Saturday 14 December 2013

Explaining Consciousness Isn't Difficult!

Consciousness has evolved because it has proved to be adaptive. An organism is more likely to survive if it has an accurate model of its immediate environment. However, there is a trade-off between consciousness and other adaptive faculties in terms of the metabolic opportunity cost. The result has been that the characteristics/degree of consciousness varies between species. But what exactly is consciousness? I suggest that consciousness can be described simply as the model of reality that emerges when individual senses - sight, hearing, smell etc - are integrated with each other and with available cognition.

Thursday 17 October 2013

From Overt to Concealed Ovulation in Humans: Theory Note

Females of the ape-like predecessors of Homo sapiens almost certainly exhibited overt ovulation. Over the ensuing 5-6 million years, this has completely changed; modern males have little idea of when a female is ovulating since she provides no visual clue. Why has this change occurred?

The hominid group that discovered bipedalism found important new uses for the forelimbs that had been released from locomotive duties; fighting, gesturing, making tools, building lairs etc. Size of brain became strongly selected as the ability to handle higher levels of intentionality became more relevant to survival and procreation. The size of the birth-canal became a bottle-neck as the head of the hominid baby became bigger to accommodate the expanding brain. Since upright walking was compromised by widening the hip structure, the optimal solution was to opt for earlier birth and therefore a very immature baby. Females then found it impossible to nourish themselves and their highly dependent baby without the assistance of a male. The problem was twofold: firstly, how to get the father to help with the nurture of the child and secondly, how to get the father to stay to protect the female and her child from predators and other males in the longer term.

Attracting a multitude of sexual encounters during ovulation increased the chance of becoming pregnant but resulted in no particular male knowing whether or not he was the father. Therefore no male assistance with child-rearing. Overt ovulation had to go. But what are the advantages of covert ovulation? Males are attracted to copulate by (a) the genetically mediated desire to pass on their genes (b) hormonally-driven sexual desire and (c) enjoying the companionship and comforts provided by the female together with its status enhancing effect. Covert ovulation would mean that (a) could be moderated and copulation not confined to a relatively short period. Consequently, the relative importance of  (b) and (c) would be increased. Furthermore the father would be more inclined to pair-bond and stay on to protect his female and her/ his offspring in the longer term.

Female emancipation, the availability of child-care, the welfare state and the rule-of-law mean that - these days - our new mother no longer needs a male. What next I wonder? Back to overt ovulation? Suggestions please!




Tuesday 25 June 2013

The Famous Rainham Diamond Necklace

Dianne and John are in the cellar. They are searching for the famous Rainham Diamond Necklace. They've been tipped-off that it's hidden somewhere down here; in the cellar. Finding it isn't going to be easy. The unlit room is full of junk. Dianne has a torch with very low power but its weak beam lights a wide area. John also has a torch but, although powerful, it lights just a small area. It leaves the rest of the room in darkness. Dianne suggests they use her torch but John argues that his torch is more likely to assist their search. What a silly story I hear you say; why don't they use both torches?  Why don't they indeed!

The strength of the female brain is that it tends to illuminate the world broadly but tends to sacrifice detail. The strength of the male brain is that it tends to be bright/ sharply focused but very narrow.

I simply want to suggest that we always use both torches!

This doesn't only apply when making decisions in heterosexual relationships. It has implications in boardrooms and politics too. Whenever and wherever decisions are made, it pays to get both a male and a female perspective on the issues involved.


Thursday 20 June 2013

Men are stronger, taller and faster than women. Right?

Men are stronger, taller and faster than women. Right? Of course not right! Try again. Men tend to be stronger, taller and faster than women. Right? Of course right! There are evident differences between the sexes but they are tendencies; not immutable and universal facts. Psychologists have found that these 'tendencies for sexual difference' are not just physical; they are also mental. Men tend to be more narrowly focused than women. Women do tend to be better at multi-tasking. Men tend to be more systematic in their thinking than women. Women tend to be more empathetic than men. I could go on.

In summary: men and women should obviously have equal rights but men and women are not the same.

There are important consequences to these observations. If more boys than girls chose to opt to study the physical sciences, we need be neither surprised nor concerned. If more women than men chose to nurture the children, we need be neither surprised nor concerned. If we find more men than women choosing a political career, likewise. If we find more women than men choosing to become nurses, so not surprising.

Society and, in particular feminists, needs to stop fretting about these differences in outcome for men and women. They are unsurprising when seen in the light of the different tendencies of the sexes; both physical and psychological.

Wednesday 15 May 2013

'Beeeeeeeeeeeeeeeeeep or just Beep?

According to the Highway Code, your car-horn has just one function; to warn other road-users that you are there. However we all know that, in practice, it is often used as a reprimand to another road-user and it is understood to mean 'where the f**k are you goin. Get out the soddin way'! So often is it used and interpreted in this way that many drivers are inhibited from using the horn appropriately as per the Highway Code. This is potentially dangerous.

It is important to let other road-users know you are there when they may be unsighted or otherwise unaware of your trajectory. If drivers are unwilling to use the horn in these circumstances, a nasty accident may be the result. So, what can be done? Here is my solution.

Always use a short sharp 'beep' rather than a long 'beeeeeep'! I am aware that this is not always easy with some horns. I therefore want to suggest that all cars be fitted with a button on the steering wheel that only enables the driver to sound a short, sharp beep. It could be made more recognizable as an information-signal rather than a reprimand-signal by using a different tone to the one we are used to.

What do you think?

"Don't Split; Will Ya"

I must have been about seven years old and the war had just ended. We had been evacuated to Leeds in 1944 while the Nazis tried to blow Southern England to smithereens with V1 and than V2 rockets. Now it was 1945 and we had returned to London to be rehoused on a sprawling council estate in Hackney, East London. There were several large blocks of flats. We had number 25, Woolpack House. Close by there was a sizable bomb-site that we - my friends and I - called 'the ruins'.

One summer afternoon I was wandering on my own in the ruins when I came across Brian Poor and Barbara Deadman in the long-grass. I was startled. They were older than me; perhaps twelve or thirteen. "Don't split, will ya" said Brian rather imperatively. I had no idea what he meant. For some reason, my best guess was that he was suggesting that I shouldn't fart. Don't ask me why this was my best interpretation but I remember quite distinctly that it was. Perhaps my unconscious mind was centered on my sphincter at that moment. "I won't", I mumbled and wandered on, somewhat relieved.

For the record, I didn't split - until now!

I sometimes wonder what became of Brian and Barbara.

Tuesday 30 April 2013

Bee Lucky!

Houston, we've got a problem. Honeybees are dying in their millions. They are essential pollinators of most of the foods we eat. Scientists think that a particular kind of pesticide, called the neo-nicotinoids are to blame. But these pesticides are essential to protect our food from bugs. So; what to do?

Notice that some honeybees are NOT dying. Do they have particular genetic mutations that are more resistant to the pesticides? If they do, we need to encourage the more resistant bees to breed together and produce lots of little pesticide-resistant baby bees don't we?

A simple application of evolutionary theory to the rescue?

Tuesday 12 February 2013

WHAT CAME FIRST; CHICKEN OR EGG?

This issue is often quoted as an example of a question that is impossible to answer. But evolutionary theory tells us that the short answer to the question is 'the chicken'. Although the first chicken to lay an egg almost certainly looked very different from the chickens we are familiar with today. The egg evolved as a good way to give birth to offspring that could survive until the chick was mature enough to 'stand on its own two feet' (so to speak). Before egg-laying evolved, chickens would have 'carried' their young for longer and given birth to chicks that did not have the benefit of the nutrition and protection provided by the egg. Laying eggs was simply a better solution to the multiple needs of survival/ development in the environment of the species. These needs include; ability to get through the birth canal, continuing nutrition, warmth and protection from harm. In chickens, the best compromise was to lay eggs with 'in-house' nutrition and to keep them warm outside the body. In humans, it was to detach from the internal womb/ placenta and feed outside the body with milk. Evolution always 'chooses' the best compromise when there are multiple considerations.

Wednesday 30 January 2013

GENETIC PRIMING; HOW ADAPTIVE BEHAVIOUR SHAPES THE GENOME


ABSTRACT


With regard to Organic Selection, it is suggested that the prevalent step-by-step, incremental hypothesis is logically possible but unlikely to account for much of the adaptive behaviour that we witness in nature. An alternative, hypothetical process - Genetic Priming – is described that is considered more likely. It proposes that there is no assimilation of the behaviour into the species genome at all. It suggests that, over the course of many generations, the relevant genes change to variants that support/ encourage the particular adaptive behaviour. Just a simple environmental trigger is then required for the behaviour to be produced. A number of studies are cited and outlined that have given results that appear to be inconsistent with the incremental hypothesis but consistent with the Genetic Priming hypothesis.


ADDITIONAL KEYWORDS: Species genome – organic selection – gene variants – alleles – assimilation – environmental trigger – incremental hypothesis – religiosity.

INTRODUCTION

The modern version of Organic Selection suggests that the evolutionary trajectory of living organisms is not totally dependent on random genetic mutation. It hypothesizes that to some extent and in some way organisms, unconsciously of course, participate in guiding their own evolution. The – rather patchy – history of scientific interest and theoretical/research activity in this area has been set out elsewhere and will not be duplicated here (see e.g., Weber & Depew, 2003; Corning, 2013). In this short paper, I want to suggest that a persistent adaptive behaviour can indeed impact the species genome, and I describe a mechanism – which I call Genetic Priming – that would enable this to occur.
Of course, this is not to suggest that behaviour is the sole driver of Organic Selection. It is well established that a change to the environment can generate a response via phenotypic plasticity. The various molecular processes involved – DNA methylation, histone acetylation etc – have recently been well described and substantiated in Carey (2012). There is substantial evidence that these epigenetic modulations to the genome are often heritable (see in particular Waddington, 1953, 1957; Jablonka & Lamb, 2005). Of course, an environmental change will often be accompanied by a change in behaviour. Where this occurs, I suggest that these epigenetic modulations run alongside and may even interact with the Genetic Priming process.
            The suggestion that behaviour can, in due course, be assimilated into the genome – later called ‘The Baldwin Effect’ by Simpson (1953) – had been proposed by the original Organic Selectionists such as Baldwin, Morgan and Osborn at the end of the 19th Century. Their suggestions for the mechanism in operation were understandably fuzzy; Mendel’s laws were only just being rediscovered at that time and the discovery of genes/genomes was yet to come. More recent work (e.g. Bateson, 2004; Jablonka & Lamb, 2005), has described a step-by-step incremental assimilation of adaptive behaviour into the genome. Bateson (2004: 289) describes the following scenario with regard to the Galapagos woodpecker finch that pokes sharp sticks into holes to get at insect larvae.
            “In the first stage, a naïve variant of the ancestral finch, when in foraging mode, was more inclined to pick up sharp sticks than other birds. This habit spread in the population by Darwinian evolution because those behaving in this fashion obtained food more quickly. At this stage, the birds still learn the second part of the sequence. The second step is that a naïve new variant, when in foraging mode, was more inclined to poke sharp sticks into holes. Again this second habit spread in the population by Darwinian evolution. The end result is a finch that uses a tool without having to learn how to do so.”
            But much adaptive behaviour does not lend itself to a step-by-step incremental process of this kind. Is it likely that the rooting reflex of the primate neonate was assimilated into the primate genome in this way? Also, at each stage in the process, the new partial implementation must be more adaptive than the last one. Is a finch that carries a sharp stick but doesn’t know what to do with it yet at a fitness advantage to a finch that doesn’t have the stick-carrying fetish? I think not; it would obviously be a hindrance. Finally, the process as described would result in a full assimilation into the genome. However, there is empirical evidence that suggests that an environmental trigger is often necessary. I will present examples of this evidence later in this paper. I suggest that the incremental assimilation procedure is logically possible but unlikely to account for much of the adaptive behaviour that we witness in nature.
            In West-Eberhard (2003), the author takes an alternative approach to describing the impact of organic selection on the relevant genome. She writes: “Generations of organic selection can lead to genetic (congenital or phylogenetic) change that makes the accommodation the norm in the population. Note that this does not imply that the advantageous response becomes genetically determined or genetically assimilated, only that the ability to produce the response becomes more common or fixed due to genetic change.” The Genetic Priming hypothesis that I will now outline goes on to suggest the inter-generational positive feedback mechanism between adaptive behaviour and positively associated gene-variants (alleles) that causes this to occur, and that an environmental ‘trigger’ will always be necessary for the adaptive response to be manifested.


GENETIC PRIMING

The Genetic Priming hypothesis is an alternative suggestion to explain how an adaptive behaviour shapes the genome. In common with West-Eberhard (2003), it proposes that there is no assimilation of the behaviour at all; merely that, over the course of many generations, the relevant genes change to variants that support or encourage the particular adaptive behaviour.

The hypothesis can be summarised as follows:

Living organisms have, over evolutionary time, acquired genetically-mediated predispositions (in terms of allele-sets) that promote/ encourage behaviours that have proven to be adaptive for their species. These genetically primed behaviours are then able to be invoked/ manifested by simple environmental triggers.

Within a population of a given species, suppose that an adaptive behaviour (AB) is performed for the first time by a particular individual in generation (g), and that this individual consistently manifests AB thereafter, whenever it is appropriate to do so. Suppose also that certain genetically mediated predispositions affect the likelihood that AB will be manifest, and that this particular individual is well-endowed with these predispositions by having alleles that facilitate the expression of AB. Let us imagine that the predispositions are Intelligence and Creativity, for example. The adaptive behaviour may well result in relatively more offspring in generation (g + 1) and a tendency for these individuals to have high values for the positively associated predispositions; with a corresponding high likelihood that AB will be performed by greater numbers in generation (g + 1). This may well be magnified by culturally mediated learning/copying behaviour between parent and offspring. Over evolutionary time, AB will spread through the population by this inter-generational positive feedback between AB and the positively associated predispositions. Selection pressure may well result in the behaviour becoming ubiquitous and occurring earlier and earlier in individual life-cycles. However, AB will never become innate. The predisposition for the behaviour among the population will become widespread and stronger, but an environmental trigger will always be necessary for the behaviour to be manifest.
            To take a specific example; the human tendency toward religiosity appears to be genetically mediated. This is supported by fairly recent empirical studies with young children by Keleman (2004), and also by Barrett (2012). Several twin-studies have also found a significant genetic component in religiosity (e.g. Vance et al., 2010). I suggest that Genetic Priming is the mechanism that has, over evolutionary time, turned the strong potential for religious behaviour into an innate human trait.
Presumably, at some point in our evolutionary past, an individual started to perform the first proto-religious act. Let us imagine that, every morning, he prayed to the god-of-the-mountain. His behaviour may well have enhanced his status in the group and therefore increased his relative fitness via sexual selection and, possibly, the protection of him and his children by group members. In order for the process that I have described above to operate we need to make the (reasonable) assumption that such behaviour would have been positively associated with genetically-mediated predispositions.
Theoretical work in the psychology of religion presented by Atran (2003) and Boyer (2001) reveals three strong contender predispositions. They and other authors have suggested that innate belief in a god is a by-product of the following genetically-mediated predispositions: child/parent attachment, assumed parental authority by children, and the teleological assumption. An example of the last is the adaptive assumption that any unexpected noise from nearby bushes may well be a predator. A false-positive will cost the energy required to run away, but a false-negative will give the predator an easy meal. Our present innate religiosity needs a simple trigger to become manifest. In modern western societies, for example, the reassurance to a bereft small child from a main-carer that their pet is “playing happily in heaven” may be sufficient to provide such a trigger.
            If the Genetic Priming hypothesis is correct, there will always be a number of adaptive behaviours ‘trying’ to prime the genome at any one time. Some will involve predisposition gene-sets that overlap and the various behaviours may well ‘want’ to prime the same genes toward different variants. No adaptive behaviour will ever get its optimal set of alleles; compromise and sub-optimisation for any particular adaptive behaviour are inevitable.
            As an adaptive behaviour spreads in the population it becomes, in effect, part of the environment to which the genome is adapting. New mutations as well as existing allele configurations that support/ encourage the behaviour will bring about positive selective pressure. This is simply Natural Selection at work. Several recent authors have highlighted the importance of particular adaptive behaviours to human evolution – for example Wrangham (2009) on the impact of fire and cooking, Wells (2010) on the impact of farming and animal domestication, and Taylor (2010) on the impact of technology. Once an adaptive behaviour starts to become ubiquitous, Genetic Priming and Natural Selection will often work in concert, concurrently.
            Many evolutionary biologists have suggested that post-weaning lactose tolerance developed in humans in temperate regions where cattle were farmed. In this case the adaptive behaviour was successful milk consumption (Vitamin D enables absorption of calcium; particularly important in temperate regions), dependent on the associated subset of the genome involved in controlling lactose tolerance. The positive feedback process explained above has resulted, in these regions, in the ubiquitous priming of the human genome toward post-weaning lactose tolerance – but not in a genetically assimilated tendency to consume milk! There has been no assimilation of the adaptive behaviour; only Genetic Priming of the associated subset of the genome to facilitate it. This is clearly a case of Organic Selection since the behaviour has impacted the species genome. However, the ubiquity of the behaviour has been environmentally constrained because not all geographical regions are suitable for cattle husbandry.


SOME RELEVANT EMPIRICAL STUDIES

Watson & Rayner (1920) demonstrated that we are born with the ability to feel fear. Although a baby will show fear of a loud noise, it will not show fear of a close naked flame until it is brought close enough to be uncomfortably hot. A baby is able to feel the 'fear emotion' but fear will only be manifested once the danger source is physically experienced. Anticipation of danger will only manifest fear once the danger has been associated with the trigger of an unpleasant physical outcome.
The experiments performed on infants by Watson & Rayner would now be considered unethical, and could not be repeated. A relevant and confirmatory study was carried out by Hunt & Smith (1967) on the pecking behaviour of newly-born chicks. They found that the chicks would only peck at "shiny, high contrast targets". In particular, they would peck at their own toes until, by chance, they hit upon food or water. This 'environmental experience/trigger' was found to be necessary before they pecked only at food or water and not their own toes. If their toes were initially masked, and no other shiny targets were available, they didn't peck at all. They appeared to be genetically primed to peck at shiny objects but needed an environmental trigger to peck only at food or water.
            LoBue et al. (2010) found that human neonates exhibited no fear of spiders. However, when tested again two years later, there was pronounced fear. Since the children tested had experienced no harm from spiders in the interim, the authors concluded that the fear had probably been triggered by seeing parental/sibling fearful reactions to the concept and/or presence of spiders.
            Marler & Sherman (1985) identified innate differences in the singing behaviour of male swamp and song sparrows by rearing males from the egg in the laboratory, in complete isolation from adult conspecific song. Isolation-reared males of both species displayed several abnormal song features including reduced numbers of notes per song, longer durations of notes and inter-note intervals, and fewer notes per syllable. Despite these and other abnormalities, many species differences emerged that matched differences in the natural singing behaviour of the two species. Subsequently, songs only became normal for their species when the singing of normally reared adult conspecifics was experienced by the birds.
It could be suggested that the abnormal songs of isolation-reared birds may be a partial assimilation of the behaviour into the genome. However, I propose an alternative explanation. The abnormal songs suggest a rough 'sketch' of the complete songs of normally reared birds rather than the assimilation of a discrete part of the songs. The abnormal songs described by the authors would be as expected from the spontaneous behaviour of birds with the same physical vocal equipment as normally-reared birds, but without the experience of hearing the 'trigger'; the musical detail of the normal song for the species. I suggest that the results reported are consistent with the Genetic Priming hypothesis.
Until recently, Anorexia Nervosa was considered to be a purely psycho-social behavioural disorder. However, more recent work has provided evidence that both genes and environment are implicated in the pathology of the disease. It has been found that particular gene/epigenetic variants render individuals more susceptible. For these people, environmental/experiential conditions such as strict dieting and/or depression are liable to trigger the onset of Anorexia Nervosa (Woerwag-Mehta & Treasure, 2008). Some researchers in this area (e.g. Guisinger, 2003) have suggested that the underlying predispositions referred to may have been adaptive deep in our evolutionary past. Guisinger in particular suggests that they may have enabled survival when famine threatened. This gene/ environmental account of the aetiology of Anorexia Nervosa is also consistent with the Genetic Priming hypothesis, as it appears that a once adaptive – now potentially pathological – predisposition can be triggered by particular present-day environmental/ experiential factors.
            In each of these research programmes, the adaptive behaviour in question appeared to need an environmental trigger to be manifested. The behaviour was not produced – in whole or part – in the absence of such a trigger. This would seem to indicate that the behaviour had not been assimilated into the genome. These results are inconsistent with the step-by-step incremental mechanism mentioned in the Introduction because such a process would be expected to result in genomic assimilation without the need for an environmental trigger. Therefore this hypothesis should be rejected. On the other hand, the results are consistent with the Genetic Priming hypothesis.


SUMMARY

Many biologists accept that, over evolutionary time, adaptive behaviour can impact the species genome. In this brief account I suggest that the leading hypothesis to explain the process – I have referred to it as the step-by-step incremental approach – is inadequate. Building on the work of Mary Jane West-Eberhard (summarised by West-Eberhard, 2003), I propose a new hypothesis, Genetic Priming, as a more likely explanation of the mechanism that drives the phenomenon. Genetic Priming suggests that adaptive behaviour is never assimilated by the genome but, instead, the genome is ‘shaped’ to favour gene-variants that facilitate the adaptive behaviour. A simple environmental ‘trigger’ is then necessary for the behaviour to be expressed. A number of empirical studies are cited that are consistent with this hypothesis.


REFERENCES

Atran S. 2003. In Gods we Trust: The Evolutionary Landscape of Religion. New York, Oxford University Press.

Barrett JL. 2012. Born Believers: The Science of Children’s Religious Belief. New York: Free Press.

Bateson P. 2004. The Active role of behaviour in evolution. Biology and Philosophy 19: 283–298.

Boyer P. 2001. Religion Explained: the Evolutionary Origins of Religious Thought. New York: Basic Books.

Carey N. 2012. The Epigenetics Revolution. London: Icon Books.

Corning P. 2013. (in press) Evolution “on purpose”: how behaviour has shaped the evolutionary process. Biological Journal of the Linnean Society.

Guisinger S. 2003. Adapted to flee famine: adding an evolutionary perspective on Anorexia Nervosa. Psychological Review 110(4): 745–761.

Hunt GL, Smith WJ. 1967. Pecking and initial drinking responses in young domestic fowl. Journal of Comparative and Physiological Psychology 64(2): 230–236.

Jablonka E, Lamb MJ. 2005. Evolution in Four Dimensions. Cambridge, Mass.: MIT Press.

Keleman, D. 2004. Are children intuitive theists? Reasoning about purpose and design in nature. Psychological Science 15(5): 295–301.

LoBue V, Rakison DH, DeLoache JS. 2010. Threat perception across the life span: Evidence for multiple converging pathways. Current Directions in Psychological Science 19(6): 375–379.

Marler P, Sherman V. 1985. Innate differences in singing behaviour of sparrows reared in isolation from adult conspecific song. Animal Behaviour 33(1): 57–71.

Simpson GG. 1953. The Baldwin Effect. Evolution 2: 110–117.

Taylor T. 2010. The artificial ape: how technology changed the course of human evolution. Basingstoke, UK: Palgrave Macmillan.

Vance T, Maes HH, Kendler KS. 2010. Genetic and environmental influences on multiple dimensions of religiosity. Journal of Nervous and Mental Diseases 198: 755–761.

Waddington CH. 1953. Genetic assimilation of an acquired characteristic. Evolution 7: 118–126.

Waddington CH. 1957. The Strategy of the Genes. London: Allen & Unwin.

Watson JB, Rayner R. 1920. Conditional emotional reactions. Journal of Experimental Psychology 3(1): 1–14.

Weber BH, Depew DJ (eds). 2003. Evolution and Learning: the Baldwin Effect Reconsidered. Cambridge, Mass.: MIT Press.

Wells S. 2010. Pandora’s Seed: the Unforeseen Cost of Civilisation. New York: Random House.

West-Eberhard MJ. 2003. Developmental Plasticity and Evolution. Oxford: Oxford University Press.

Woerwag-Mehta S, Treasure J. 2008. Causes of Anorexia Nervosa. Psychiatry.7(4): 147–151.

Wrangham R. 2009. Catching Fire: How Cooking Made Us Human. XXXX: Basic Books.