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.


Wednesday, 28 November 2012

The Danger of Adversarialism in Western Society


In an earlier entry (August 2012), I considered inter-personal argument and contrasted two alternative epistemologies that can underpin such exchanges; Arguing to Win (ATW) and Discussing to Reveal (DTR). I was making the case for DTR and against the ATW rules-of-engagement. I now want to go further and suggest that pernicious ATW has become the norm and is just one facet of a more general societal malaise; adversarialism. I define adversarialism as any system that encourages or tolerates participants acting to defeat the opposition by fair means or foul.

It is not just apparent in person-to-person exchanges. It is endemic to our justice system (contrast with France), our politics (watch/ listen to "Today in Parliament"), in Business activities (example: tax avoidance), in 'sport' (thankfully not all) and in our entertainment (film/ video games). With regard to 'sport' it is likely to be experienced  both on the field of play and on the terraces. Drug-taking and 'professional fouls' are just two aspects of adversarialism in 'sport'. In our culture, adversarialism is so blatant and ubiquitous that I don't feel it necessary to support these contentions with specific examples.

The most serious aspect of the adversarial tendency relates to the activities of children and young adults. They are often avid participants in sport; both as actual participants and spectators. They play video games that mainly encourage combat to the death and eschew fair-play. Adversarialism is becoming the norm for many of our children. Concepts like sportsmanship, live-and-let-live, credit-where-credit-is-due, cooperation, fair-play and good manners are being left far behind. Yet surely these are the essential markers of a truly civilized society.

I suggest that the decline needs to be stopped if we want to progress toward the civilized, contented and fair society that we all (?) want. Teach fair-play to the children and steer them toward the relevant role-models. Discourage ATW and encourage DTR in their discussions and always set them a good example in this regard.

If I were invited to leave just one piece of advice to the societies of the world to serve as my personal legacy, it would be this one.


Thursday, 25 October 2012

Why I'm Not an Atheist!!

Religion's trump card is our inability to explain 'First Cause'. Since any suggested explanation will always encounter the infinite regress objection, I don't believe that science will ever explain how something came from nothing. If all the religions agreed to drop their scriptures and fairy-stories and simply regard God as the unknowable 'First Cause', in this sense, I would no longer be an atheist. Does anyone else feel the same way?

Friday, 5 October 2012

THE ‘DRIVERS’ OF HUMAN BEHAVIOUR

Introduction

Social psychology is concerned primarily with human behaviour and emotions. Behaviour is simply what we do. My dictionary defines it, curtly, as “How we conduct ourselves” but that implies that we are always in conscious control of our behaviour and we all know that this isn’t the case.  I will say more about this later in the note. Our behaviour is externally observable whereas emotions are how we feel; they are experiential. They cannot be experienced externally although their existence in an individual can sometimes, wittingly or unwittingly, become apparent to others, e.g. blushing, facial expressions. This paper addresses behaviour rather than any concomitant emotions. It therefore sidesteps the complications that would be introduced by a consideration of the emotions and the interaction between behaviour and emotions. The subject of social psychology is also concerned both with ‘normal’, healthy behaviour and with pathological behaviour. This note focuses on healthy behaviour. However, the issues it raises are just as relevant to the study of pathological behaviour.

The question under consideration in this note is “What are the root causes, or ‘drivers’ of our behaviour?”  This is clearly a seminal issue for social psychology. A clear exposition would have the potential, not just to clarify and provide an analysis of the determinants of behaviour, but also to integrate a number of disparate approaches to the subject of psychology itself. Both the theory and practice of social psychology is bedevilled by schisms euphemistically called ‘perspectives’. For example, we have biological psychology that concentrates on the role of genes/ hormones in generating behaviour, social-constructionist psychology that emphasizes social and cultural factors in accounting for it, the psycho-dynamic (notably Freudian) approach that majors on early nurturing in explaining behaviour, cognitive psychology centred mainly on the role of attention/ cognition and humanistic psychology that considers the role of human free-will in regulating behaviour. Some psychologists regard themselves as just that; ‘psychologists’. Many more in my experience will use an epithet to qualify their professional descriptor; Freudian psychologist, humanistic psychologist, cognitive psychologist, etc. Pity the poor client looking for assistance from a psychologist! She doesn’t know or care about the particular epistemology favoured by the practitioner, she just wants help from someone qualified to diagnose and treat an unwanted psychological condition. In passing I would suggest that the profession would do well to move towards greater integration in this regard.

If this is to happen, we need more integrated hypotheses, theories and experimentation. The only relevant work I am currently aware of is called ‘Trimodal theory’ and is described in Stevens (1998). The author distinguishes three ‘bases (or sources) for action’; biological processes, symbolic processes and reflexive awareness. He relates these to a number of perspectives. For example, he notes that both social constructionism and psychoanalysis depend on symbolic processes to provide a basis for action. He concludes that “  --  Given the argument here that human personal and social life involves a mixture of all three sources, this would imply that we need a broad range of perspectives in order to represent all three modes, and that such perspectives are therefore to be regarded as essentially complementary rather than mutually exclusive.” From my previous comments you will be able to anticipate that I agree enthusiastically with this latter conclusion. I believe Richard Stevens is right; the perspectives do relate to “bases for action”. I would add, however, that they often operate concurrently.

The Drivers

Using a physical analogy, I hypothesize that the individual drivers are like a set of forces acting on an object. In physics, the resulting direction and velocity of the object is called the 'resultant' of the contributory forces. In the same way, behaviour may be thought of as the resultant of a number of these drivers that may be acting on the individual. Any particular behaviour will be the resultant of one or more drivers. Drivers may act positively, encouraging action, or negatively, inhibiting action. What are these drivers? The following seven are proposed:-

Biological
1. Genetically mediated propensities
Propensities to express certain types of behaviour are the result of basic, common human drives (e.g. to assuage hunger, sexual desire etc) together with other psychological propensities that arise from particular gene/allele patterns.
2. Concurrent somatic condition
Behaviour will be affected by concurrent hormonal levels and the general somatic condition.
Social
3. Behaviour patterns learned from early nurturing relationships
Psycho-dynamic (Freudian) factors including ego defences.
4. Relevant learned social/cultural norms
The recognised norms within the culture and social 'milieu' in which the behaviour takes place.
Cognitive
5. Cognitively developed patterns of behaviour
Stereotypic attitudes that provide cognitive short-cuts to formulaic patterns of behaviour. These may have been 'inherited' from primary carers or from exposure to particular social representations during development. 
6. Free cognition
Free-thinking from basic principles and the detail of the particular situation. 
7. Reflexive consideration 
Critical reconsideration of past thoughts, feelings and actions.

An example will illustrate some of the points made.
I am walking down a crowded Oxford Street in London; on the pavement but close to the kerb. A man walking toward me does not appear to be giving me any room to pass. I don't think it's safe to step into the road so I push back at him as we collide and say, in a loud voice, "Why don't you look where you're going?" A few yards on I look back, and, for the first time, and to my horror and acute embarrassment, see he is carrying a white stick. I shout my apology and hope he hears me. Before I fall asleep that night I resolve to be more circumspect before losing my rag in future.
Walking down Oxford Street can be stressful and it is highly likely that my active stress hormones, such as adrenelin and cortisol, will be above ambient levels in the hypothetical scenario described above. If this is so, the 'Somatic' driver (Driver 2) will have played a part in my initial, somewhat aggressive reaction. The genetically mediated 'fight or flight' response (Driver 1) would also have played a part in this reaction. A Driver 1 component can be fast-acting and difficult to control; as in this case. It is also possible that a 'Cognitive Pattern', (Driver 5) was a component; e.g. "I won't be intimidated by inconsiderate walkers!"
My feelings of shame and embarrassment and my shouted apology when I see that the gentleman is blind, will have been generated from Driver 4, 'Social Norms' acting with Driver 6, 'Free Cognition'; while my nocturnal resolution to ensure that I have all the facts before engaging my big mouth would have involved 'Free Cognition', again, and 'Reflexive Consideration' (Driver 7). 
It is interesting to note that, at the time that the behaviour occurs, the model suggests that the only driver under full conscious control is ‘Free Cognition’ (Driver 6). I would suggest that this provides a possible answer to the time honoured question about the contribution of “freewill” to our behaviour. The possibility of engaging ‘Reflexive Consideration’ (Driver 7) at some later time is another aspect of freewill that enables us to modify relevant, subjective ‘Cognitive Patterns’ (Driver 5) and hence learn from our experience.

Conclusions

In this short paper I have suggested a model for approaching the aetiology of human behaviour. It may well need discussion and amendment. However, I believe that it makes a useful start and contend that the need for such a model is overwhelming in order to integrate the existing approaches to the discipline of psychology. As it stands, the various flavours – cognitive, psycho-analytic, humanistic etc are a source of confusion for our clients and a source of unnecessary discord within the profession.
It also suggests an answer to the question about how much free-will we have in the manifestation of our behaviour.

Reference.

Stevens, R (1998), ‘Trimodal theory as a model for interrelating perspectives in psychology’. In Sapsford, R (ed.), Issues for Social Psychology, Open University.



John Jacob Lyons, 17 Jan. 2012

CONSCIOUSNESS: TOWARDS A SOLUTION TO THE ‘HARD PROBLEM’?

The “hard problem of consciousness was formulated by David J Chalmers in 1996. Simply stated it concerns the issues; what is consciousness; why do we have it and how do patterns of neuronal firing in the brain generate the subjective experience of being conscious?

I think of consciousness quite simply as our subjective awareness of ourselves, our surroundings and the relationship between these two entities. I believe that consciousness evolved because it provided an adaptive integrated model of reality from the, individually evolved, sensory inputs we are able to receive from outside the body and from the body itself. Such a model is adaptive since it speeds up our evaluation of confirmatory/ contradictory evidence when making conscious decisions about the actions we need to take in response to the state of world and/or our physical needs. It is also an essential tool in making adaptive moral judgements. See Marc D Hauser, ‘Moral Minds’, p29.

In a moving, talking picture, the fact that the dynamic visual image is synchronized with the sound results in consilience between the words heard and the lip movements produced by the actors. This results in an emergent subjective experience that seems to the viewer to be an acceptable model of our usual real-life subjective model of reality. My hypothesis is that there is a similar relationship between our sensory inputs, which are, to all intents and purposes, also experienced in a synchronized fashion, and objective reality.

This emergent model of reality that we call ‘consciousness’ also enables us to take ‘snapshots’ of states of the world associated with emotionally charged experiences. These may then be stored in long-term memory and used, unconsciously, to pattern-match to real-time experiences and thus enable very fast, unconsciously mediated and adaptive actions to be generated when similar states of the world are encountered.

But how do we explain our subjective experience of being conscious in terms of its neurological basis? In other words, how do we explain the translation from a pattern of electro-chemical pulses in neural brain tissue to the subjective model of reality that we call our consciousness?  I have described consciousness as an integrated model of reality based on our sensory inputs. Since our experience of each of these inputs (sight, for example) is understood by science in terms of specific neuronal activity and the physiology of the sensory organs, the ‘hard problem’ seems to disappear when described in this way.

So, what is consciousness? It is a subjective model of reality. Why do we have it? We have it because it proved to be an adaptive facility that emerged spontaneously with the phylogenic development of the senses. How does neuronal activity generate subjective experience? Sensory input, the functionality of the sensory organs combined with appropriate neural activity generate synchronized sensory experiences that result in the subjective, integrated, emergent model of reality that we call ‘consciousness’. Where does this analysis leave the concept “unconsciousness”?

If one accepts the notion that neural activity mediates both my conscious processes such as deciding to write this note, and my unconscious processes, such as those controlling my somatic-homeostatic functions, I see no problem in hypothesizing that consciousness is a sub-set of brain processes. There appears to be constant movement, however, between the conscious sub-set and the unconscious sub-set; as when we suddenly become conscious that someone within ear-shot has mentioned our name. I accept that the explanation of consciousness I am putting forward in these notes leaves the neuronal source of ‘attention’, as yet, unexplained.

The question arises, “What distinguishes the conscious sub-set of neuronal activity from the unconscious sub-set?” I would hypothesize that the conscious sub-set is a logically distributed module within neuronal architecture that contains the results of synchronized sensory processing as previously described which has access to long-term memory/ reasoning and which allows input from emotional circuits. The unconscious sub-set also has access to emotional circuits in order to produce fast responses by pattern-matching. Any particular emotional event may, unconsciously, trigger a match with previous emotionally-laden memories. These memories will there-by be etched deeper. The emotion generated by the event will also be consciously experienced as ‘feeling’ thus allowing later reflection on the event, any action/inaction taken in response and the result.

Thursday, 13 September 2012

Dawkins v Sacks: Science v Religion: A False Dawn?

Did you see the discussion between Richard Dawkins and Jonathan Sacks; "Rosh Hashanah: Science v Religion", 11:15 pm, BBC1, Wednesday 12 September 2012?

This was a very interesting and amiable discussion between two very intelligent men of goodwill. However, it ended on a note of false harmony that reminded me of the written 'agreement' between Chamberlain and Hitler immediately prior to World War 2. The only difference was that, in this case, both parties were being suckered into believing they had achieved 'peace in our time', not just the one.

During the discussion, Dawkins accepted that the application of science is capable of doing as much harm as religion. He affirmed that " Science can be hideously misused. Indeed, if you want to do terrible things, you need to use science to do it ---". Straight into the philosophical trap of confusing 'means' with 'motivation'. Yes, science has provided the means to inflect hell-fire and brimstone on one's enemies but religion has often provided the motivation to do so. The 'Social Darwinism' that, to a degree, underwrote the misdeeds of the Third Reich was the exception that proves the rule. Admittedly, this was a genuine motivational misuse of 'science'. However, it was not just a misuse of science; it was also a misinterpretation of science. It was incorrect science. So-called 'Social Darwinism' interprets the evolutionary theory, incorrectly, as meaning that nature works on the principle of 'the survival of the fittest'. The word 'fittest' in the last sentence is the usual one; the strongest, the best, the ones that can vanquish the weak. Natural Selection doesn't use the word 'fittest' in this way. In Natural Selection, the fittest refers to the individuals best suited to surviving and reproducing in the relevant environment. This makes all the difference since the ability to cooperate becomes at least as important as the ability to enforce. There is nothing truly Darwinian in so-called Social Darwinism. Dawkins is, of course, well aware of this. He should have ensured that the distinction was apparent to Sacks and thus cleared correct science - unlike correct religion - of the charge that it has ever been implicated in the motivation of harm.

During the programme, Sachs said "Belief in god doesn't require a suspension of our critical faculties". However he also said "My view is that god made us in his own image. He marked us out from other animals by giving us freewill, morality and conscience". I suggest that the claim of the first of these three sentences is 'called out' by the second and third sentences. Faith always involves a suspension of one's critical faculties. Of course, theologians can argue with each-other about the real meaning of bits of scripture; and that requires them to engage their intellect. However, this always takes place within the questionable epistemology of an unquestioning faith.

This brings us to the nub of the matter. At the end of the programme, Sachs claims that he and Dawkins have agreed that they can collaborate in a common pursuit of truth for the common good. He speaks of a breakthrough; even "an epiphany". Poppycock! However well-meaning and charming the proponents, science will never be able to cooperate with those that pursue truth with a methodology, an epistemology, that is based on faith rather than evidence. Sorry; no deal!


Tuesday, 14 August 2012

DTR IS BETTER THAN ATW

Think about all the disagreements you've ever had with a partner, friend, colleague, relation, fellow internet-poster or even the bloke behind you in the queue. What proportion of these exchanges could best be described as 'Arguing to Win' (ATW) and what proportion would be better described as  'Discussions to Reveal' (DTR)? My guess is that your ATW figure is far higher than your DTR figure. Right?

We are all familiar with the ATW strategy. You put forward your view; then back it up with all the sub-arguments, examples/ illustrations and supporting evidence you can muster. You sidestep any good counter-arguments from your 'opponent' and rubbish his/her evidence. You are operating as an advocate rather than as a judge. We have all done it. It's such a familiar procedure that I don't think I need to give you examples.

The DTR strategy may be less familiar. Once again you state your opinion. But this time you are less dogmatic. This is your opinion at this time; you're prepared to modify or even change it completely if given relevant counter-evidence. You listen carefully to your 'opponent' and give him/her credit for points made that you believe to be correct. He/she does the same for you. You are on a joint enterprise to find the truth/ fairness. Of course, in due course, you may have to agree to disagree. This may not be a blanket disagreement. You may  well agree on some points, disagree on others and need more information on yet others. You have both been operating as judges rather than advocates.

I want to suggest to you that this is a very important distinction. Just imagine a world in which everyone used the DTR rather than the ATW strategy. What do you see? More harmony/ happiness or less harmony/ happiness? I see much more.

I think we would do well to teach DTR to our children. Of course, you may well have different ideas. I'm listening    --------------