Human Genetics and the Image of God

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Dr Graeme Finlay delivered the lecture "Human Genetics and the Image of God" on 7th November 2006 at Queen's Lecture Theatre, Emmanuel College, Cambridge. The lecture was followed by questions from the audience and later a dinner/discussion at St Edmunds College. A transcript of the lecture follows.

Our retroviral heritage
Furtive DNAzens of the genome
Genes from junk
Genes that make us human
Genes for religion
Genes and experience
Humanity and the gracious Other
References and notes


Some people still deny that extensive evolutionary change (macroevolution) has occurred. They deny that the existing mammalian orders or the primates (including Homo sapiens) could have evolved from founding progenitors. Others deny that evolutionary mechanism is compatible with the biblical assertion that God is Creator of the spectacularly diverse biosphere of which we are a part. We are told that once we understand the mechanism of our evolution, we can no longer think of ourselves as having a divinely ordained purpose. An answer to the ‘how’ question supposedly eliminates the ‘why’ question.

Such controversies are eminently resolvable. Genome science has generated accessible and compelling evidence that dispels uncertainty as to human evolutionary origins. Our genetic connectedness to (other) apes cannot call into the question the primary datum of our lives: that we are relational beings. Indeed it is our relationships with other people (and, I believe, with God) that constitute us as human. The basis of christian faith is that a personal God has revealed himself in personal terms as a person, Jesus of Nazareth.

An implication of biblical faith (that recognises the Bible as God’s authoritative Word ‘in all matters of faith and conduct’) is a high valuation of science. The historian of science Gingerich has stated that ‘the very expression “laws of nature,” from the time of Boyle and Newton, derives from the concept of divine law, and it is probably not accidental that science arose in such a philosophical/theological environment’. 1 Its first practitioners had encountered God as the Redeemer who brought life out of death and therefore they recognised him as the Creator who brought order out of chaos.

Wolpert has said that the Templeton Foundation supports courses and meetings on the topic of science and faith in ‘an attempt to reconcile religious belief and modern science.’ 2 I seek rather to clarify the nature of science and of christian faith, both of which are sorely misunderstood. They are different perspectives on reality. When these are understood, reconciliation can look after itself.

Our retroviral heritage

In the early 1980s, I started surveying evolutionary genetics from the vantage point of cancer cell biology. Stories about retroviruses and oncogenes were transforming our understanding of cancer. The dramatic story of the first human oncogenic retrovirus, the human T cell leukaemia virus (HTLV-1) was being told by Japanese researchers investigating an aggressive leukaemia that afflicted adults in Japan and elsewhere. 3

Retroviruses such as HTLV-I are skilled parasites. During the infection cycle, the retroviral genome (genetic material) is copied from RNA into DNA by a viral enzyme (a ‘reverse transcriptase’). The freshly made DNA is spliced into the chromosomal DNA of the infected (‘host’) cell. The insertion event is initiated by another viral enzyme (an ‘endonuclease’), which recognizes a short sequence of bases in the DNA of the host cell, and cuts each DNA strand (so that the two cuts are separated by a few bases). This creates a gap into which the viral DNA is inserted. The loose ends are filled in and joined. The resulting retroviral DNA insert (the ‘provirus’) is recognized by its set of genes (gag, prt, pol, and env), its ‘long terminal repeat’ (LTR) sequences at each end, and flanking short ‘target site duplications’ (TSDs) of host DNA.

host cell DNA-TSD-[LTR-gag-prt-pol-env-LTR]-TSD-host cell DNA

host cell DNA-TSD

These insertional events occur randomly at sites that exist at myriad places in the host cell genome. Early in infection, many distinguishable provirus insertions are found in a cell population. Years later, when a leukaemia appears as a result of the infection, all the leukaemic cells have an HTLV-1 provirus integrated at precisely the same site. 4

Why should all the cells in a cancer have the same inserted retrovirus? There is no way that a segment of HTLV-1 DNA could integrate faithfully into the same site of chromosomal DNA in a large population of cells. There is one conceivable explanation. The impulse to develop into a cancer was initiated in one cell harbouring one particular provirus. This cell and its offspring were driven by the provirus (and by later genetic changes) into a programme of uncontrolled multiplication, producing an expanding clone of descendents, all of which inherited the original provirus from the founding cell. The billions of cancer cells possess the same HTLV-1 proviral insertion because they inherited it from the one progenitor cell. 5

It has been found that everyone possesses retroviral proviruses in their DNA. These proviruses (or ‘endogenous retroviruses’, ERVs) did not enter our DNA by the familiar process of infection, but they were inherited from our parents, just as genes are. All humans have inherited the same zoo of 100,000 ERVs, classified into 80 families. If one includes related elements that possess LTRs there are 400,000 elements and 200 families constituting 8% of our DNA. 6 Regardless of our ethnicity, we are one-twelfth virus. Our DNA is a detailed historical record of past retroviral insertions into the germ-line DNA of our forbears. 7

For all humans to possess the same set of ERVs as part of their common genetic endowment, the germ-line cells sustaining the original infections must have been ancestral to us all. When did the common ancestor(s) live? In the 1980’s some reports suggested that humans and chimpanzees possessed ERVs at the same sites in their respective genomes. At that time, it was not established that the ERVs were precisely the same in the two species (same class of virus, insertion site, orientation, TSD). 8 But it looked like it. The implications were clear. If humans and chimps did in fact possess the same ERV inserts, then both species would have inherited their collection of ERVs from a lineage of common ancestors. Human and chimps would be clonal with respect to each shared (but uniquely arising) ERV.

ERV inserts

The fact that humans and chimps possess in common a set of ERVs was confirmed by a study of six ERVs, present in the DNA of humans and chimps, and of other primates. Three of the ERVs were found in the African great apes. They had integrated into the primate germ-line prior to the human-chimp-bonobo-gorilla radiation. The other three are present in Old World Monkeys (OWMs) and hominoids (apes including humans), but not NWMs. They entered the primate germ-line in an ape-OWM ancestor. Each ERV established that humans, chimps (and other primates that possess it) are descended from the one reproductive cell that sustained the insert. 9

Confirmations accumulated in the literature. Representative insertions of ERVs or their LTRs are shown. In most cases, the undisturbed integration site has been characterised in species that had branched off on another evolutionary trajectory before the integration event. 10

ERVspeciesinsertion site with target site duplication, underlined
 gorilla…not determined…[ERV]TGAGACAGCAT…
 orangutan …GAATCTGAGAC   AATAT…
 orangutan …GAATGATTAT   GATGT…
 orangutan…GTTAT CCAAC  TAAAT…

ERVs have been instrumental in structuring our genomes. 11 Genome sequencing has shown that nearly all of the 400,000 ERV and related LTR-like sequences in the human genome are shared with chimps. There are about 100 human–specific and 300 chimp-specific ERVs. We share a long and unbroken pedigree with (other) apes. 12

Furtive DNAzens of the genome

Our DNA is populated by many other genetic parasites (or ‘transposable elements’). They do not travel between cells. Instead, they track from one generation to the next, as part of the germ-line DNA, copying-and-pasting themselves as they go.

Long interspersed elements (LINEs) are parasites of unknown origin. LINEs produce a protein that acts as an endonuclease (to initiate the insertion event), and a reverse transcriptase (to copy the RNA version of a LINE into the chromosomal DNA version).

How retrotransposons copy and paste

LINE-1 (‘L1’) elements are the most abundant class in human DNA, with over 500,000 copies (17% of our DNA). The insertion process is haphazard, but the mechanisms by which LINEs copy-and-paste themselves are yielding to investigation. 13 Many LINE-1 segments lack TSDs, and may have arisen as repair patches at DNA breaks. 14

Several dozen LINE-1 families are found in human DNA.

When the insertion sites occupied by some 500 human–specific LINE-1 elements were investigated in non-human primates, in no case was an independent insertion found at the corresponding sites in those other species. The probability of two LINE-1 elements independently integrating in the same site in two different species is thus negligible. 19 If two species possess the same insert they have inherited it from the one progenitor.

Transposable elements are powerful markers for delineating lines of descent. An example is found in the centromere of the X chromosome. This LIPA7 insert is present in the great apes and OWMs, descendants of the one reproductive cell in which the insertion occurred. 20

 left flanking sequence[ L1PA7 insert ]right flanking sequence

Genome comparisons have shown that there are 2,000 human-specific and 2,000 chimp-specific LINE-1 sequences. These inserted after the human and chimp lineages diverged. The other half million LINEs we possess are shared with the chimps – a staggering weight of evidence of common ancestry. 21

LINE-1 elements provide other cogent evidence of common ancestry. When LINE-1 RNA is being copied into DNA, the reverse transcriptase can switch from the LINE-1 RNA and start copying a bystander RNA molecule. The resulting insert will be a chimaera: part-LINE-1, part-bystander RNA, joined at a unique point. One such element contains 476 bases of L1 sequence, 40 bases copied from a nearby ERV, and another 40 bases of cellular DNA adjacent to the ERV. This unique chimaera is present in humans, chimps and bonobos. The three species that possess it acquired it by inheritance from a common ancestor. 22 Over 80 of these singular patchwork inserts reside in human DNA. They have been accumulating in primate DNA since before the origin of the simians. 23

Short interspersed elements (SINEs) possess no genes. They co-opt the proteins made by LINEs in order to copy-and-paste themselves into new sites in the genome. The most abundant SINEs in our genome are the primate-specific ‘Alu’ elements, originally derived from a small cellular (7SL RNA) gene, and now numbering 1.1 million inserts (11% of human DNA). The LINE-1-dependent copying-and-pasting of Alu elements has been studied in cultured cells. SINEs are parasites’ parasites. 24

Alu elements multiply through the genome largely by the activity of a few highly active ‘master’ elements. Some can lie in a quiescent state for aeons before bursting into retrotranspositional activity. Some ancient elements may still be active. 25

Major Alu families

relative agefamily extent of divergence age, my

Human-specific Alu subfamilies

subfamilytotal numberdimorphic, %reference

Nearly all (>99%) of the Alu elements in our DNA are shared with other primates. Shared elements do not arise independently: when >2500 insertions of human-specific Alu families were characterised, in no case was an insertion found in a corresponding site in a non-human species. 31 If multiple species possess a particular insert, those species are descended from the one individual in which that unique insert occurred.

The AluYa5 and AluYb families are still expanding in human genomes. They arose from Alu founder elements that inserted into hominoid (ape) ancestors. 32 Potentially active Alu elements can lie in waiting for a million generations, poised to become active when conditions become permissive.

The Yd3 and Ye5 families have been colonising ape genomes for a long time. In one study, 9 elements were shown to be present in humans and chimps but not in gorillas (pointing to a human-chimp ancestral lineage). More remotely, 45 Alu elements are shared by humans, chimps and gorillas (confirming an African great ape ancestral lineage). An additional 38 elements are shared by humans, chimps, gorillas and orangutans, and 65 by the great apes and the lesser apes (gibbons). The apes are ‘monophyletic’ – clonally derived from each progenitor cell that sustained the DNA insertion of one of these Alu elements. 33

Alu inserts: markers of hominoid evolution

The distribution of Alu elements has outlined the phylogenetic development of the OWMs and of the New World Monkeys (NWMs). The OWMs are known to be monophylic (derived from one lineage of common ancestors) on the basis of 35 Alu elements found only in their genomes. 34 The NWMs are known to be monophyletic on the basis of 84 Alu elements shared by NWMs alone. 35

Apes, OWMs and NWMs are simian (anthropoid) primates. More distant primate relations, the prosimians include the tarsiers, and the galago-loris-lemur group. The relationships between these groups have been controversial for a long time. The presence of four ancient Alu inserts in anthropoid primates and tarsiers but not in lorises or lemurs shows that the Anthropoidea and Tarsioidea are derived from a common lineage. 36 Alu sequences and other SINEs have elucidated the phylogenetic development of the galagos, lorises and lemurs. 37

Genes from junk

We have co-opted genes donated by the DNAzens of the genome, as exemplified below.

(1) The env gene of infectious retroviruses enables the virus particles to stick to cells. The human genome possesses 16 ERVs that retain env genes with the capacity to produce intact proteins. These env genes have remained intact far longer than would be expected if they were junk. 38 These env proteins may function to induce the fusion of their adopted cells, as in the formation of the placental syncytiotrophoblast.

Endogenous retroviruses in our DNA that contain intact envgenes

ERVtime of insertionname of env proteinref ERV-FRDsimian ancestor syncytin-239 ERVPbOWM ancestor, or possibly before-40 ERV3OWM-ape ancestor-41 ERV-WE1OWM-ape ancestorsyncytin-142

The insertion site of the ERVWE1 provirus is shown below:


The expression of the ERV-WE1 env gene is regulated by both ERV-WE1 sequences, and by sequences of an upstream LTR-containing element of the MaLR class. ERV-WE1 has undergone a 12-base deletion that enhances its ability to induce cell fusion. This unique deletion has been shown in 8 OWM species and 6 hominoid species, and demonstrates their common ancestry.

(2) The insertion of an Hsmar1 transposon has contributed to the assembly of a new gene. The insertion of the Hsmar1element (and of an Alu element), and a 27-base deletion (required for the incorporation of the Hsmar1 sequence into a pre-existing gene), occurred in ancestors of the simian primates. The Hsmar1 and Alu element insertions occur at exactly the same point.

speciesflank del[ Alu insert ][ hMAR insert ]flank
tarsier (prosimian)…AGTGGCATG   TATCT…

The unique 27-base deletion is preserved in all the simian species. 43 A concatenation of random and unique events has assembled the Hsmar1 gene.

human…AACATCAGTT [          27  base deletion         ] GTGGAAAT…
chimp…AACATCAGTT [          27  base deletion         ] GTGGACAT…
gorilla…AACATCAGGT [          27  base deletion         ] GTGGAAAT…
orang…AACATCAGTT [          27  base deletion         ] GTGGAAAT…
siamang…ATCATCAGTT [          27  base deletion         ] GTGGAAAT…
green mo (OWM)…AACATCAGTT [          27  base deletion         ] GTGGAAAT…
macaque (OWM)…AACATCAGTT [          27  base deletion         ] GTGGAAAT…
owl mo (NWM)…AACATCAGTT [          27  base deletion         ] GTGGAAAT…
galago (prosimian)…AACATCAATTAGGAAGGAA…

(3) The GLUD2 gene produces an enzyme called glutamate dehydrogenase in the brain. It is a ‘processed gene’: a messenger RNA copy of the parent gene was inserted into primate DNA by LINE-1 enzymes.

Retrogenes: genes copied and pasted

The insert, target site duplication (underlined) and an extra CAG are identical in all the ape species. This event occurred in an ape (hominoid) ancestor. The target site in OWMs is empty. 44

 left flanking sequence[ gene ]right flanking sequence 

Such irreducible complexity arising de novo is a recurring theme. Over 100 such ‘retrogenes’ have been discovered in the human genome. Complexity does arise from randomness. 45

Genes that make us human

In summary,

The publication of the human and chimp genomes has meant that ‘scientists can address anthropology’s fundamental question at a new level: what are the genetic changes that make us human?’ 46 Many features characterise us as human, 47 but given that ‘our cognitive abilities, more than anything else’, have defined our distinctive evolutionary niche, states Sikela (2006), 48 ‘there is a general consensus that it is our brain and its unusual talent for complex thought that is the most significant.’ 49

The task of relating our genome to our biology is daunting. Human DNA differs from that of chimps by base substitutions (35 million), inserts and deletions (five million), 50 large duplications >51 and other rearrangements. The contribution of any one of these is not obvious. Most changes will represent random drift. Half of the changes will reflect chimp-specific alterations. The significant changes in the human lineage may have occurred in coding genes, in regulatory regions of coding genes, or in the vast expanse of non-coding ‘dark matter’. 52

It may be simplistic to search for ‘the genes that made us human’ in events that have occurred since our common ancestor with chimps. Goodman et al (2005) argue that the evolution of genes since the era of the earliest primates has contributed to our current nature. 53 ‘The proposal to sequence an entire chimpanzee genome was based on the premise that this genome sequence would be needed to search for the genetic basis of being human. … it is also true that many traits used to define humanity have much deeper roots. Indeed, to identify the genetic roots of being human the comparative primate genomic data need to be enlarged and placed into a phylogenetic framework that encompasses the entire order Primates.’ The sequences of multiple primate genomes are required.

Relating genetics to human biology will be a huge task. Carroll (2003) wrote: 54 ‘Despite our enhanced understanding of functional genetic architecture, there remains a tendency to associate the development, function or evolution of a trait with single genes (genes ‘for’ speech, cancer and so on). The ghost of ‘hopeful monsters’ still haunts biology and is, unfortunately, a prevalent misconception in the scientific and general press ... It seems unlikely that the traits that interest us most – bipedalism, skeletal morphology, craniofacial morphology, brain size and speech – were the products of the selection of just a few genes’. It may be the interacting indivisible entirety of our genome that specifies the indivisible entirety of our biology. Carroll concludes: ‘The sequencing of the chimpanzee genome will reveal no more directly about the origin of human traits than the sequence of the human genome tells us about how to construct a health baby’. 55

Genetics are unable to describe fully what make us human. ‘A complete understanding of uniquely human traits will, however, include more than DNA. Scientists may eventually circle back to those long-debated traits of sophisticated language, culture and technology, in which nurture as well as nature plays a leading role. We’re in the age of the genome, but we can still recognise that it takes much more than genes to make the human.’ 46

Explaining “humanness” is … not easily approached using the genome alone. We prefer to use the term “the human condition” to refer to the entire suite of characters that make humans different from the great apes. What it means to be human involves quantitative aspects of biochemistry, physiology and morphology as well as more qualitative arenas such as cognition, behaviour, symbolic communication, and culture.’ 47

Darwin’s friend and most ardent supporter in America was the Harvard botanist Asa Gray (a devout christian). He said that man ‘is as certainly and completely an animal as he is certainly something more’. 56 An American Professor of Biology Rick Colling has recently said the same thing: ‘We are fully biological but also much more.’ 57

The differences in the biology of the human animal and other great apes are specified in our DNA. This whole area is open to scientific investigation. But the system may be vastly more complex than some ‘genes-that-make-us-human’ enthusiasts have allowed. If our minds and culture are emergent properties of matter and genetics, then genes will never tell the whole story of our humanity.

Genes for religion

Wolpert has suggested that there may be ‘circuits in our brain set up by the genes that predispose us to have religious and mystical beliefs’. 58 If that were completely true, it would have no bearing on whether a transcendent being, the focus of such beliefs, exists independently of our minds. The spiritual faculty – a yearning for the transcendent – may have been of selective advantage because God is the source of the physical and moral order that makes our existence intelligible. A mental faculty that arises by natural selection need not for that reason be unconnected to an independent objective reality.

However, we should not accept Wolpert’s thesis without critical reflection. He compares the tendency to ‘religious belief’ (considered to be genetically encoded) with science: ‘Scientific thinking is not programmed in our brains’. 60 This provides the underlying structure to his book, and the basis of the exalted status given to science. However, ‘science’ and ‘religion’ are not comparable concepts. The equivalent of ‘science’ is ‘theology’. It is these that are systematic, rigorous, scholarly, communal activities, not genetically encoded. Science seeks understanding of natural history (such as primate evolution); Christian theology seeks understanding of God’s actions in concrete human history. The basis of each intellectual discipline is the empirical world. The equivalent of ‘religion’ (causal beliefs regarding the spiritual world) is that set of causal beliefs that interprets the material world. The capacity to entertain such beliefs, whether spiritual or physical in nature, may well reflect genetically encoded, specifically human neural circuits. To be human is to engage in the spectrum of causal beliefs. All of our causal beliefs need to be critiqued at the bar of the appropriate discipline.

Wolpert is a developmental biologist, but he does not discuss the limits of genetics as seen in the plasticity of the brain. Genes provide the neural substrate upon which experience acts to mould our brains. With a faculty as basic even as that of sight, it is experience that turns potentiality into actuality. ‘If babies born with cataracts fail to have them removed within their first year or so, it avails little to remove them, for the vision tuning program has shut down…’. 61 This is an instance of amblyopia, and reflects experience–dependent circuit refinement during an all-important critical period: ‘the seemingly innocuous act of covering an eye can profoundly alter the physical structure of the brain’. 62 The brain develops anatomically in response to environmental inputs, experience, and training. This has been shown by quantifying morphological changes in the brains of musicians, jugglers, taxi drivers, and university students. 63

Genes and experience

The physical structure and the function of the brain, genetics and all, is moulded early in life by the attention and love of those to provide care. Neural and behavioural abnormalities occur in young children who have suffered socio-emotional deprivation. Brain imaging (PET using 2-deoxy-2-[ 18F]-glucose/MRI) has shown reduced metabolic activity in certain parts of the brain of children adopted from institutions where they experienced severe neglect. This is associated with structural abnormalities in the white matter tract (left uncinate fasciculus) which connects the malfunctioning regions. 64

Perry has stated that ‘Genes are designed to work in an environment ... Genes are expressed by microenvironmental cues, which in turn are influenced by the experiences of the individual.’ In the just fertilised ovum, the chemical processes that drive development essentially genetically-determined. By birth, ‘environmental cues mediated by the senses play a major role in determining how neurons will differentiate, sprout dendrites, form and maintain synaptic connections, and create the final neural networks that convey functionality. By adolescence, the majority of the changes that are taking place in the brain of that child are determined by experience, not genetics.’ 65

Sensory neglect in childhood leads to abnormal brain development. ‘In the development of socio-emotional functioning, early life nurturing appears to be critical. If this is absent from the first three years of life, and then a child is adopted and begins to receive attention, love and nurturing, these positive experiences may not be sufficient to overcome the malorganisation of the neural system mediating socio-emotional functioning.’ 66

These ‘experiments’ of nature are not true experiments. All variables (alchohol exposure in utero, nutrition) cannot be controlled. However, experiments in non-human primates have established that boring environments make for plain-looking brains. ‘On the other hand, enriched animal environments – enclosures that stimulate the complexity of a natural habitat – lead to dramatic increases in both neurogenesis and the density of neuronal dendrites, the branches that connect one neuron to another. Complex surroundings create a complex brain.’ Our environments can profoundly influence the structure of our brain. 67 In the study of brain pathology, environmental enrichment has been a poor cousin to genetics and pharmacology, but exerts ‘a range of dramatic effects’. 68

‘As with other brain-mediated capabilities, the capacity to form relationships results from the experience-based expression of an underlying genetic potential … The somatosensory bath – the smells sights, sounds, tastes and touch – of the loving caregiver provides the repetitive sensory cues necessary to express the genetic potential in this infant to form and maintain healthy relationships.’ 69

Anyone with an a priori commitment to describe humanity in exclusively physical (genetic) terms has a problem. Our brains, minds and humanity arise not only from our genes, but from non-quantifiable (‘spiritual’) qualities such as love, joy, peace, patience, kindness, goodness, faithfulness, gentleness, and self-control – all of which are invisible to the tools of science. That which is spiritual must be admitted as constitutive of my neural development as a human person.

Such a tangible reality as human ‘life’ requires such an apparently intangible thing as communication, relationship, and words. Take the words quoted by Jesus at his temptation:

Man shall not live by bread alone, but needs every word that God speaks. (Matt:4:4; from Dt 8:3)

or by Peter when Jesus asked his disciples whether they would leave him:

You have the words that give eternal life. (Jn.6:68)

Supremely, consider the words of St John:

The Word was the source of Life. (Jn 1:4)

We write to you about the Word of life’ (1Jn 1:1)

Here the writer uses the concept ‘logos’ that would be meaningful to both Jewish and Greek readers, to refer to Christ, who as the ‘Word’ was God’s personified self-expression to humanity. As God’s Word he is life-giving.

Spiritual life is life in relation to God. This life comes from experiencing the grace of the One into whose society we are graciously included. Here is a concept of the concreteness of life arising from the apparent abstractness of personal relationship. It is a concept that the reductionistic materialist may not see. Mackay said 40 years ago, ‘Just as we see psychological life embodied in the physical brain, so we can see spiritual life embodied in the psychological mechanisms of a person. Just as psychological life is related to the activity of nerve cells, so spiritual life is related to the scientific mechanistic structure of psychological theory. 70

Humanity and ‘the gracious Other’

Our humanity is not guaranteed by the possession of a human genome. The development of our humanity is consequent upon such a non-material and vulnerable reality as inter-personal relationship. The Franciscan Friar Salimbene relates a story about the Emperor Frederick II of Hohenstaufen, who was intrigued about the origins of language. He ordered that some children be raised from birth in complete silence, in order to ascertain what language they would speak. Perhaps they might spontaneously speak the Language of Heaven.

Frederick’s experiment was performed by ‘bidding foster-mothers and nurses to suckle and bathe and wash the children, but in no wise to prattle or speak with them; for he would have learnt whether they would speak the Hebrew language (which had been the first), or Greek, or Latin, or Arabic, or perchance the tongue of their parents of whom they had been born. But he laboured in vain, for the children could not live without clappings of the hands, and gestures, and gladness of countenance, and blandishments.’ 71

It seems that the children never learnt to speak any language. Their genes for humanity and for religion did not kick in. They died in infancy. We live, develop and grow as human, not according to some deterministic genetic blueprint, but by being immersed in the nurture, love and encouragement of a prior human community. The action of genes in our brains is modulated by the experience of communicated care. ‘The untouched newborn may literally die.’ 72

Much may be learned from children who have spent their earliest years apart from human company, either because of severe neglect, or because they were separated from society and raised by animals. An example of this has come to light recently in the Pacific, where a boy was kept with the chickens, pecked his food from the ground, and when found, did not learn to speak or enter into society. 73

Stories of neglect (Genie) or of separation (Amala and Kamala) may be found in the ‘Feral Children’ website. 74 When introduced into society, such children do not learn to speak, or develop a sense of ‘I’ as a human being, or become socialised. The neglected child Genie, for example, could not grasp the meaning of pronouns. She used ‘I’, ‘me’, and ‘you’ interchangeably. 75 Language is learned only in the companionship of others and may be necessary for human consciousness. 76

When it comes to being fully human, genetics counts for nothing if an infant is separated from humanity. Our humanity is the outcome of ‘three kinds of adaptive history’: the influence of biological evolution through the genes, the evolution of neural circuits through experience, and the influence of cultural evolution. It seems that ‘culture and speech are essential for the making of the human mind’. The situation is complex, because ‘it could be that the lack of a social trigger at the right moment, meant that certain genetic programmes failed to kick in’. 77

Steeves has said that ‘Defining “human” by means of distant hairy relatives or genetic tests capable of being run only by a few experts in our society is just as unfulfilling as defining “human” as a creature with a chin. …Perhaps being human is best understood as being a particular character in the intertwining stories of the living world. … What I have in mind is the notion that the burgeoning consciousness of the infant will not necessarily develop into human intentionality on its own but rather requires the presence of a Significant Other who is human. This “gracious act of attention” is thus responsible for “creating” a human-person … Without a human Other to attend to the child as human, the child does not become human – which is not to say that feral children have no sense of Self or Other, but rather that such senses do not include “humanity” ... Humans we know are not defined genetically or anthropologically …Humanity is in some respect the result of specific treatment within one’s community … Being human is being treated by humans as human.’ 78

When I studied for my BTh with the open University of South Africa, I came across and was hugely impressed by the Xhosa saying ‘umuntu ngumuntu ngabantu’ or ‘a person becomes a person through persons’. 79

Our genes are absolutely necessary but completely insufficient to define our humanity. Our status as human beings arises from personal knowledge. What our genetics do is to give us the ability to receive the love of others which in fact confers upon us our humanity. This is congruent with the words of Christ:

And eternal live means knowing you the only true God, and knowing Jesus Christ, whom you sent (John 17:3).

In his first letter, St John spelled out a similar concept:

the Son of God has come and has given us understanding, so that we know the true God. We live in union with the true God – in union with his Son Jesus Christ. This is the true God and this is eternal life (1John 5:20).

As human beings we transcend our genes because they could never make us human. It is the love of humans who have made us human. In being known and loved we know and love. In similar manner I believe that we are socialised into the community of God only by the communication of his grace. No extra material is added to our humanity, but just as we have human life through knowing, so we have spiritual life - the fullness of life – in knowing the WORD of God, spoken in Jesus Christ. 80

I believe that the words of St Paul, written to the christian community at Philippi, reveal the apogee of authentic humanity:

‘All I want is to know Christ and to experience the power of his resurrection, to share in his sufferings, and become like him in his death, in the hope that I myself will be raised from death to life.’ (Phil 3:10-11)

References and notes

1. Gingerich O (2006). God’s Universe. (Cambridge MA: Harvard University Press), p.72

2. Wolpert L (2006). Six Impossible Things Before Breakfast. (London: Farber and Farber), p.214

3. Karpas A (2005). Human retroviruses in leukaemia and AIDS: reflections on their discovery, biology and epidemiology. Biol Revs Camb Philos Soc79, 911

4. Mortreux F, Gabet A-S and Wattel E (2003). Molecular and cellular aspects of HTLV-1 associated leukemogenesis in vivo. Leukemia17, 26; Tsukasaki K, Koeffler P and Tomonaga M (2000). Human T-lymphotropic virus type I infection. Best Pract Res Clin Haematol13, 231

5. An artificial retrovirus carrying a therapeutic gene has also produced leukaemia. In each patient, one insertion event targeted and dysregulated a key (LMO2) gene. Every derived leukaemic cell possessed the same (clonal) provirus insert. See Hacein-Bey-Abina S, Von Kalle C, Schmidt M et al (2003). LMO2-associated clonal T cell proliferation in two patients after gene therapy for SCID- X1. Science302, 415

6. International Human Genome Sequencing Consortium (2001). Initial sequencing and analysis of the human genome. Nature409, 860; Li W-H, Gu Z, Wang H and Nekrutenko A (2001). Evolutionary analysis of the human genome. ibid, 847; Bannert N and Kurth R (2004). Retroelements and the human genome: new perspectives on an old relation. Proc Natl Acad Sci USA101 suppl 2, 14572.

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11. Hughes JF and Coffin JM (2001). Evidence for genomic rearrangements mediated by human endogenous retroviruses during primate evolution’, Nature Genet 29, 487; Hughs JF and Coffin JM (2005). Human endogenous retroviral elements as indicators of ectopic recombination events in the primate genome. Genetics171, 1183; Romano CM, Ramalho RF and de A Zanotto PM (2006). Tempo and mode of ERV-K evolution in human and chimpanzee genomes. Arch Virol in press.

12. The Chimpanzee Sequencing and Analysis Consortium (2005). Initial sequence of the chimpanzee genome and comparison with the human genome. Nature437,69;

Polavarapu N, Bowen NJ and McDonald JF (2006). Identification, characterization and comparative genomics of chimpanzee endogenous retroviruses. Genome Biol7, R51; Lopez-Sanchez P, Costas JC, and Naveira HF (2005). Paleogenomic record of the extinction of human endogenous retrovirus ERV9. J Virol79, 6997.

13. Zingler N, Willhoeft U, Brose J-P et al (2005). Analysis of 5’ junctions of human LINE-1 and Alu retrotransposons suggests an alternative model for 5’-end attachment requiring microhomology-mediated end-joining. Genome Res50, 780. Of LINE-1 elements with TSDs, 15% are full-length (6,000 bases long), 66% are partial (truncated) and 19% are truncated with partial inversions. Models of transposition are: (i) full-length (or truncated without micro-homologies at the junction of cellular and L1 DNA): template jump model; (ii) truncated with micro-homologies: micro-homology-mediated end-joining model; (iii) truncated and inverted: twin priming.

14. Morrish TA, Gilbert N, Myers JS et al (2002). DNA repair mediated by endonuclease-independent LINE-1 retrotransposition. Nature Genet31, 158

15. Khan H, Smit A and Boissinot S (2006). Molecular evolution and tempo of amplification of human LINE-1 retrotransposons since the origin of primates. Genome Res16, 78.

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17. Deininger PL and Batzer MA (1999). Alu repeats and human disease. Molec Genet Metab67, 183; Ostertag EM and Kazazian HH (2001). Biology of mammalian L1 retrotransposons. Annu Rev Genet35, 501; Chen J-M, Stenson PD, Cooper DN and Ferec C (2005). A systematic study of LINE-1 endonuclease-dependent retrotranspositional events causing human genetic disease. Hum Genet117, 411; Callinan PA and Batzer MA (2006). Retrotransposable elements and human disease. Genome Dyn1, 104. For a detailed study of an Alu retrotransposition into the renal chloride channel gene CLCN5 resulting in Dent’s disease of the kidney, see Claverie-Martin F, Gonzalez-Acosta H, Flores C et al (2003). De novo insertion of an Alu sequence in the coding region of the CLCN5 gene results in Dent’s disease. Hum Genet113, 480; Claverie-Martin F, Flores C, Gonzalez-Acosta H et al (2003). The Alu insertion in the CLCN5 gene of a patient with Dent’s disease leads to exon 11 skipping. J Hum Genet50, 370; for a consideration of the SVA class of SINEs that currently retrotranspose in humans, see Ostertag EM, Goodier JL, Zhang Y and Kazazian HH (2003). SVA elements are nonautonomous retrotransposons that cause disease in humans. Am J Hum Genet73, 1444; a recent example is provided by Watanabe M, Kobayashi K, Jin F et al (2005). Founder SVA retrotransposal insertion in Fukuyama-type congenital muscular dystrophy and its origin in Japanese and northeast Asian populations. Am J Med Genet Part A138A, 344. In this case, disruption of a gene by insertion a particular SVA element causes serious neurological disease in Japanese populations. This insertion is present at a frequency of ~0.5% of these populations. Because the insert is the same in all those who have the element, it is accepted that it arose in a unique event (estimated to be about 2-2.5 thousand years ago), and everyone who now possesses the element received it by inheritance from the original founder.

18. Bogerd HP, Wiegand HL, Hulme AE et al (2006). Cellular inhibitors of long interspersed element 1 and Alu retrotransposition. Proc Natl Acad Sci USA103, 8780; Stenglein MD and Harris RS (2006). APOBEC3B and APOBEC3F inhibit L1 retrotransposition by a DNA deamination-independent mechanism. J Biol Chem281, 16837.

19. Vincent BJ, Myers JS, Ho HJ et al (2003). Following the LINEs: an analysis of primate genomic variation at human-specific LINE-1 insertion sites. Mol Biol Evol20, 1338; Ho HJ, Ray DA, Salem A-H et al (2005). Straightening out the LINEs: LINE-1 orthologous loci. Genomics85, 201

20. Schueler MG, Dunn JM, Bird CP et al (2005). Progressive proximal expansion of the primate X chromosome centromere. Proc Natl Acad Sci USA102, 10563. Note a particular 7-base deletion shared by the OWMs. This shared novelty is evidence of descent from a unique OWM ancestor in which the deletion occurred.

21. CSAC, ref 12; an analysis that considered only elements with intact TSDs generated comparable although slightly lower figures. Mills RE, Bennett EA, Iskow RC et al (2006). Recently mobilized transposons in the human and chimpanzee genomes. Am J Hum Genet78, 671

22. Ling J, Zhang L, Jin H et al (2004). Dynamic retrotransposition of ERV-9 LTR and L1 in the b-globin gene locus during primate evolution. Molecular Phylogenet Evol 30, 867

23. They are chimaeras of LINE-1 and Alu elements, small nuclear RNAs, messenger RNAs, and ribosomal RNAs. Many are shared by other primate species. Buzdin A, Ustyugova S, Gogvadze E et al (2002). A new family of chimeric retrotranscripts formed by a full copy of U6 small nuclear RNA fused to the 3’ terminus of L1. Genomics80, 402; Buzdin A, Gogvadze E, Kovalskaya E et al (2003). The human genome contains many types of chimeric retrogenes generated through in vivo RNA recombination. Nucleic Acids Res31, 4385; Gogvadze EV, Buzdin AA and Sverdlov ED (2005). Multiple template switches on LINE-directed reverse transcription: the most probable formation mechanism for the double and triple chimeric retroelements in mammals. Russ J Bioorg Chem31, 74.

24. for a review, see Batzer MA and Deininger PL (2002), ref 16; Dewannieux M, Esnault C and Heidmann T (2003). LINE-mediated retrotransposition of marked Alu sequences. Nature Genet35, 41; Schmid CW (2003). Alu: a parasites’ parasite? Nature Genet35, 15

25. Cordeaux R, Hedges DJ and Batzer (2004). Retrotransposition of Alu elements: how many sources? Trends Genet20, 464; Shaikh TH and Deininger P (1996). The role and amplification of the HS Alu subfamily founder gene. J Mol Evol42, 15; Johanning K, Stevenson CA, Oyeniran OO et al (2003). Potential for retrotransposition by old families. J Mol Evol56, 658; see also the supplementary data provided by Mills et al (2006), ref 21

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27. Cordaux R, Lee J, Dinoso L and Batzer MA (2006). Recently integrated Alu retrotransposons are essentially neutral residents of the human genome. Gene in press

28. Garber RK, Hedges DJ, Herke SW et al (2005). The Alu Yc1 subfamily: sorting the wheat from the chaff. Cytogenet Genome Res110, 537

29. Han K, Xing J, Wang H et al (2005). Under the genomic radar: the stealth model of Alu amplification. Genome Res15, 655; Gibbons R, Dugaiczyk LJ, Girke T et al (2004). Distinguishing humans from Great Apes with AluYb8 repeats. J Mol Biol339, 721

30. Salem A-H, Kilroy GE, Watkins WS et al (2003). Recently integrated Alu elements and human genomic diversity. Mol Biol Evol20, 1349

31. Roy-Engel AM, Carroll ML, El-Sawy M et al (2002). Non-traditional Alu evolution and primate genomic diversity. J Mol Biol316, 1033; Salem et al (2003), ref 30; Salem et al (2003), ref 33 below

32. Shaikh and Deininger (1996), ref 25; Han et al (2005), ref 29

33. Xing J, Salem A-H, Hedges DJ et al (2003). Comprehensive analysis of two Alu Yd subfamilies. J Mol Evol57, S76; Salem A-H, Ray DA, Xing J et al (2003). Alu elements and hominid phylogenetics. Proc Natl Acad Sci USA100, 12787; Salem A-H, Ray DA, Hedges DA et al (2005). Analysis of the human Alu Ye lineage. BMC Evol Biol5,18

34. Xing J, Wang H, and Han K et al (2005). A mobile element based phylogeny of Old World monkeys. Molec Phylogenet Evol37, 872

35. Ray DA, Xing J, Hedges DJ et al (2005). Alu insertion loci and platyrrhine primate phylogeny. Molec Phylogenet Evol35, 117; for an earlier study on the distribution of Alu elements in the NWMs, see Singer SS, Schmitz J, Schwiegk C and Zischler H (2002). Molecular cladistic markers in New World monkey phylogeny (Platyrrhini, Primates). Molec Phylogenet Evol26, 490

36. Reviewed by Schmitz J, Roos C and Zischler H (2005). Primate phylogeny: molecular evidence from retroposons. Cytogenet Genome Res108, 26; Schmitz J, Ohme M and Zischler H (2001). SINE insertions in cladistic analyses and the phylogenetic affiliations of Tarsius bancanus to other primates. Genetics157, 777

37. Roos C, Schmitz J and Zischler H (2004). Primate jumping genes elucidate strepsirrhine phylogeny. Proc Natl Acad Sci USA101, 10650

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39. Blaise S, de Parseval N, Benit L and Heidmann T (2003). Genomewide screening for fusogenic human endogenous retrovirus envelopes identifies syncytin 2, a gene conserved on primate evolution. Proc Natl Acad Sci USA100, 13013

40. Aagaard L, Villesen P, Kjeldbjerg AL and Pedersen FS (2005). The ~30 million-year-old ERVPb1 envelope gene is evolutionarily conserved among hominoids and Old World monkeys. Genomics86, 685. This ERV is one of family of only four.

41. Herve CA, Forrest G, Lower R et al (2004). Conservation and loss of the ERV3 open reading frame in primates. Genomics83, 940. Of note is the fact that the env gene is truncated by a ‘stop’ mutation at the same point in all species tested (baboon, macaque, orang, gibbon, chimp, human). The same mutation could not be expected to have occurred independently in all six species; rather these species have all inherited the mutation from the one individual in which the mutation uniquely occurred. This ERV has been described independently by Kim H-S, Yi J-M, Hirai H et al (2006). Human endogenous retrovirus (HERV)-R family in primates: chromosomal location, gene expression, and evolution. Gene in press

42. Mallet F, Bouton O, Prudhomme S et al (2004). The endogenous locus ERVWE1 is a bona fide gene involved in hominoid placental physiology. Proc Natl Acad Sci USA101, 1731; Bonnaud B, Bouton O, Oriol G et al (2004). Evidence of selection on the domesticated ERVWE1 env retroviral element involved in placentation. Mol Biol Evol21, 1895; Prudhomme S, Oriol G and Mallet F (2004). A retroviral promoter and a cellular enhancer define a bipartite element which controls env ERVWE1 placental expression. J Virol78, 12157; Caceres M, NISC Comparative Sequencing Program and Thomas JW (2006). The gene of retroviral origin syncytin 1 is specific to hominoids and is inactive in Old World Monkeys. J Hered97, 100; Bonnaud B, Beliaeff J, Bouton O et al (2005). Natural history of the ERVWE1 endogenous retroviral locus. Retrovirology2, 57. The ERV env gene has accumulated various inactivating mutations in the OWM lineage, starting with an inactivating ‘stop’ mutation that occurred soon after the ERV was integrated:

TGC (encodes the amino acid cysteine) ® TGA (a ‘stop’ signal)

However, env gene function was retrieved in an ape ancestor when a second mutation converted the ‘stop’ into an amino acid-specifying triplet:

TGA (a ‘stop’ signal) ® CGA (encodes the amino acid arginine)

43. Cordaux R, Udit S, Batzer MA and Feschotte C (2006). Birth of a chimeric primate gene by capture of the transposase gene from a mobile element. Proc Natl Acad Sci USA103, 8101

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46. Culotta E (2005). What genetic changes made us uniquely human? Science309, 91; see also Orwant R (2004). What makes us human? New Scientist21 February, 36; Ruvelo M (2005). Comparative primate genomics: the year of the chimpanzee. Curr Opin Genet Dev14, 1; Li W-H and Saunders MA (2005). The chimpanzee and us. Nature437, 50

47. Varki A and Altheide TK (2005). Comparing the human and chimpanzee genomes: searching for needles in a haystack. Genome Res15, 1746-1758; others list sophisticated tool-making, bipedality, culture, language, humour, a big brain (Culotta 2005), ref 46, small canine teeth, changes in skeletal features associated with chewing of food, reduced hair cover, perspiration as an efficient means of thermoregulation, long distance-running capacity, and increased lifespan (Sikela 2006), ref 48, below

48. Sikela KM (2006). The jewels of our genome: the search for the genomic changes underlying the evolutionarily unique capabilities of the human brain. PLoS Biol2, e80

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50. Kehrer-Sawatzki H and Cooper DN (2006). Understanding the recent evolution of the human genome: insights from human-chimpanzee genome comparisons. Human Mutation, in press

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52. Popesco MC, MacLaren EJ, Hopkins J et al (2006). Human lineage-specific amplification, selection , and neuronal expression of DUF1220 domains. Science313, 1304; Pollard KS, Salama SR, Lambert N et al (2006). An RNA gene expressed during cortical development evolved rapidly in humans. Nature443, 167

53. Goodman M, Grossman LI and Wildman DE (2005). Moving primate genomics beyond the chimpanzee genome. Trends Genet21, 511-517; for a summary of primate genomes on the sequencing track, see Dennis C (2005). Branching out. Nature437, 17

54. Carroll SB (2003). Genetics and the making of Homo sapiens. Nature 422, 849

55. Similarly, Lahn has said, ‘If you didn’t tell me that humans were special biologically, I wouldn’t have predicted it looking at the human genome’; quoted by Holms R (2004). Chimp genome preview: the great invertors. New Scientist21 (February), 41-43

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58. Wolpert, ref. 2, p.217. Other postulates include: ‘brain function in relation to belief has a strong genetic basis’ (p.35); ‘our brain has a natural tendency to find consistent and reasonable explanations for important events, and so religious beliefs are most likely partly genetically determined’ (p.137); ‘religious beliefs have a genetic component’ (p.138). These statements seem to boil down to the notion that the capacity to engage in religious or metaphysical beliefs (including ‘reductionist materialist atheist’ ones, p.x) arise from a genetically-encoded neural potentiality.

59. Colling, ref.57, p.147

60. Wolpert, p.201

61. Leiber J (1997). Nature’s experiments, society’s closures. Journal for the Theory of Social Behaviour27, 325

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64. Decreased metabolic activity has been demonstrated in the orbital frontal gyrus, the infralimbic prefrontal cortex, the amygdala and head of the hippocampus, the lateral temporal cortex and in the brainstem: Chugani HT, Behen ME, Muzik O et al (2001). Local brain functional activity following early deprivation: a study of postinstitutionalized Romanian orphans. NeuroImage14, 1290; Eluvathingal TJ, Chugani HT, Behen ME et al (2006). Abnormal brain connectivity in children after early severe socioemotional deprivation: a diffusion tensor imaging study. Pediatrics117, 2093; for a review, see MacLean K (2003). The impact of institutionalization on child development. Development and Psychopathology15, 853. Effects of institutionalisation included abnormal intellectual and physical development, behavioural problems (stereotyped behaviour, attention difficulties, problems relating to peers), indiscriminate friendliness, and loss of attachment.

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66. Perry, p.87

67. Lehrer J (2006). The reinvention of the self. Seed2, 58. This article discussed the work of Elizabeth Gould and Ronald Duman.

68. Nithianantharajah J and Hannan AJ (2006). Enriched environments, experience-dependent plasticity and disorders of the nervous system. Nature Reviews Neuroscience7, 697

69. Perry. p. 94-95

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75. Lieber, p.329

76. Lieber, p.335

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78. Steeves HP (2005). Illicit Crossings: the Other at the Human/Animal Boundary. Rhetoric of Identify: Conference paper, Centre for Rhetorics and Hermeneutics (see

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80. One other point must be made about Wolpert’s ‘religion-is-in-the-genes’ hypothesis. Nowhere did he engage the truth claims of Christianity. When were the gospels written? Did Jesus live as the gospels say he did? Did he claim to come from God? Did the first Christians really believe that Jesus was risen? The record of our evolution as inscribed in our genes reveals an epic story in all its contingent particularity. All creatures that possess a particular ERV or SINE are the descendents of the one organism in which the instance of insertion occurred. The biblical understanding of God has likewise grown as an epic story of unique events in history. The particularities of an Abraham, a Moses and an Isaiah (refugees from the all-encompassing polytheism of the magnificent civilisations of Ur, Egypt and Babylon) are sources of my awareness and understanding of God. Supremely the uniqueness of ‘God’s great historic act in Christ … imposes an inescapable scandal of particularity’ (John Polkinghorne, Science and Christian Belief, p.186). It is history, not genetics, that confronts us with God – a God who is strikingly different to what we may naturally intuit. The singular, radically counter-intuitive teachings of Jesus (‘happy are you who poor’; ‘love your enemies’) speak not of genetics but of encounter with Someone who takes us by surprise.