The fragile biology of social genes and the evolution of human societies

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Work with different animal species has shown that a mutation in a single gene can convert an asocial species into a social one. With a prevalence of human developmental and psychiatric conditions whose primary symptoms are social dysfunction, depression caused by problems with social relationships, and increasing interest in sex without social commitment, are we destined to evolve into an asocial species? Are males who are often less socially adept than females, and more susceptible to conditions such as autism and schizophrenia, most at risk?

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Professor Keith Kendrick


Many of my previous lectures have considered different social behaviours in humans as well as in other mammals and birds. The purpose of this lecture is to look in a little more detail about the purpose and evolution of social behaviour and in particular it’s genetic control and the impact of an individual’s physical and social environment.

What is social behaviour?

Social behaviour is simply defined as interactions among individuals, normally within the same species, that are usually beneficial to one or more of them. It is displayed by a wide variety of animal species from insects to humans and, like any other characteristic is considered to have been selected for as an adaptive trait since individuals engaging in it were more likely to survive and reproduce. While this has been difficult to prove as a concept it has recently been shown that in female baboons sociability is positively associated with improved infant survival independent of dominance rank, group membership and environmental conditions (Silk et al 2003).

However, the quality and complexity of human social behaviour and personality are viewed by many as being culturally derived and governed less by hard genetics and the principles of random genetic mutations selected for by their adaptive value. Indeed, flowing the founding of the field of Sociobiology, particularly through the work of E.O.Wilson on invertebrate species, it took many years for it to gain acceptance. Even today many still find the idea of a strict hard-genetic basis for human social behaviour and personality difficult to accept, particularly in the context of our cherished concept of free-will.

In his Essay “Why Socialism” published in the first issue of Monthly Review in May 1949, Albert Einstein wrote an insightful description of man’s social nature and of the relative contributions of genetic inheritance and experience within society:

‘Man is, at one and the same time, a solitary being and a social being. As a solitary being, he attempts to protect his own existence and that of those who are closest to him, to satisfy his personal desires, and to develop his innate abilities. As a social being, he seeks to gain the recognition and affection of his fellow human beings, to share in their pleasures, to comfort them in their sorrows, and to improve their conditions of life. Only the existence of these varied, frequently conflicting, strivings accounts for the special character of a man, and their specific combination determines the extent to which an individual can achieve an inner equilibrium and can contribute to the well-being of society. It is quite possible that the relative strength of these two drives is, in the main, fixed by inheritance. But the personality that finally emerges is largely formed by the environment in which a man happens to find himself during his development, by the structure of the society in which he grows up, by the tradition of that society, and by its appraisal of particular types of behavior. The abstract concept "society" means to the individual human being the sum total of his direct and indirect relations to his contemporaries and to all the people of earlier generations. The individual is able to think, feel, strive, and work by himself; but he depends so much upon society—in his physical, intellectual, and emotional existence—that it is impossible to think of him, or to understand him, outside the framework of society. It is "society" which provides man with food, clothing, a home, the tools of work, language, the forms of thought, and most of the content of thought; his life is made possible through the labor and the accomplishments of the many millions past and present who are all hidden behind the small word "society." ‘

So just what are the relative contributions of genes and experience to social behaviour? Let’s first take a step back and consider why being social should be an advantage at all.

What are the advantages of being social?

This is a question that taxes most evolutionary biologists. At the heart of all social behaviour are the key defining features of co-operation and altruism. The apparent problem in squaring social behaviour with an individual wanting to promote their own genes is that co-operation and altruism have an associated cost to them in that they may reduce their chances of reproducing themselves if they spend time helping others to do it.

The classic example of this is parental behaviour which I have discussed in a previous lecture (Is having a good parent more important than having good genes? – December 2002). By definition, parenting is nurturing offspring at cost to oneself and is mainly carried out by females who have more invested in their limited supply of eggs than males do with their plentiful supply of sperm. However, in a few monogamous mammals and a large proportion of birds Dad is dragged in as well because Mum has difficulty in doing it successfully on her own. Indeed, as we will see later, parents can have considerable influence on the social behaviours of their offspring.

The most extreme example of reproductive sacrifice in a social community is that found in eusocial animal societies such as in some species of ants, termites and bees where individuals take on specific functional support roles within their society and the business of reproduction is carried out by “queens”. Indeed, those in supporting roles are usually rendered sterile which seems like a kind of insurance policy to make sure they don’t step out of line and cheat!

There are even now two identified species of eusocial mammals. The first of these is the naked mole rat (Heterocephalus glaber). Naked mole rats are hairless and virtually blind and live in large (up to 300 individuals) subterranean colonies in north-eastern Africa. They are Eusocial because only one female and her 1-3 mates actually reproduce. Everyone else is involved in cleaning, defence and looking after the kids (which is similar to eusocial ants and bees). As with queens in other eusocial species, mole rat queens undergo morphological changes compared with the workers. They actually get elongated, forming new ribs so they can carry more offspring during pregnancy but without getting wider since that would prevent them from negotiating the regulation sized tunnels dug by the workers! The Damaraland mole rat (Cryptomys damarensis) is also eusocial.

So what might lead to these kinds of cooperative and altruistic behaviours in different species? The evolutionary biologist W.D. Hamilton proposed some 40 years ago that selfish genes can lead to co-operation and altruism. This is because a gene can spread by helping other individuals reproduce that carry copies of it. The idea is that this is best achieved by assisting kin (so kin selection or “inclusive fitness” rather than individual selection) who are most likely to have similar genes and explains also why species tend to have developed efficient strategies for recognising kin, often using odour cues. This theory provides a good explanation for aspects of social behaviour in eusocial insects and naked mole rats for example and in colonies of these latter species there is very small genetic variation between individuals. However, it is well known that social co-operation in many other species often extends beyond kin. This has led to other theories being proposed. For example Robert Triver’s theory of reciprocal altruism where unrelated individuals may cooperate if the cost of doing so is low and can result in favours being reciprocated and improving fitness.

In humans, cooperation can even occur between unrelated individuals where there is no reciprocation however. This has led to another recent theory proposed by Ernst Fehr and Simon Gächter (2000) that strong reciprocity of cooperation can be maintained in species which incorporate ‘altruistic punishment’ of non-co-operators.

Whatever the explanation for social co-operation and altruism may be however the cost of this must always be less than the benefits in order for it to be maintained. Arguably there also have to be significant costs associated with cheating.

Social genes

Across the animal kingdom from insects to primates one can find examples of species who are relatively solitary and asocial and those who are gregarious and prosocial. In invertebrates in particular, different sub-species of ants, bees, flies and locusts can have dramatically different social phenotypes. This is also true of mammals, most notably in moles and voles and also cats. One obvious approach has been to try to identify genetic differences between such species.

However, at the same time within species some individuals are more social than others and again one can try to identify genetic differences between them. Indeed, variability in social behaviour within a species can be extensive. Again in invertebrates such as worms, locusts and even bees social phenotypes within species can be influenced by environmental conditions. For example desert locusts can switch from solitary to gregarious when unavoidably exposed to other locusts and this causes morphological and physiological as well as behavioural changes. In a collaborative study we have carried out with the University of Cambridge we have found that switching to social mode provokes wide ranging changes in brain neurochemistry (Rogers et al, 2004).

Increasingly what is being found is that despite the obvious complexity of social behaviour very often a single gene polymorphism or deletion can have a very significant impact on it. This is certainly surprising, and while there are other examples of this with non-social behaviours one can quickly be drawn into a tentative hypothesis that social behaviour is designed to be highly vulnerable to genetic mutation effects so it is highly adaptive in terms of being able to change in response to altered environments. One can contrast this for example with control of appetite where large numbers of genes play important roles and this makes it highly robust as a behaviour and very difficult to interfere with or to control therapeutically following manipulation of a single gene or protein.

Hard and soft inheritance

Before looking at some examples of genetic influences on social behaviour it is important to set out the ground rules of the different mechanisms that can be involved. Most people are familiar with the concept of what is termed “hard” inheritance which is the nucleotide-based (DNA) genes you inherit bi-allelically from your mother and father (one copy from each) and which are carried on the chromosomes. Following on from Darwin, a cornerstone of modern genetics theory is that changes in these involve random mutations that may or may not be taken advantage of depending upon whether they convey a reproductive advantage. So phenotypic adaptations by this random route are usually slow.

Prior to Darwin, the idea that organisms could inherit experience acquired traits was first proposed by Jean-Baptiste Lamarck (1744-1829). His theory, while attractive in some ways, was discredited. Taken to extreme it did seem far-fetched with a possible example used being an antelope stretching its neck to reach higher branches turning into a giraffe! However, Darwin and others acknowledged him as the forerunner of evolution. Indeed, Darwin did admit in “Origin of Species” that the heritable effects of use and disuse might be important in evolution. The idea of acquired traits also received a further set back when the Soviet biologist Trofim Denisovitch Lysenko (1898-1976) claimed to have demonstrated empirically with grain seeds that by cold treating them resistance to cold could be passed on to future generations. Stalin liked the idea so much that he made Lysenko director of the Institute of Genetics of the USSR Academy of Science s and plunged Soviet agriculture and genetics research into the wilderness for 20 years!

However, a recent major discovery in biology is that layered onto the genome is an epigenome which represents a form of softer inheritance through which experience-dependent changes can occur (see Richards 2006). This extra layer of instructions which is passed down from parent to child in a less reliable manner and can tell genes whether they should become more of less active or even remain completely silent. It does not however influence the nucleotide sequences of the genes themselves but can modify their activity through methylation changes and histone modifications, particularly at transcription sites. These are referred to as epigenetic marks and are scattered throughout the genome to provide a remarkable way through which experience can interact with it by permanently altered patterns of gene expression. As changes occur developmentally they can be maintained in new cells through mitosis. Differential changes in these epigenetic marks have been shown to increase in monozygotic twins as they age and show fewer and fewer behavioural and physiological similarities (see Fragaetal 2005).

An important qualification on this though is that changes in epigenetic marks during the course of an individual’s life are rarely translated into their germ cells (sperm or eggs) and so are not passed on to the next generation. However, there are a growing number of examples where this does happen so it seems Lamarck was not so wide of the mark after all! I must emphasise though that at this point in time no epigenetic changes influencing social behaviour have been shown to do this.

Epigenetics also plays an important role in the control of imprinted genes which I discussed in the context of sexual conflict in a previous lecture (Sexual conflict and the emergence of sexual equality and monogamy – 7 th November 2002). Whereas the majority of genes are biallelically expressed there a small number of so-called "imprinted" genes where the gene from one parent carries a mark that identifies its origin. This allows either the paternal or maternal copies of these genes in the cells of a particular tissue to be effectively "silenced" by demethylation. In this way, offspring only functionally express copies of such genes from one parent or the other (see Constancia et al 2004). This allows mother and father to effectively compete by promoting different characteristics in their offpsring. Possibly as few as 100 of the 30,000 or so genes in the human genome are imprinted in this way although it is already becoming clear that they play very important roles in foetal development as well as in control of social and cognitive functioning in adults. Also, because only one copy of the gene from a particular parent is expressed this increases the potential risk of mutagenic interference with normal expression. Such disruptions in this gene family are implicated in a number of human neurological and mental disorders many of which also have altered social behaviour (Prader-Willi, Angelman and Tourette Syndromes, Autism, Bipolar affective disorder, Epilepsy and Schizophrenia).

So it can readily be seen that social behaviour can be altered both by hard and soft inheritance and now we can move on to consider some examples of both.

Contributions of genes to social behaviour and identifying them

In all species it is recognised that there is a strong genetic component to social behaviour. In humans comparisons between monozygotic and dizygotic twins have estimated this to be around 40% when one is talking about aspects of social responsibility (altruism, empathy, nurturance and low aggression). A further 23% is down to shared rearing environment and the rest to non-shared environment (Rushton, 2004). The latter two will of course be contributed to strongly by differential epigenetic effects.

To better identify candidate genes a number of gene expression profiling experiments are being carried out to identify social genes. While in invertebrate species these can sometimes provide reliable guides for predicting changes in social behaviours they do tend to still involve large numbers of genes (see Whitfield et al, 2002). So far this approach has been used less in mammals, although as more genomes are sequenced this is likely to be an increasingly important approach in the search for key social genes.

Effects of gene deletions and polymorphisms

While there are undoubtedly large numbers of genes involved in the control of different aspects of social behaviour a remarkable finding across species has been that single gene deletions or polymorphisms can nevertheless cause profound changes to overall patterns of sociability.

An example of this in invertebrates is a cell signalling gene called DIF-1 in amoeba which is linked to cooperative behaviour that actually leads to death of many of the organisms. This suicidal co-operative behaviour occurs when the normally solitary species forms social aggregates as a result of food being scarce. This allows just a small number to reproduce successfully on the shoulders of the supporting cast who die to help them achieve success (Foster et al. 2004). Not many would perhaps contemplate the concept of altruistic amoeba! An interesting development that stops “cheating” death by somehow silencing this DIF-1 gene is that it is also required for successful reproduction so without it you might survive but you also can’t reproduce. This seems a neat biological trick to ensure social cooperation without cheating.

In fire ants, sub-species where workers support and recognise multiple queens have polymorphisms in a specific gene called Gp-9 which distinguish then from species that only have a single queen. This gene appears to regulate discrimination of pheromones that allows altered capacity to recognise and serve multiple queens (Krieger and Ross, 2002). As we will see in a minute in mammals too, social genes often appear to be linked to social recognition by smell.

In honey bees, the switch between worker bees staying in the hive as cleaners and nurturers and then suddenly turning into pollen gathering foragers working outside of the hive is regulated by a single gene, called ‘for’ (Ben-Shahar et al. 2002). Apparently this same gene also shows increased expression in fruit flies that play a roving foraging role rather than a baby sitter one. I am not aware of any human equivalent to this gene being found although were it to be the case it might help distinguish between “roving” and “stay at home” males!

In mammals genetic differences have been investigated in social monogamous species of vole (prairie voles) and asocial promiscuous ones (meadow voles). These have focussed on two small peptides, oxytocin and vasopressin, and their respective receptors. In the social species oxytocin and vasopressin stimulate bonds between mates whereas in asocial ones they do not (Insel and Young, 2001). This has been found to be associated with differences in the localisation of receptors for the two peptides within the brain. In social species there are large numbers of receptors localised in brain reward centres (nucleus accumbens and ventral pallidum) which contain dopamine. When this happens the peptides can act to release dopamine within these centres. Thus, when the sensory cues from a prospective partner, and particularly having sex with them, release oxytocin or vasopressin there is also release dopamine and the animals experience pleasure. In this way social and sexual interactions between partners are reinforced and a bond is formed between them. The same happens in sheep bonding with their lambs and probably in humans bonding with babies and romantic partners as well. In asocial voles this link between release of the peptides and dopamine is much weaker and so social bonds are not formed.

Both oxytocin and vasopressin release in social voles and other species such as sheep also facilitate the development of smell recognition memory for a partner or offspring. In this case it is through modulation of another neurotransmitter important for learning – noradrenaline. So there is a strong link in mammals between prosocial genes and their protein products and social recognition in the same way as there is in the humble fire ants where the Gp-9 gene is involved.

As one would anticipate mice that lack functional expression of the oxytocin gene or the vasopressin receptor gene (v1ar) have problems in some aspects of social behaviour and also with social recognition memory using smell cues.

The work with voles has so far not found an explanation for the different distribution of the oxytocin receptor gene in social and asocial species. However, for the vasopressin v1ar receptor a polymorphism has been found where the addition of small microsattelite repeats in one of the coding regions for the gene promotes the “social” distribution of this receptor in dopamine reward areas of the brain. Interestingly this same longer form of the gene is also found in humans and in our highly social relations, the Bonobos, but not in chimpanzees (Hammock and Young 2005).

Recent experiments have carried out the ultimate proof of the importance of this version of the gene for social behaviour by using methods to express it just within a brain reward centre of an asocial meadow and showing that it became more social and bonded with a mate in the same way a social monogamous prairie vole would (Limetal. 2004). Thus a small polymorphism in a single gene in a mammal can have a fundamental effect on its social and bonding behaviour.

Another interesting gene that has been shown to be linked with social behaviour in mammals is the Foxp2 gene. Through initial studies in a human family with inherited difficulties with language production the genetic defect was first localised to chromosome 7 and then to the Fox2pgene. Language is obviously very much a social communication behaviour and a recent study on transgenic mice lacking this gene has found that they too have problems with producing ultrasonic vocalisations which communicate social stress. (Shu et al, 2005).

Altruism genes

A recent study on 354 families has identified a gene variant on chromosome 11 linked to altruism (Bacher-Melman et al 2005). This gene is involved in the control of the dopamine D4 receptor which I have previously discussed as being linked to “risk-taking” behaviour (Why do we gamble and take needless risks? – 2 nd March 2006 ). However, for risk taking it turns down the activity of the receptor whereas for altruism it turns it up. So in a simplistic way risk taking and altruism are at opposing ends of a spectrum. dopamine acting on the D4 receptor promotes feelings of pleasure and reward and so the argument goes that altruistic individuals are likely to be more easily pleased by any kind of activity whereas “risk-takers” require greater thrill seeking and novelty. Arguably altruism does not normally rate as a high intensity rewarding behaviour!

Human genetic disorders with social behaviour dysfunction

In humans a number of genetic disorders are associated with problems relating to social behaviour although this is usually one of a broader spectrum of problems.

Autism and Aspergers

These disorders particularly impact on social behaviour in humans and currently may affect as many as 1 in 100 individuals (taking into account the full spectrum of disorders classified in this category). Many reports, particularly from the US have reported progressive increases in the incidence of autism disorders over the last 10 years in particular and there has of course been a link claimed with the MMR vaccine. There are a wide range of behavioural, cognitive, language and emotional as well as social components that can be affected in autism. As yet no full understanding has emerged as to the likely causes although genetic links remain one of the main areas of investigation. While it is currently thought that maybe a dozen or more genes are involved it is interesting that both the oxytocin and vasopressin systems in the brain have been linked to autism.

A positive link has been reported between the oxytocin receptor gene in a Chinese Han population (Wuetal. 2005) and blood oxytocin levels are lower in autistic than in other children (Modahl et al. 1998). Intranasal infusions of oxytocin promote social trust (Kosfeld et al 2005) and resistance to psychosocial stress (Heinrichs et al 2003). They also reduce repetitive antisocial behaviours in individuals with autism and Aspergers (Hollander et al, 2003).

A link between autism and the human vasopressin receptor gene (avpr1a) has been reported in terms of a transmission disequilibrium in a microsattelite within a region controlling its expression (Kim et al 2001). The link was strongest in autistic individuals without language impairment. Indeed there is now growing evidence that there may be different genetic components to the social and other aspects of the autism spectrum disorder.

Williams’s syndrome

This is a neurodevelopmental disorder caused by a deletion of a region on chromosome 7 containing around 28 genes. It affects as high as 1 in 7,500 individuals and accounts for around 6% of cases of mental retardation with a genetic origin. Apart from a mild to moderate mental retardation it is associated with cardiovascular abnormalities, growth retardation and a distinct facial appearance. However, in the context of social and emotional behaviour individuals are distinctive in being highly gregarious and social, with increased empathy and overfriendliness. This is associated with a reduced responsivity of the amygdala in the brain to threatening faces suggesting that they may lack the normal social inhibitory control that we have to modify our social responses when dealing with strangers or potentially threatening individuals. For threatening non-social scenes they are actually more responsive than control subjects. In fact, although individuals with Williams’s syndrome appear to be always happy they are actually particularly anxiety prone in non-social areas of their lives.

While a small number of the genes missing in William’s syndrome have been found to have behavioural functions through the use of transgenic mouse models, to date none has been identified that may be associated with the decreased social fearfulness (see Meyer-Lindenberg 2006 for review).

Angelman and Prader-Willi syndromes

As with Williams’s syndrome these are complex genetic disorders causing mental retardation and growth and motor problems. They both result from abnormalities in a region of chromosome 15 and have a similar prevalence to William’s Syndrome. They are both also associated with imprinted genes, with Prader-Willi involving loss of paternally expressed genes and Angelman from loss of maternally expressed ones, notably a gene known as UBE3A. From the view point of social behaviour dysfunction the two syndromes appear to have opposite effects with individuals with Angelman syndrome exhibiting an excessively happy, smiling demeanour and inappropriate laughter (somewhat similar to Williams’s syndrome). On the other hand Prader-Willi syndrome is associated with temper tantrums and obsessive compulsive mannerisms (more similar to autism). These, and other imprinting disorders such as Turner’s syndrome, have led to the speculation that in terms of sexual conflict theory the paternal genome is trying to promote prosocial behaviour in offspring whereas the maternal one is not. However this is likely to be a gross oversimplification.

Transgenic mice have been produced that lack expression of the UBE3Agene and while these have learning and memory dysfunction and abnormal brain electrical patterns they have yet to be shown to have any problems with their social behaviour (Miura et al 2002).

Epigenetic contributions to social behaviour

This is very much an exciting and growing area in behavioural genetics in general as well as in the specific context of socio-biology. It is clear that in the next few years there will be an increasing number of epigenetic modifications to gene transcription identified which can exert life long, and perhaps potentially inheritable, changes to social behaviour.

By far the most investigated epigenetic effect on aspects of social as well as stress behaviour is that discovered in rats by Michael Meaney’s group in Montreal. Some time ago they identified different groups of rats which either exhibited low or high frequencies of licking, grooming and arched-back nursing behaviours towards their pups. This resulted in increased stress responses being shown by their offspring in adulthood as well as altered cognitive function. The offspring also maintained the same pattern of maternal behaviour as their mothers. However, they found that if they cross-fostered offspring from low licking and grooming mothers to high licking and grooming ones they developed the same behavioural phenotype as their foster mother. The same was true of pups born to high licking/grooming mothers being nurtured by low licking and grooming foster mothers. This showed that the social, stress and cognitive changes were caused by early life experience rather than by some form of hard genetic inheritance. Indeed, the researchers found that changes only occurred in response to experience during the first week of life.

They have subsequently identified that the effects of early experience are mediated by altered epigenetic marks on the glucocorticoid receptor (GR) gene within the hippocampus. This is ultimately important for controlling stress hormone (cortisol) release from the adrenal glands. These changes appear to be mediated by altered release of the neurotransmitter, serotonin and a nerve growth factor NGF1-A binding site on the GR promoter. (Meaney and Szyf 2005). Altered epigenetic marks are evidenced by the finding of increased methylation across the promoter region of the GR gene in the low licking/grooming/nursing group of animals.

In a recent study the group have shown that erasing these epigenetic marks with a histone deacetylase inhibitor, trichostatin A, turned offspring from low licking and grooming mothers into the phenotypic equivalent of high licking and grooming ones (i.e. low stress and high nurturing). This effect could be produced even when infusions were made in adulthood.(Weaver et al 2004 and 2006).

One of the interesting aspects of this research that is often overlooked is that what is triggering the behavioural changes in the poorly nurtured rats is not that they have bad mothers but that they are not receiving the optimal amount of tactile stimulation. Indeed, the effects of having a low licking and grooming mother can be prevented just by giving the offspring more tactile stimulation with a brush. Tactile stimulation is at the heart of social behaviour and bonding and in primates in particular mutual grooming behaviours are highly regulated in terms of how much each individual expects to receive and give. Pro-bonding peptides such as opioids and oxytocin can also elicit grooming behaviour in species. Mutual tactile stimulation is something that in many developed cultures has been progressively reduced and yet it seems likely to have long lasting effects in promoting sociability. Experiencing touch in a social context may therefore have a profound influence on promoting sociability!

There are a number of other social, anxiety and aggression traits that are strongly influenced by parental care in animals that I have discussed in previous lectures. It seems likely that many of these will also ultimately be explained by changes in the epigenome and perhaps send out a strong message that parents can alter the behaviour of their offspring throughout their whole lives through promoting them. A sobering thought perhaps for both parents and children!

So what might be the future of human social behaviour?

It is tempting to conclude from the examples I have given of how social behaviour can be dramatically altered by simple single gene polymorphisms and deletions, and by experience dependent epigenetic modifications, that it is both highly flexible and also vulnerable to mutation effects and to cultural change. The proof of this is born out by the number of genetic disorders that impact on aspects of sociability as does the fact that so many species can switch between social and asocial phenotypes. Were we as humans to adopt a progressively asocial lifestyle it seems likely we would quite rapidly embrace genetic changes to establish this as an inherited trait.

Arguably, in many human cultures in the developed world anti-social behaviour patterns are on the increase and pro-social ones on the decrease. We are also moving slowly back towards individual rather than societal based cultures as family, local, national and international boundaries blur and resources become easier to obtain by individuals. Co-operation is also progressively more about joining forces in resource acquisition than it is strictly about reproductive support. As such it has far less of a firm basis in providing improved reproductive fitness.

At this stage it seems reasonable to speculate that humans could evolve a relatively asocial inheritable phenotype quite rapidly if altered cultural values promoted it. If sociability has primarily evolved as an optimum form of reproductive support then, if it is less required in this context, the associated high cost paid through exhibiting altruistic and co-operative social behaviours is less likely to outweigh reproductive benefits. This could lead to a more individual based selfish and relatively asocial strategy for mankind.

Some final conclusions

Social behaviours improve reproductive fitness


Are under strong genetic control


Even co-operation and altruism have genetic components


Both genetic and epigenetic mechanisms are involved


Parental influences play a key role in epigenetic effects


Touch during early social interactions may be important


Single gene deletions and polymorphisms can have major effects


There are many human genetic disorders with altered social behaviour


Many other species can switch from being asocial to social


It would be relatively easy for humans to evolve into an asocial species


Selected references:

Bacher-Melman et al (2005) Dopaminergic polymorphisms associated with self-report measures of human altruism: a fresh phenotype for the dopamine D4 receptor. Molecular Psychiatry 10:333-335.

Ben-Shahar Yetal (2002) Influence of gene action across different time scales of behaviour. Science 296:741-744.

Constancia Metal (2004) Resourceful imprinting. Nature 432:53-57.

Foster KR et al (2004) Pleiotropy as a mechanism to stabilize cooperation.Nature 431:693-696.

Fraga MF et al (2005) Epigenetic differences arise during the lifetime of monozygotic twins. Proceedings of the National Academy of Sciences USA102:10604-10609.

Francis D et al (1999) Non-genomic transmission across generations in maternal behaviour and stress responses in the rat. Science 286:1155-1158.

Hammock EAD and Young LJ (2005) Microsatellite instability generates diversity in brain and sociobehavioural traits. Science 308:1630-1634.

Heinrichs Metal (2003) Social support and oxytocin interact to suppress cortisol and subjective responses to social stress. Biological Psychiatry54:1389-1398.

Hollander E et al (2003) Oxytocin infusion induces repetitive behaviours in adults with autistic and repetitive disorders. Neuropsychopharmacology28:193-198.

Insel TR and Young LJ (2001) Neurobiology of social attachment. Nature Neuroscience 2:129-136.

Kim S et al (2001) Transmission disequilibrium testing of arginine vasopressin receptor 1A (AVPRIA) polymorphisms in autism. Molecular Psychiatry 7:503-507.

Kosfeld Metal (2005) Oxytocin increases trust in humans. Nature 435:673-676.

Krieger MJB and Ross KG (2002) Identification of a major gene regulating complex social behaviour. Science 295:328-332.

Lim MM et al (2004) Enhanced partner preference in promiscuous species by manipulating the expression of a single gene. Nature 429:754-757.

Meaney MJ and Szyf M (2005) Maternal care as a model for experience-dependent chromatin plasticity. TRENDS in Neurosciences 28:456-463.

Meyer-Lindenberg A et al (2006) Neural mechanisms in Williams syndrome: a unique window to genetic influences on cognition and behaviour. Nature Reviews Neuroscience 7:380-393.

Miura K et al (2002) Neurobehavioral and electroencephalographic abnormalities in Ube3a maternal-deficient mice. Neurobiology of Disease9:149-159.

Modahl C et al (1998) Plasma oxytocin levels in autistic children.Biological Psychiatry 43:270-277.

Richards EJ (2006) Inherited epigenetic variation – revisiting soft inheritance. Nature Reviews Genetics 7:395-401.

Rogers et al (2004) Substantial changes in central nervous system neurotransmitters and neuromodulators accompany phase change in the locust. Journal of Experimental Biology 207:3603-3617.

Ross KG and Keller L (1998) Genetic control of social organization in an ant. Proceedings of the National Academy of Sciences USA 95:14232-14237.

Rushton JP (2004) Genetic and environmental contributions to pro-social attitudes: a twin study of social responsibility. Proceedings of the Royal Society London Biology B 271:2583-2585.

Shu W et al (2005) Altered ultrasonic vocalization in mice with disruption in the Foxp2 gene. Proceedings of the National Academy of Sciences USA102:9643-9648.

Silk JB et al (2003) Social bonds of female baboons enhance infant survival. Science 302:1231-1234.

Weaver ICG et al (2001) Epigenetic programming through maternal behaviour. Nature Neuroscience 7:847-854.

Weaver ICG et al (2006) Maternal care effects on the hippocampal transcriptome and anxiety-mediated behaviours in the offspring that are reversible in adulthood. Proceedings of the National Academy of SciencesUSA 103:3480-3485.

Whitfield CW et al. (2003) Gene expression profiles in the brain predict behaviour in individual honey bees. Science 302:296-299.

Wu S et al (2005) Positive association of the oxytocin receptor gene (OXTR) with autism in the Chinese Han population. Biological Psychiatry58:74-77.


©Professor Keith Kendrick, Gresham College, 18 May 2006

This event was on Thu, 18 May 2006

professor keith kendrick

Professor Keith Kendrick

Professor of Physic

Professor Keith Kendrick is Systems and Behavioural Neuroscientist and was Gresham Professor of Physic between 2002 and 2006.

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