Friday 24 April 2009

Sleep Elaboration–Awake Pruning (SEAP) memory theory

The Sleep Elaboration–Awake Pruning (SEAP) theory of memory: Long term memories grow in complexity during sleep and undergo selection while awake. Clinical, psychopharmacological and creative implications

Medical Hypotheses; 73: 1-4

Bruce G. Charlton and Peter Andras



Long term memory (LTM) systems need to be adaptive such that they enhance an organism’s reproductive fitness and self-reproducing in order to maintain their complexity of communications over time in the face of entropic loss of information. Traditional ‘representation–consolidation’ accounts conceptualize memory adaptiveness as due to memories being ‘representations’ of the environment, and the longevity of memories as due to ‘consolidation’ processes. The assumption is that memory representations are formed while an animal is awake and interacting with the environment, and these memories are consolidated mainly while the animal is asleep. So the traditional view of memory is ‘instructionist’ and assumes that information is transferred from the environment into the brain. By contrast, we see memories as arising endogenously within the brain’s LTM system mainly during sleep, to create complex but probably maladaptive memories which are then simplified (‘pruned’) and selected during the awake period. When awake the LTM system is brought into a more intense interaction with past and present experience. Ours is therefore a ‘selectionist’ account of memory, and could be termed the Sleep Elaboration–Awake Pruning (or SEAP) theory. The SEAP theory explains the longevity of memories in the face of entropy by the tendency for memories to grow in complexity during sleep; and explains the adaptiveness of memory by selection for consistency with perceptions and previous memories during the awake state. Sleep is therefore that behavioural state during which most of the internal processing of the system of LTM occurs; and the reason sleep remains poorly understood is that its primary activity is the expansion of long term memories. By re-conceptualizing the relationship between memory, sleep and the environment; SEAP provides a radically new framework for memory research, with implications for the measurement of memory and the design of empirical investigations in clinical, psychopharmacological and creative domains. For example, it would be predicted that states of insufficient alertness such as delirium would produce errors of commission (memory distortion and false memories, as with psychotic delusions), while sleep deprivation would produce errors of memory omission (memory loss). Ultimately, the main argument in favour of SEAP is that long term memory must be a complex adaptive system, and complex systems arise, are selected and sustained according to the principles of systems theory; and therefore LTM cannot be functioning in the way assumed by ‘representation–consolidation’ theories.


The nature of long term memory: instructionist or selectionist?

What follows is an ‘in principle’ argument about the basic nature of human long term memory. Although the details of real human memory may differ; if the premises concerning the nature of complex systems are correct, then memory ‘must’ work in something like the way we describe [1].

Human long term memory is typically described as a brain system for the storage of information about what has happened to an organism, so that the organism will be able to use this information in the future in order better to survive and reproduce (i.e., to increase its ‘fitness’). The kind of thing which is ‘stored’ in the long term memory system includes external stimuli (perceived via the five senses) and internal body states (perceived via the autonomic nervous system and messenger molecules such as hormones) [2]. Long term memories (LTMs) are typically conceptualized in terms of changes to brain circuitry [3], for example changes in the pattern of synaptic sensitivities [4].

The vast capacity of human long term memory implies that memory must be an extremely complex system, and all complex systems share basic formal properties [1], [5] and [6].

The usual description has memories as ‘representations’ of environmental entities being formed while an animal is awake and alert; after which these memories are edited, sorted, combined, selected or pruned (i.e., ‘consolidated’) while the animal is asleep. This could be termed an awake elaboration–sleep simplification theory of memory, or an awake representation–sleep consolidation theory.

In contrast, we propose almost the opposite idea: that memories are elaborated mostly during sleep (when the brain is more-or-less cut-off from interaction with its environment) and these memories are then selected or ‘pruned’ by interaction with other brain communications when awake. Our theory could be termed the Sleep Elaboration–Awake Pruning (or SEAP) theory of memory.

The traditional ‘representation–consolidation’ view of memory is ‘instructionist’ because the environment is seen as instructing the brain during awake periods. In other words, the complexity of memory is ‘exogenous’ because it originates in the environment; and complexity is transferred from the environment into the brain such that brain complexity ‘represents’, or in-effect mirrors, environmental complexity; then subsequently this complex information in the brain is summarized and thereby simplified mainly during sleep (i.e., the ‘consolidation’ phase).

By contrast, we see the complexity of memories as having an endogenous origin: i.e., originating within the brain. We suggest that complexity of memories is generated within the brain during sleep, to create elaborate memories which are then simplified (‘pruned’) mainly during the awake period of alertness, when the brain is brought into a more intense interaction with both its internal and external environment.

So the SEAP theory sees complexity as arising in the brain (mostly during sleep), and the editing of this complexity as a secondary consequence of the brain interacting with the environment when the animal is awake and behaving. Instead of the complexity of memories deriving from the environment, the complexity of memories is reduced by interaction with the environment – such that (for instance) in response to experience some memories are lost, others are abbreviated, while other connected memories are separated.

The SEAP theory is therefore akin to ‘selectionist’ accounts of neurobiology such as those provided by Edelman [7] and Gazzaniga [8]. SEAP is a selectionist theory of memory in which random variation and combination generates non-adaptive complexity; and in which complexity is reduced and adaptiveness emerges by a competitive selection mechanism of differential growth and extinction of complex systems. The complex systems which survive selection and grow are those which are more adaptive in that particular selection environment.

Like Edelman and Gazzaniga we regard memories as a consequence of the generation of diversity and selection among variants. But we also believe that only systems of communications [5] undergo selection, and therefore it is not necessarily or usually the brain’s physical units (such as neurons) which are selected [1] and [6].

SEAP is therefore based on the axiom derived from Luhmann’s theory of complex systems [5] that systems of communications are primary, and the communicating components of these systems (such as neurons) are secondary [6]. So that long term memories should properly be conceptualized as abstract systems of communications between neurons; and not the particular pattern of anatomical entities such as neurons or synapses.

Growth of memory systems

Memory systems need to be self-reproducing in order to maintain their complexity of communications over time in the face of the universal tendency for entropic loss of organised complexity: i.e., loss of information. In other words, the intrinsic tendency is for memories to be lost [4], and memory systems need a mechanism whereby complexity can be generated and information can be maintained despite this entropic tendency.

According to the SEAP theory, self-reproduction of memories generates surplus memory communications and a tendency for expansion in complexity of the memory system. So that self-reproduction of the memory system randomly generates memory complexity, and growth of new memories and combinations of memories will in turn create competition between the newly-generated memories.

This competition between new memories leads to differential survival and extinction of memories and is the basis of the process of selection among memories in a manner precisely analogous to natural selection in biology, or the selection processes of the immune system. All types of selection share basic formal properties [6] and [9]. Natural selection and immune system selection both lead to adaptation to the environment, but by the generation of random complexity being subjected to pruning of ‘maladaptive’ (or, more exactly, less-adaptive) variants via interaction with the environment.

Hence memory systems must tend to grow to ensure their own survival, and growth in this systemic sense entails growth in complexity. So the conclusion is that memory systems must have a tendency to grow in complexity; and superimposed on this tendency to growth are selection mechanisms that enforce adaptiveness.

Selection of endogenously-generated memories occurs by interaction with other memories within the long term memory system, and also from the memory system’s interaction with other brain systems. Interaction between memories and their environment probably happens at the level of neurons – which are the units generating and receiving communications in the memory system. Presumably, individual long term memory (LTM) neurons will typically participate in ‘coding’ (communicating) more than one memory; and some LTM neurons will also participate in other neural systems.

Selection of memory systems

Selection is a consequence of these interactions at the neuron level between more than one memory sharing a particular neuron, and between memories and other brain functions in which that neuron participates. For example, a cortical neuron may participate in several memories relating to an individual person, and also in the awake processing relating to visual perception [4]. Some of these networks of communication will be compatible, and memories then may be combined and thus grow to generate more complex memories by including more neurons into the communications network, or by triggering more frequent communications from neurons already in the network.

This may be conceptualized as memories being selected by their compatibility with ongoing personal experience. ‘False’ memories are therefore those contradicted by perceptions, while ‘true’ memories are those compatible with perceptions.

And memories will also conflict and interfere, such that one memory system may suppress neuronal participation in another memory system; and such memories cannot be combined and cannot grow in complexity. Such memory systems are more likely to become extinct, and these memories be lost.

The rationale by which memories either grow and increase in complexity, or interfere and reduce in complexity, are the structural and functional properties of the long term memory system – which are currently poorly understood. Presumably the sketchy current knowledge of how and why memory associations form, or how and why some memories rapidly disappear, are preliminary evidence concerning the structural and functional properties of the long term memory system.

Memories are therefore subject to continual selection and reshaping by the organism’s ongoing waking experience, and each night memories will be elaborated and combined, so that the interaction between nocturnal memory growth and diurnal pruning means that memories will tend to evolve over time. Most memories will become extinct, but those which are not ‘contradicted’ by awake experience will continue to increase in complexity (mainly during sleep) until such a point that they do eventually lead to contradiction after which the erroneous memories will be pruned-back.

Cyclical nocturnal growth of complexity and diurnal competitive pruning by the perceptual system is therefore the process by which long term memories on the one hand overcome the continuous tendency to loss of information by random entropic processes, and on the other hand maintain their adaptive relevance such that the long term memories (on average, and in the environment where they evolved) will tend to be fitness-increasing.

The function of sleep in memory

While sleep is advantageous to reproductive fitness in most (although not all [4] and [10]) animals, nonetheless understanding the ‘function of sleep’ has proved elusive [11]. While sleep very probably has to do with the editing and maintenance of long term memory [4], the specifics of this have proved hard to pin-down (e.g. [12] and [13]).

The reason sleep remains poorly understood, we suggest, is that sleep does not really have ‘a function’ in terms of the organism as a whole. Rather, according to SEAP theory, sleep is the behavioural state during which most of the internal processing of the system of long term memory (LTM) occurs. The primary ‘function’ of sleep is therefore maintenance and increase of LTM complexity. Or, the function of sleep is the expansion of long term memories.

This implies that serving as an adaptive ‘memory’ system for the organism is merely a secondary function of memory; and that sleep does not exist to improve the ‘accuracy’ (or adaptive relevance) of memories but instead to generate the complexity of memories.

The main requirement for LTM is among complex animals living in complex and changing environments – i.e., situations in which organisms have a repertoire of potential behaviours, where each day generates different challenges, and when therefore animals stand potentially to benefit from memories of their previous experiences [4]. In such animals (including humans) LTM often has a vast information capacity, and therefore necessarily memory is vastly complex.

The complexity of a system can be defined in terms of its having a much greater density of internal communication than its interactions with the non-system environment: in principle, the quantitative differential between internal communications and external interactions is a measure of system complexity [5] and [6]. Such internal complexity appears to an external observer as memory activity ‘autonomous’ from the rest of the organism, and with little or no communication between the LTM and its environment.

In other words, the memory system (like any complex system) needs to be relatively cut-off from environmental interactions (especially the computationally-heavy load of visual stimulation). The long term memory system likewise needs to be all – but disengaged from initiating ‘action’ – therefore not engaged in purposive movement, with the organism either temporarily inert or merely performing repetitive and stereotyped motor behaviour. This set of conditions is closely approximated by the state of sleep [3] and [4].

Sleep may therefore be considered as the cycle during which memory systems are most engaged in their primary activity of internal processing. There is a great deal of evidence to suggest that sleep is important for memory functions [14] – but the perspective of abstract communication systems goes considerably further than this.

From the perspective of the long term memory (LTM) system, sleep processing is its main activity; sleep allows its maintenance, self-reproduction and increase in complexity, and the ‘memory function’ of the LTM system is a subordinate activity which has evolved to enable the LTM system to emerge, survive and thrive in the context of the rest of the brain.

In a metaphorical sense, the ‘memory function’ is merely rent paid by the LTM system to the organism.

Clinical and behavioural implications of the SEAP theory


Sleep disturbances – reduced amount or quality of sleep – are an extremely common aspect of clinical practice. Lack of alertness is another common clinical problem. According to the SEAP theory, both sleep disturbance and impaired alertness would both be expected to impair memory – but in different ways.

Insufficient or too-often-interrupted sleep would presumably result in a reduction of complexity of communication in LTM: that is, a reduction in informational capacity of LTM. In summary, after sleep deprivation memories would be accurate and correct, but there would be a loss of content. The consequences of reduced complexity might include a reduction in potential total memory capacity of LTM, simplification of memories (less informational content, less combination of individual memories to form scenarios), and a greater probability of loss and extinction of memories. All of these predicted effects would be in principle measurable by properly designed memory tests.

Because the SEAP theory predicts that the accuracy of memories is mainly a consequence of selection processes during the awake and alert period; so that a major consequence of reduced alertness would be reduced accuracy of memories. So long as sleep was un-impaired; lack of alertness would be expected to produce inaccurate or false memories but not to cause memory losses. There would be plenty of memories, and memories would not be lost to entropy, but memory information would be inaccurate, unreliable, maladaptive. This inaccuracy would happen because memories had not undergone effective selection by interaction with perceptual systems and other pre-existing memories which had themselves undergone selection. So memories might be incompatible with direct experience and also with previous knowledge.

This situation of distorted and incoherent memories resembles the bizarre delusions which occur in psychotic states; and many psychotic states are associated with impaired alertness or ‘delirium’ [15]. Of course, sleep deprivation can itself be a cause of reduced alertness by causing increased sleepiness/impaired consciousness [16].

So specific states of insufficient alertness would be expected to produce errors of commission (memory distortion, false memories, memory inaccuracy), while sleep deprivation would produce errors of memory omission (memory loss). These predictions are testable, given the development of specific psychological measurement instruments to distinguish these types of memory error.

However, the specific consequences of sleep deprivation may be hard to predict without knowledge of the principles (or contingencies) of internal organization of the LTM. Furthermore, there may be various combinations of sleep loss and lack of alertness. One confusing factor is that sleep loss can itself produce drowsiness/delirium/lack of alertness (see below). These factors might explain the difficulties that sleep and memory researchers have experienced in precisely defining the function of sleep. For instance, the effects of ‘pure’ sleep deficiency on memory would be expected to be seen in terms of impairing the complexity of memories – but not necessarily on reducing the accuracy of memories.


The SEAP theory implies that there is likely to be a trade-off and a phasic effect in the memory effects of some psychotropic drugs.

There are many sedative drugs (e.g., benzodiazepines, sedative antihistamines) that improve sleep; and also several psychostimulant drugs (e.g., dexamphetamine, methylphenidate) that improve alertness. However, these mainstream drugs lack specificity of action, because sedatives tend to have hangover effects of drowsiness after wakening, while stimulant drugs tend to have ‘hangover’ effects of insomnia and other types of sleep disturbance [17].

Therefore, the expected memory effect of sedatives might (assuming that sleep really is improved) be first to improve the recall of memories; but the secondary effect would be to impair the accuracy of memories (due to hangover and reduced alertness). The effect of psycho-stimulants might be the opposite: firstly to improve the accuracy of memories, then (when sleep disturbance became a problem) secondarily to impair sleep and increase the problem of memory losses.

Perhaps no single drug would therefore be expected to improve memory, and the most likely possibility for pharmacological enhancement of memory would be alternate and sequential circadian dosages of short-acting stimulants and short-acting sedatives.

Another possibility for memory enhancement might be methods for direct and specific brain stimulation – if it became possible technologically to initiate at will both restorative sleep and an awake and alert state of consciousness, and to impose these states alternately and sequentially.

Creative trance

It can be seen that the elaborative phase of long term memory bears considerable resemblance with the process of creativity as we usually understand it [18]. This suggests that most creative activity is likely to occur during sleep – indeed the characteristic ‘wide associative field’ of creative thinking has long been recognized as similar to the mental processes of dreaming. However, some creative people seem able to engage in associative thinking while relatively awake and alert – especially in a ‘trance’ state of altered consciousness of a kind traditionally associated with religious, spiritual, artistic and scientific breakthroughs and ‘eureka’ moments [19].

Since the process of elaborative memory is prone to maladaptive errors of commission, the SEAP theory emphasises that the creative trance is also likely to suffer from the same errors of commission as occur during other states of impaired alertness – and the products of a creative trance state therefore typically require pruning or ‘editing’ by the alert mind (or by other people) in order to eliminate this type of error.

Indeed, this two stage procedure of generation of raw material in a trance state of ‘impaired consciousness’ followed by the period of revision of critique in a state of alertness and clear consciousness is frequently seen in accounts of creativity. For example, the English poet and novelist Robert Graves described his writing procedure in precisely these terms: as firstly a self-induced trance state which generated the primary ‘raw material’, then a stage of making multiple revisions and re-shapings to the raw material when in a ‘normal’ state of alertness and concentration [20]. And the same stages are also observed in some examples of scientific creativity – the ‘breakthrough’ coming in a visionary state of actual sleep, sleepiness or some other altered state of consciousness – followed by a period of checking and validating [19].

This model may also explain the role of alcohol in creativity, since a high proportion of creative geniuses (especially in the arts) also ‘abuse’ alcohol [18] and [22]. A very intelligent and knowledgeable person may find their creativity limited, and use the sedative (alertness-reducing) properties of alcohol to enable the associations which form the basic raw material of their creativity (so long as the dose of alcohol is not so great as to lead to inertia). The alcohol-fuelled raw material is then selected, pruned and revised when sober.

Furthermore, creative geniuses may exhibit a phasic pattern of asocial versus social behaviour: a phase of solitude when they are cut-off from interaction with others so that their ideas (memories) may increase in complexity; followed by social engagement when these ideas are selected by interaction with the peer group.

Autodidacts, who lack interaction with a peer group; are often very creative and original but their ideas often also tend to be wrong or ‘crazy’ because they have lacked the selection process of peer interaction. They have too much solitary introspective brooding, and not enough interaction. However, professionals working in institutions tend to generate ideas that are sensible and correct but which tend to be dull and unoriginal – merely incremental extrapolations from existing knowledge. They exhibit too much peer interaction, and not enough solitary brooding.

The SEAP theory may therefore explain why most creative people are introverted [18], but that intermittent periods of peer interaction are also usually necessary.

The Sleep Elaboration–Awake Pruning theory of memory is not merely a reversal of the mainstream instructionist theory of memory since the putative memory processes are quite distinct. In particular, SEAP regards the complexity of memories as being endogenously-derived rather than ‘representing’ environmental complexity; and SEAP replaces the concept of ‘consolidation’ during sleep with interactional pruning while awake. Ultimately, the main argument in favour of SEAP (or something similar) is that long term memory must be a complex adaptive system, and that complex systems arise and are sustained along the lines we have described, and not in the way assumed by ‘representation–consolidation’ theories of memory.

Therefore, by re-conceptualizing the relationship between memory, sleep and the environment; SEAP provides a radically new framework for memory research, with implications for the measurement of memory and the design of empirical investigations in clinical, psychopharmacological and creative domains.


[1] Charlton BG, Andras P. Complex biological memory conceptualized as an abstract communication system–human long term memories grow in complexity during sleep and undergo selection while awake. In: Perlovsky LI, Kozma R, editors. Understanding complex systems (series): neurodynamics of cognition and consciousness,; 2007 [accessed 12 March 2009].

[2] A.R. Damasio, Descartes error: emotion, reason and the human brain, Putnam, New York (1994).

[3] J.A. Hobson, The dream drugstore, MIT Press, Cambridge, MA, USA (2002).

[4] J.L. Kavanau, Memory, sleep and dynamic stabilization of neural circuitry: evolutionary perspectives, Neurosci Biobehav Rev 20 (1996), pp. 289–311.

[5] N. Luhmann, Social systems, Stanford University Press, Palo Alto, CA (1996).

[6] B.G. Charlton and P. Andras, The modernization imperative, Imprint Academic, Exeter, UK (2003).

[7] G.M. Edelman, Neural Darwinism: the theory of neuronal group selection, Basic Books, New York (1987).

[8] M. Gazzaniga, Nature’s mind: biological roots of thinking, emotions, sexuality and intelligence, Penguin, London (1994).

[9] D.L. Hull, Science and selection, Cambridge University Press, Cambridge, UK (2001).

[10] J.L. Kavanau, Is sleep’s ’supreme mystery’ unraveling? An evolutionary analysis of sleep encounters no mystery; nor does life’s earliest sleep, recently discovered in jellyfish, Med Hypotheses 66 (2006), pp. 3–9.

[11] J.M. Siegel, Why we sleep, Sci Am (November) (2003), pp. 92–97. View Record in Scopus | Cited By in Scopus (18)

[12] P. Maquet, The role of sleep in learning and memory, Science 294 (2001), pp. 1048–1052.

[13] J.M. Siegel, The REM sleep–memory consolidation hypothesis, Science 294 (2001), pp. 1058–1063.

[14] M.P. Walker and R. Stickgold, Sleep, memory, and plasticity, Ann Rev Psychol 57 (2006), pp. 139–166.

[15] B.G. Charlton, Theory of mind delusions and bizarre delusions in an evolutionary perspective: psychiatry and the social brain. In: M. Brune, H. Ribbert and W. Schiefenhovel, Editors, The social brain – evolution and pathology, John Wiley & Sons, Chichester (2003), pp. 315–338.

[16] B.G. Charlton and J.L. Kavanau, Delirium and psychotic symptoms – an integrative model, Med Hypotheses 58 (2002), pp. 24–27.

[17] D. Healy, Psychiatric drugs explained (4th ed.), Churchill Livingstone, Oxford (2004).

[18] H.J. Eysenck, Genius: the natural history of creativity, Cambridge University Press, Cambridge, UK (1995).

[19] B.G. Charlton, Alienation, recovered animism and altered states of consciousness, Med Hypotheses 68 (2007), pp. 727–731.

[20] M. Seymour-Smith, Robert Graves: his life and work, Paladin, London (1982) p. 99–100 [1987 edition].

[22] B.G. Charlton, Scientific discovery, peak experiences and the Col-oh-nell Flastratus! phenomenon, Med Hypotheses 69 (2007), pp. 475–477.

Thursday 2 April 2009

Robert 'Humphrey' Havard - Medical 'Inkling'

Charlton, BG. Reflections on a scientific paper of 1926 by the medical ‘Inkling’ Robert Emlyn ‘Humphrey’ Havard (1901–1985). Medical Hypotheses. 2009; Volume 72: Pages 619-620


Robert Emlyn Havard (1901–1985; general practitioner and sometimes medical scientist) was the only non-literary member of the Inklings – a1930s and 1940s Oxford University club which included Lewis and Tolkien. Despite spending most of his time in family medicine, Havard was a productive medical scientist. While still a student at Cambridge University, Havard co-authored an influential study published in the Journal of Physiology of 1926 entitled ‘The influence of exercise on the inorganic phosphates in the blood and urine’. The style and structure of this paper provides a charming window into the elite medical science of the 1920s.
Article Outline

Havard: The medical Inkling

The Inklings was a group of friends and colleagues who gathered around Lewis in Oxford University during the 1930s and 1940s [1]. The group would meet weekly after dinner in the evening at Lewis’s rooms in Magdalen College to read works-in-progress, and more informally to converse in the Eagle and Child (‘Bird and Baby’) pub in St Giles.

Lewis is now world famous as author of the Narnia fairy stories, and was probably the greatest lay Christian writer of the 20th century. The other world famous Inkling was Tolkien, author of The Hobbit and The Lord of the Rings. Charles Williams the novelist, poet and theologian was a later member. Other well-known Inklings included the philosopher Owen Barfield, Nevill Coghill – who became known as a Shakespearian director and published the best known modern English version of Chaucer’s Canterbury Tales, the ‘angry young man’ novelist and literary scholar John Wain, and the biographer Lord David Cecil. Lewis’s brother Warren (‘Warnie’) was usually in attendance: he was a popular historian of the France of Louis XIV. Tolkien’s youngest son Christopher later joined, and is now the only surviving Inkling – Christopher Tolkien is the most important scholar of his father’s work.

In a recent book on the Inklings, The company they kept [2], Diana Pavlac Glyer notes that almost all of the regular members of the group were active authors – producing academic books, essays, novels, stories, plays and poems. The Inklings essentially functioned as a writers’ group that provided mutual encouragement, criticism and editorial assistance. Superficially at least, the odd-man-out was Robert Emlyn Havard (1901–1985), who was a general practitioner and sometimes medical scientist and the family physician for both Lewis and Tolkien.

Havard appears in fictional form as the somnolent but shrewd character ‘Dolbear’ in Tolkien’s posthumously published story The Notion Club papers [3]; and Lewis’s Prince Caspian is dedicated to Havard’s daughter [4]. He had various nicknames bestowed on him by the group including ‘Humphrey’, ‘the Red Admiral’ (due to a beard grown while in the navy) and UQ – which stood for the ‘Useless Quack’. Indeed, in his sneering and pervasively unreliable biography of Lewis, Havard is depicted by AN Wilson as something of a buffoon [5].

This was far from the case, as can be seen from Havard’s early career as a medical scientist. The most complete account of Havard’s life so-far is by Walter Hooper in his Lewis: a companion and guide [6]. Havard began by taking a first class degree in chemistry at Keble College, Oxford then studying medicine at Gonville and Caius College, Cambridge and Guy’s Hospital in London to graduate with the Oxford medical degree of BM BCh in 1927. He took an Oxford DM (Doctor of Medicine) in 1934 while working at Leeds University in the Biochemistry Department, and in the same year returned to Oxford as a research fellow in The Queen’s College, and around this time became a general practitioner.

Despite spending most of his time in general medical practice, Havard was a productive medical scientist with his name on more than two dozen papers published in first rank journals such as Nature, the Lancet, Biochemical Journal and the Journal of Physiology. He had three spells of research and publication – the first mainly to do with human biochemistry during the mid 1920s while he was still a medical student; a second studying more clinical aspects of biochemistry from the early 1930s as a medical graduate doing a doctorate in Leeds and Oxford, and the third from the early 1940s when working on anti-malarial drugs while an above-conscription-age volunteer for military service during world war two [2].

Exercise, phosphates and fun

During his days as a medical undergraduate in Cambridge, Havard co-authored (with George Adam Reay) an influential study published in the Journal of Physiology of 1926 entitled ’The influence of exercise on the inorganic phosphates in the blood and urine’. It was this amiable paper, with its depictions of a time when doing science was akin to an undergraduate ‘jape’, that provoked the following reflections.

This paper was certainly not earth-shattering, nonetheless seems to have been one of the most cited of that year’s volume of J. Physiol. There are currently 13 references to be found on the Google Scholar database ( (quite a lot for such an old paper) with the most recent reference in 1971.

The style and structure provides a charming window onto the very different science of the early 1920s; with its un-translated ‘varsity’ slang, ‘clubby’ style of referencing which lists only authors surnames without initials (in 1926 the membership of the Physiological Society was less than 400 [7]) and delightful vignettes concerning the conduct of experiments.

One striking feature is that the experimental methodology reported in the paper is described as having changed significantly throughout the period of the experiment, and results are given both for before and after these trial-and-error modifications. A modern scientific paper would surely omit the earlier failed attempts. Indeed, the style of this article is less like a modern paper than a slice of laboratory life. The impression is that these scientific pioneers wanted to share not just their results, but the nuts and bolts of how results were generated.

Havard and Reay describe how ‘the exercise took the form of the subject running up and down the laboratory stairs, 40 ft in height, until he was exhausted’ during and after which many one cubic centimetre blood samples were taken from the subject’s finger in order to measure the phosphate etc. – which seems likely to have been a painful procedure. However, one of the main subjects listed was ‘R.E.H.’ himself, so he could not be accused of inflicting on others something he avoided himself.

Indeed, all the experimental subjects are listed by their initials, and presumably therefore identifiable by those ‘in the know’ (so, none of our present-day worries about ‘confidentiality’ are in evidence). In one of the tables we are told that that subjects include G.B. described as ‘A rowing man’, W.E.T. a ‘Rugby “Blue”’ (a ‘Blue’ was awarded to Oxford undergraduates for competing at the highest level of university sport), H.K.B.O. a ‘Running “Blue”’, E.H.F a ‘Sprinter’; and again Havard himself who is, by contrast to these athletes, only ‘Partly trained’.

Collecting urine samples was a problem – we are informed that H.K.B.O. (despite – or maybe because? – of being a Running Blue) was unable to produce a urine sample for 7 min after his exercise. In another experiment R.H.B (‘Running’) was ‘as exhausted and distressed as any of the untrained subjects’ – which must have been rather humiliating for him. But then R.H.B seems not to have been a Blue.

Three women were included as subjects. Miss (I assume it was a Miss) M.M. did exercise which was rather disdainfully dismissed as ‘not very vigorous’; Miss B.E.H. managed ‘more vigorous’ exercise; while the Amazonian Miss C.E.L. was able to perform ‘very vigorous’ exercise – unfortunately however after these exertions she was depicted as ‘very exhausted’. Havard noted, with obvious regret, that the women produced ‘anomalous results’ which were ‘difficult to account for’.

In conclusion the authors reported that phosphate goes up a little then markedly down on exercise, and that trained men show less of these exercise-induced changes in their blood inorganic phosphate.

A snapshot from a lost era

My interest in this paper was stimulated because it presents in microcosm a snapshot of science from an all-but lost era of the ‘invisible college’ of collaborating and competing researchers who knew each other well-enough to dispense with formalities, and whose world was essentially private despite publication in widely circulated journals [8]. To the hard-nosed professional modern scientist, such early 20th century papers look eccentric and idiosyncratic. The paper is indeed ‘amateur’, but mostly in a desirable sense of describing science as an avocation done for intrinsic reasons and the esteem of peers, rather than a vocation rewarded by a secure income and managerial power.

But much more important and striking is the total absence of exaggeration, hype, or spin: the paper’s openness, candour – in a word honesty. This marks the biggest and most dismaying contrast between publications of the science of 80 years ago and of modern science. There has indeed been a loss of innocence, collegiality and fun; but a loss of unvarnished truthfulness is the most serious change against current practice [9].

I have said that Havard was not himself a writer, but on the evidence of this early article, Havard was an unusually vivid scientific author from his mid-twenties. Indeed he wrote essays and journalistic reviews dating back to his student days and continuing through into the 1950s. Furthermore, Havard contributed posthumous memoirs of both Lewis [10] and Tolkien [11].

All of which helps explain why, despite not being a literary man, ‘Humphrey’s’ presence at the Inklings meetings was so highly valued.


I am grateful to Robert Havard’s eldest son John, who kindly gave me a list of some of his father’s publications, and provided fascinating background information by means of e-mail and telephone conversations. John Havard’s brother Mark (i.e. RE Havard’s second son) also corresponded, and reminded me that the doctor in CS Lewis’s 1943 novel Perelandra was named ‘Humphrey’.

[1] H. Carpenter, The inklings, George Allen and Unwin, London (1981).

[2] D.P. Glyer, The company they keep: CS Lewis and JRR Tolkien and writers in community, Kent State University Press, Kent, Ohio (2007).

[3] J.R.R. Tolkien, The Notion Club papers, Morgoth’s ring: history of middle earth volume IX, HarperCollins, London (1992).

[4] C.S. Lewis, Prince Caspian, Geoffrey Bles, London (1951).

[5] A.N. Wilson, CS Lewis: A biography, Collins, London (1990).

[6] R.E. Havard and G.A. Reay, The influence of exercise on the inorganic phosphates of the blood and urine, J Physiol 61 (1926), pp. 35–48.

[7] W.F. Bynum, A short history of the physiological society 1926–1976, J Physiol 263 (1976), pp. 23–72. View Record in Scopus | Cited By in Scopus (0)

[8] T. Kealey, Sex, science and profits: how people evolved to make money, William Heinemann, London (2008).

[9] B.G. Charlton, The vital role of transcendental truth in science, Med Hypotheses 72 (2009), pp. 373–376.

[10] R.E. Havard, Philia: Jack at ease. In: T. James and C.S. Como, Editors, Lewis at the breakfast table and other reminiscences, Harvest/HBJ Book, New York (1979), pp. 215–228.

[11] R.E. Havard and J.R.R. Professor, Tolkien: a personal memoir, Mythlore 17 (1990), pp. 61–62.