should note that while selection pressures are relaxed in some areas, such as the risk from predators and many infectious diseases, new selection pressures arise in other areas. Humans, of course, remain vulnerable to old threats such as microorganisms (old and new), while new pressures such as the stresses of modern life and technology are having currently unknown effects on fitness and hence on the composition of the human genome of future generations. Therefore, selection pressures are different, not absent.
1.4.1 OpportunitiesWe have argued in this chapter that evolutionary science presents a range of advantages for psychiatry. The advantages can be summarised as follows (Nesse, Reference Nesse2005):
(1) Asking new questions about why evolution has left us all vulnerable to mental disorders;
(2) Providing a way to think clearly about development and the ways in which early experiences influence later characteristics;
(3) Providing a foundation for understanding emotions and their regulation;
(4) Providing a foundation for a scientific diagnostic system;
(5) Providing a framework for incorporating multiple causal factors that explain why some people get mental disorders while others do not.
However, it is important to emphasise that evolutionary psychiatry does not seek to replace mainstream psychiatry. It supplements, informs and augments mainstream psychiatric thinking. Evolutionists fully accept the current ethical principles that govern the practice of psychiatry in which the interests of individual patients, their welfare and the reduction of harm to patients and others remain the central concerns. Furthermore, evolutionary psychiatrists fully subscribe to the principles of evidence-based medicine and do not suggest or prescribe untested treatments to patients based on purely theoretical formulations. Evolutionary thinking can and does generate theories regarding causation that can lead to proposals for novel treatments. However, any such treatments should be subjected to the same rigorous assessments using the standard scientific methodology currently in use in mainstream medicine and psychiatry. Evolutionary psychiatry has no connection to the ideological and unscientific doctrines of social Darwinism and eugenics (see Wilson, Reference Wilson2019). Hence, evolutionary psychiatry aims to utilise our understanding of human vulnerabilities arising from evolutionary processes to help alleviate distress and aid the recovery of individual patients in every ethical and evidenced-based way possible (Troisi, Reference Troisi2015).
1.4.2 Clinical Utility
There are currently only a few examples of psychological/psychiatric interventions based on evolutionary theory. These include compassion-focused therapy (Gilbert, Reference Gilbert2020) as well as a new type of cognitive behavioural therapy (Abrams, Reference Abrams2020). Nevertheless, we would argue that evolutionary knowledge can be useful to both the patient and the clinician in clinical practice even when not administering specific therapies (e.g. through enhancing empathy, greater attention to context and deeper understanding of the evolved function(s) of emotions). However, evolution’s main utility is in helping us to understand health and disease in populations rather than individuals. Evolutionary science is therefore more analogous to epidemiology than therapeutics. It is important to appreciate that, like all models of health and disease, evolutionary theory does not instantly solve all outstanding problems. Issues in psychiatry are particularly complex, and therefore expansive claims of the efficacy of any particular approach are simply not credible. However, evolutionary theory has already been of immense value in multiple areas of biology. As a greater understanding of the human genome will take medicine towards individualised treatments, taking an evolutionary approach can offer invaluable insights. For example, evolution reminds us that there is no such thing as a normal genome. There are only genes that construct phenotypes that result in higher or lower reproductive success in a given environment (Nesse and Dawkins, Reference Nesse, Dawkins, Warrell, Cox, Firth and Benz2010).
1.4.3 Research Implications
An evolutionary approach suggests a new class of questions about the aetiology of disease. Research to answer these questions should eventually allow the psychiatric literature to provide evolutionary considerations for each disease (Nesse and Dawkins, Reference Nesse, Dawkins, Warrell, Cox, Firth and Benz2010). The strategies for formulating such questions and hypotheses remain unsettled, and the methods for testing evolutionary hypotheses are unfamiliar to many in medicine. Nesse (Reference Nesse2011) has suggested a structure for appropriate evolutionary research that uses recent examples to illustrate successful strategies as well as some common challenges. He identifies appropriate questions to consider in testing evolutionary hypotheses. Addressing them systematically can help minimise confusion and errors.
We recognise that providing an introduction to a volume on evolutionary psychiatry that hopes to cater for both the newcomer to evolution as well as evolutionary scholars was going to be a challenge. We aimed to cover the basics of evolutionary theory while presenting current, up-to-date thinking on the subjects included. We particularly hope that those new to evolution feel better prepared to tackle the rest of this volume as a result of reading this introduction and also perhaps interested in consulting some of the references to this chapter and/or reading more widely around the rich and fascinating literature on evolutionary psychology and psychiatry.