Marsden,
P. (1998). Memetics and Social Contagion: Two Sides of the Same Coin?
Journal of Memetics - Evolutionary Models of Information Transmission,2.
http://cfpm.org/jom-emit/1998/vol2/marsden_p.html
Marsden,
P. (1998). Memetics and Social Contagion: Two Sides of the Same Coin?
Journal of Memetics - Evolutionary Models of Information Transmission,2.
http://cfpm.org/jom-emit/1998/vol2/marsden_p.html
Following a thematic overview of social contagion research, this paper examines the question of whether this established field of social science and the nascent discipline of memetics can be usefully understood as two sides of the same coin. It is suggested that social contagion research, currently lacking a conceptual framework or organising principle, may be characterised as a body of evidence without theory. Conversely, it is suggested that memetics, now over two decades old but yet to be operationalised, may be characterised as a body of theory without evidence. The article concludes by proposing a memetic theory of social contagion, arguing that social contagion research and memetics are indeed two sides of the same social epidemiological coin, and ends with a call for their synthesis into a comprehensive body of theoretically informed research.
Two centuries ago, a wave of suicides swept across Europe as if the very act of suicide was somehow infectious. Shortly before their untimely deaths, many of the suicide victims had come into contact with Johann von Goethe's tragic tale "The Sorrows of Young Werther," in which the hero, Werther, himself commits suicide. In an attempt to stem what was seen as a rising tide of imitative suicides, anxious authorities banned the book in several regions in Europe (Phillips 1974, Marsden 1998).
During the two hundred years that have followed the publication and subsequent censorship of Goethe's novel, social scientific research has largely confirmed the thesis that affect, attitudes, beliefs and behaviour can indeed spread through populations as if they were somehow infectious. Simple exposure sometimes appears to be a sufficient condition for social transmission to occur. This is the social contagion thesis; that sociocultural phenomena can spread through, and leap between, populations more like outbreaks of measles or chicken pox than through a process of rational choice.
The term contagion (kan-tã'jan) itself has its roots in the Latin word contagio, and quite literally means "and from touch". Contagion therefore refers to a process of transmission by touch or contact. The Microsoft Dictionary (Microsoft 1997) defines contagion as the
"transmission of a disease by direct contact with an infected person or object; a disease or poison transmitted in this way; the means of transmission; the transmission of an emotional state, e.g. excitement; a harmful influence."
From this definition, contagion refers to 1) the social transmission, by contact, of biological disease, and 2) the social transmission, by contact, of sociocultural artefacts or states.
The contagion concept first became popular as both a descriptive and explanatory device for social, as opposed to biological, phenomena in the late 19th century France, notably through the work of James Mark Baldwin (1894), Gabriel Tarde (1903) and Gustave Le Bon (1895). Empirical research into the phenomenon did not, however, begin until the 1950s. This more recent research has unequivocally established the fact of the social contagion phenomenon, and has identified its operation in a number of areas of social life. The implications of this social contagion research are radical: The evidence suggests that under certain circumstances, mere `touch' or `'contact' with culture appears to be a sufficient condition for social transmission to occur.
Despite this promising start, social contagion research has evolved into a field that is now unorganised, disparate and incoherent, lacking both an organising principle and a conceptual framework (Levy and Nail 1993). There is, in fact, a complete absence of agreement among researchers as to the particular mechanism that underlies social contagion. This lack of consensus has lead to a proliferation of definitions of the phenomenon which range from the vague to the plain contradictory. For example, the Penguin Dictionary of Psychology (Reber 1995) defines contagion simply as the "spread of an activity or a mood through a group". The Concise Oxford Dictionary of Sociology (Marshall 1994) adopts a similarly vague definition of "ideas moving rapidly through a group." Other definitions, whilst more extensive, provide little in the way of increased clarity or utility. The Macmillan Dictionary of Psychology (Sutherland 1995) defines contagion as "the spread of ideas, feelings and, some think, neuroses through a community or group by suggestion, gossip, imitation etc." Some definitions attempt to clarify the concept in terms of a putative uncritical and non-rational mode of inheritance/infection. Thus, The Encyclopaedic Dictionary of Psychology (Furnham 1983) defines contagion as a process and form of collective excitement "in which emotions and behavioural patterns spread rapidly and are accepted uncritically by the members of a collective." In contrast, other definitions make no mention of this uncritical nature of inheritance but specify instead the perception of non-intentionality in transmission (e.g. Levy and Nail 1993) such that contagion becomes the "spread of affect, attitude or behaviour from Person A ("the initiator") to person B ("the "recipient") where the recipient does not perceive an intentional influence attempt on the part of the initiator." A very different definition of contagion has also been proposed, referring to neither the non-intentional nature of transmission, nor the uncritical nature of inheritance, but rather to a putative phenomenon of disinhibition. Thus, Wheeler (1966) states that:
"If the set of test conditions T1 exists, then contagion has occurred if and only if Person X (the observer) performs behaviour N (BN) where T1 is specified as follows: a) A set of operations has been performed on Person X which is known to produce instigation toward BN in members of the class to which X belongs: b) BN exists in the response repertoire of X, and there are no physical restraints or barriers to prevent the performance of BN; c) X is not performing BN; d) X observes the performance of BN by Person Y (the model)." (p. 180)
Together, these very different definitions of contagion have been operationalised to produce studies that have little in common except the observable phenomenon of spread by contact. Most of these insist on the presence of a number of internal states and mechanisms (intentionality, approach-avoidance, conflict etc.) for the process to count as `true', as opposed to merely `apparent' contagion. However, these various qualifications have not only contributed to the confused nature of social contagion research, but they have also undermined the central rationale of the metaphor; that observable culture spreads as if it has contagious properties.
One of the clearest and most inclusive definitions of social contagion is that proposed by The Handbook of Social Psychology (Lindzey and Aronsson 1985). This definition refrains from positing as necessary internal states. Instead social contagion is held to be "the spread of affect or behaviour from one crowd participant to another; one person serves as the stimulus for the imitative actions of another." Such a definition has the advantage of focusing and clarifying the observable contagion phenomenon, whatever internal states may or may not be present. It should be noted however that there is no reason for the contagion phenomenon to be restricted to the crowd scenario, to be sure, the mass media allows for the possibility of contagion through dispersed collectivities.
Despite the varied definitions of contagion, the empirical research has tended to confirm that the hypothesis that human behaviour clusters in both space and time even in the absence of coercion and rationale. This tendency towards homogeneity has been identified in a number of types of behaviour using one or more of three basic approaches. In the case of dispersed collectivities or masses, evidence for and against the social contagion phenomenon has been typically drawn from correlational studies where aggregate statistics on exposure and infection are correlated, such as media reporting on suicide stories and suicide rates (e.g. Phillips 1974, Marsden 1998). In the case of local collectivities such as crowds, research methods have included field studies using participant or non-participant observation (e.g. Reicher 1984 on Bristol riots), or formal experimental studies under laboratory conditions (e.g. Freedman, Birsky and Cavoukian 1980). Bringing the disparate data from the various methods together, meta-analyses of the contagion phenomenon have also been conducted (e.g. Levy and Nail 1993).
Substantively, social contagion research can be broken down into two major areas, studies investigating emotional contagion (the spread of mood and affect through populations by simple exposure) and studies investigating behavioural contagion (the spread of behaviours through populations by simple exposure). Behavioural contagion research can itself be broken down into six broad areas, based on the nature of the behaviour that is spread; hysterical contagions, deliberate self-harm contagions, contagions of aggression, rule violation contagions, consumer behaviour contagions, and financial contagions.
A hysterical contagion is "the dissemination of a set of symptoms among a population in which no manifest basis for the symptoms may be established." (Kerckhoff and Back 1968). Also known as contagious psychogenic illness (Cohen, Colligan, Wester II and Smith 1978), hysterical contagions involve the spread by contact of reported symptoms and experiences usually associated with clinical hysteria (hallucinations, nausea, vomiting, fainting etc.) in the absence of a biological contagion. The paradigmatic example of hysterical contagion is the "June Bug" incident that occurred in a US textile factory in 1962, where 62 factory workers reported having been bitten by a mythical bug that `caused' symptoms such as numbness and nausea (Kerckhoff and Back 1968). More recently, Colligan and Murphy (1982) have analysed a further 23 examples of hysterical contagion - "the collective occurrence of a set of physical symptoms and related beliefs among two or more individuals in the absence of an identifiable pathogen", and found that it was the verbal reporting of the symptoms that spread in a contagious-like manner rather than the symptoms themselves. Their research also largely confirmed Kerckhoff and Back's theory that those susceptible to hysterical contagion were suffering from intra-psychic stress. More recently still, Showalter (1997) has suggested that chronic fatigue, Gulf war and multiple personality syndromes might spread by contagion, and Pfefferbaum and Pfefferbaum (1998) have argued post-traumatic stress disorder also spreads by contagion. The hallucinatory component of hysterical contagion may also account for the spread of supernatural phenomena such as the sightings of Diana ghosts following the death of the princess in 1997 (Marsden 1997), as well as reports of UFO sightings and alien abductions (Houran and Lange 1996, Showalter 1997).
A second class of behaviour that appears to spread through populations by contagion is rule breaking or rule violation behaviour. Evidence has tended to support the thesis that an individual's exposure to rule violations increases their likelihood of engaging in similar or identical behaviour. Such rule violation contagions have been identified in teenage smoking (Ritter and Holmes 1969, Rowe, Chassin, Presson, Edwards and Sherman 1992), speeding (Connolly and Aberg 1993), substance abuse (Ennett, Flewelling, Lindrooth and Norton 1997), delinquency (Jones 1998), youth sex (Rodgers and Rowe 1993) and criminality (Jones and Jones 1995).
A third class of behaviour, which has been the focus of empirical social contagion research, is deliberate self-harm (DSH), of which suicide is the paradigmatic example. Specifically, research has shown that suicide rates and other examples of DSH vary proportionally to the extensity, intensity and content of exposure, both in local and dispersed collectivities (Phillips 1974, 1980, 1982, Stack 1987, 1990, Higgins and Range 1996, Gould 1990, 1996, Gould, Wallenstein and Kleinman 1987, Gould, Wallenstein and Davidson 1989, see Marsden 1998 for a `memetic' overview). Contagion is now an accepted risk factor in suicide research, and the overwhelming evidence has prompted the establishment of several government programmes to minimise the effects of suicide contagion.
Another, very different focus of social contagion research has been the financial contagion phenomenon, manifested in the behaviour of stock markets which lurch from state to state as a result of selling panics and buying frenzies that sweep across the globe. Financial contagion research has tended to investigate the various factors that may exacerbate and contribute to the phenomenon such as analysis techniques, the level and nature of information available to dealers, and social communication networks (e.g. Orlean 1992, Temzelides 1997, Lux 1998).
A fifth area of contagion research has investigated the contagious properties of consumer behaviour which sometimes results in the spread of consumer fashions and fads through populations in a manner more indicative of an influenza epidemic than rational behaviour (Marsden, forthcoming b). This phenomenon has prompted the development of deterministic and stochastic models with good predictive power that forecast both sales realisation and new product adoption patterns based on the `infectiousness' of consumer goods (Bass, Mahajan and Muller 1990, Rashevsky 1939, 1951, Rapoport 1983, Rogers 1995).
A sixth focus of social contagion research has been the contagion of aggressive behaviour, a phenomenon that has been shown to operate in both local and dispersed collectivities. Whilst much of this research has been of a descriptive nature within transitory and unpredictable angry crowds (mobs) (Bandura 1973, Reicher 1984, Lachman 1996), results have been supported with experimental evidence (Bandura, Ross and Ross 1963, Wheeler and Caggiula 1966, Wheeler and Levine 1967, Wheeler and Smith 1967, Goethals and Perlstein 1978). In dispersed collectivities, where the contagion of aggression is mediated by the mass media, research has focused on measuring exposure and infection rates and then testing for correlations. (Atkin, Greenberg, Korzenny, and McDermott 1979, Sheehan 1983, Phillips 1983).
Finally, social contagion research has not only restricted itself to the spread of behaviours, a significant number of studies have identified a variety of emotional contagions. The emotional contagion phenomenon was originally defined by McDougall (1920) as "the principle of direct induction of emotion by way of the primitive sympathetic response" and more recently by Sullins (1991) as "the process by which individuals seem to catch the "mood" of those around them". The proposed mechanism for this spread of mood is an automatic and continuous human tendency to synchronise facial expressions, voices, and postures with others in the immediate environment (Hatfield, Cacioppo and Rapson 1993). These behavioural cues then appear to trigger the appropriate emotions in a system of feedback. The Emotional Contagion Scale (Doherty 1997) has been recently developed and validated to assist further research in this area, which has already identified various examples of emotional contagion including mood (Hsee, Hatfield and Chemtob 1992), anxiety (Behnke, Sawyer and King 1994), fear (Gump and Kulik 1997), appreciation (Freedman and Perlick 1979) and enjoyment (Freedman et al. 1980).
Whilst the vast majority of social contagion research has demonstrated the existence and voracity of the empirical phenomenon, the theoretical implications of the results have not been addressed. The results of contagion research suggest that just as we do not choose to be infected with, and pass on, biological contagions, we often behave as if we have little control over the culture we become infected with and consequently spread. Such an observation undermines the traditional understanding of the human subject as an autonomous agent whose action is defined by individual intentionality and rational evaluation. Whilst we may like to believe that we consciously and rationally decide on how to respond to situations, social contagion evidence suggests that some of the time this is simply not the case. Rather than generating and `having' beliefs, emotions and behaviours, social contagion research suggests that, in some very real sense, those beliefs, emotions and behaviours `have' us.
The failure of mainstream social science to take this implication of social contagion evidence seriously is certainly in part due to the above-mentioned disorganised and incoherent state of the field. However, the failure is also probably due to a fundamental incompatibility between the concept of social contagion and the Cartesian voluntarism implicit in much social science. In fact, standard explanations of social contagion can be characterised by an almost desperate attempt to restore irreducible individual agency and rational action to the phenomenon.
In trying to explain away the social contagion phenomenon, two types of theory have been developed. Firstly, a number of theories suggest that the spread of homogeneity is a consequence of conscious and deliberate imitation in situations usually defined by uncertainty or ambiguity. Secondly, contagion has been accounted for by putative latent homogeneities in terms of prior motivations that antecede the observable phenomenon.
An example of the first type of explanation is Emergent Norm Theory (e.g. Turner 1964) which states that the spread of behaviour through a population is not by contagion (contact) but is the result of conscious and deliberate attempts to adhere to norms and rules emerging out of complex and subtle interaction within collectivities. Similarly Social Learning Theory (e.g. Bandura 1971, 1986) holds that homogeneity is the result of the conscious and deliberate imitation that takes place when individuals are presented with uncertain and ambiguous situations. When we are unsure of how to react to a stimulus or a situation, these theories suggest that we actively look to others for guidance and consciously imitate them.
An example of the second type of explanation is Convergence Theory (e.g. Turner and Killian 1987) which suggests that homogeneity and clustering is not a result of contagion but the result of prior shared motivations that cause collectivities to converge in the first place. From this perspective, similarities cause collectivities and not vice versa. A similar explanation is provided by Disinhibition Theory (e.g. Freud 1922, Redl 1949, Wheeler 1966, Ritter and Holmes 1969, Levy and Nail 1993) which states that contagion is "essentially imitation mediated by restraint release due to observing another perform an action that the individual is in conflict about performing himself" (Freedman 1982). In other words, from this perspective, behaviours are not transmitted by contact; rather inhibited behaviours (sometimes unconscious and "primitive") that are already held in an individual's behavioural repertoire are simply released. Thus, homogeneity spreads as a result of the intra-psychic conflict resolution that occurs through social evidence. Another variation on the 'prior motivations' theme is Deindividuation Theory (e.g. Diener 1976, 1979, Festinger, Pepitone and Newcombe 1952, Zimbardo 1969). This theory holds that the anonymous nature of collectivities can engender a restraint reduction in individuals. This sense of anonymity is held to cause a reduction in the individual's sense of personal accountability and responsibility, allowing them to engage in behaviour from which they might otherwise abstain. When anonymity leads to restraint reduction of similar behaviours within individuals within a collectivity, this produces the appearance of contagion.
Both the `conscious choice' and `prior motivations' theories may explain the social contagion phenomenon in some circumstances, but none of them can comprehensively explain the phenomenon. Indeed, it is difficult to see how any of the theories could provide a credible explanation of either emotional or hysterical contagion, except by maintaining that we either choose illnesses or emotional states based on those that are around us, or worse we have hidden desires to be ill, angry or anxious! Social contagion stretches Cartesian rational action theory to such a degree that the latter becomes an untenable explanation of the former. Valiant attempts at squeezing irreducible individual agency and rational evaluation into the phenomenon are simply at odds with data. The evidence shows that we inherit and transmit behaviours, emotions, beliefs and religions not through rational choice but contagion. Does this rejection of rational choice/action theories mean that social contagion is a homeless body of research, a body of evidence with no theoretical home to go to? No, I think there is an alternative paradigm that has the potential to explain more of the data more of the time. That paradigm is memetics.
Social theorists often use the language of architecture, they speak of theory building, laying theoretical foundations, or constructing theoretical edifices. This is useful language, it indicates the step by step, laborious nature of their enterprise. Meme theory is no different in this respect, many problems still have to be resolved within the new paradigm (Rose 1998). However, meme theory is developed enough to be operationalised conservatively by adopting what could reasonably be called a memetic stance. Not a fully blown theory, the memetic stance is more of a way of looking a the world, a set of guiding principles, a useful heuristic, based on some hopefully important insight into the nature of the social world. Whether the memetic stance turns out to be an explanatory device in an evolutionary extension of folk psychology, or a proper theory of mind where memes are internally instantiated in the neural networks of our brains is an issue that will one day have to be resolved empirically. For now, by adopting the memetic stance, these issues may be bracketed, and research can proceed based on the utility of this ontologically minimalist heuristic.
So what exactly is the memetic stance? The memetic stance states that human condition is minimally defined by two selective processes operating in two different substrates, the biological and social (Marsden forthcoming a). This is because the necessary conditions for the evolutionary loop of replication, variation and selection are present in the two substrates. This is not contentious in itself, what is more contentious is that the memetic stance sees these processes operating at the level of what is being replicated, that is, the gene and the meme. Thus, the memetic stance involves taking a meme's-eye perspective and understanding of the social world, thinking not in terms of selfish genes, but selfish memes. Taking this memetic stance has allowed researchers to explain the spread of non-rational behaviour in terms of the fitness of that behaviour itself. Examples include altruism (Allison 1992, 1993, Blackmore forthcoming) chain letters (Goodenough and Dawkins 1994, Hofstadter 1995, Allison 1993), chain e-mail (Jones 1995) religions and cults (Dawkins 1993, Lynch 1996 and Cowley 1997), political revolutions and war (Vajk 1989), religious scriptures (Pyper 1997) Usenet content (Best 1997), management practices (Price and Shaw 1996, 1998), media representations, (Rushkoff 1994), urban legends (Gross 1996) and consumer behaviour (Marsden forthcoming b, Brodie 1996).
The memetic stance suggests that design in the social world is at least partly a product of the evolutionary loop of replication, variation and selection operating on culture, or more specifically cultural instructions coding for behaviour (Cloak 1975, Marsden forthcoming a). It is not necessary to invoke conscious choice or rational evaluation by an entity - homuncular, divine or otherwise - standing miraculously outside evolution to explain design; given enough iterations, natural selection will inexorably and inevitably give rise to design.
Once we take the memetic stance, features of the world that are difficult to explain from the orthodoxy of traditional social science become non-miraculous and eminently explicable. The memetic stance can explain not only apparent design in the social world, but importantly it can also explain phenomena that seem to negate the omnipresence of individual agency in human affairs. Put simply, the memetic stance states that the reason why some social behaviour doesn't seem to make sense from the perspective of the individual is because we are looking at that behaviour at the wrong level. We are taking an anthropocentric or homuncular view of a social world that was created at least in part at a memetic level. Trying to explain the social world from the perspective of the individual is like trying to explain the movements of a car without reference to the driver. The movements of a car can be rationally described, explained and understood in terms of the car's own needs as (somewhat circuitous) trips from petrol pump to petrol pump. However, by ignoring the driver much of what is observed makes no sense at all. The same argument holds for the social world, just as we can explain much of our (somewhat circuitous) social behaviour in terms of the needs of the meme-vehicle (individual), much of what is interesting about that behaviour is overlooked. By taking the memetic stance we can account for what happens when the needs of an individual cannot explain behaviour, the equivalent of all the non-petrol seeking activity of a car, and this stance provides an evolutionary rationale for explaining why the social contagion phenomenon occurs.
Taking the memetic stance involves, to use an overused concept, a true Kuhnian paradigm shift; just as evolution in the biological world evolves according to what is better (not best) for the gene in its environment, so too does the social world evolve according to what is better for the meme. The memetic stance involves describing, explaining and understanding social behaviour from this meme's-eye perspective. From the memetic stance "What makes this person want to do x?" becomes "What is it about x that makes people want to do it?" Social contagion can be explained by the memetic stance because culture has an independent evolutionary dynamic that is derived from the genetically evolved human capacity and predisposition to replicate culture (see Flinn 1997 for a review). Because social learning is an evolved psychological trait, it follows that we have an evolved predisposition to replicating the behaviour of those around us. Successful social contagions are those elements of culture that operate as both stimulus and response, and that are adapted to the evolved architecture of the human brain. No homunculus need be invoked, only evoked imitation.
In this way, the memetic stance deconstructs the homunculus into what can be understood as replicating cultural instructions (memes). This opens up an exciting research programme for memetics, as contagion is no longer understood as a metaphor but an evolutionary process. Social contagion research, from the memetic stance could focus on the particular characteristics that render behaviours and emotions infectious. It could also investigate why certain people are immune to certain contagions, or how they develop resistance to contagion, or conversely what makes certain people particularly susceptible to contagion, and others not. Similarly, memetic research could look for the limiting factors of the contagion phenomenon in both time and space. How, for example, is social contagion bounded? Can social contagion epidemics burn themselves out and if so, how? How does a contagious epidemic become an endemic trait in the social world? Is it possible to quarantine areas exposed to contagion, or quarantine those who have been infected? Can individuals be vaccinated against contagion? How long is the incubation period, that is, the time from exposure to infection? What are the primary vectors of contagions, that is, what are the primary channels of infection? Are contagions specific or diffuse? These are all questions that are more or less precluded in a traditional paradigm dominated by a Cartesian homuncularism and rational action theory which essentially deny the existence of the social contagion phenomenon. By deconstructing the homunculus into a web of replicating instructions, the memetic stance allows the social contagion phenomenon to become a theoretically informed research enterprise.
Taking the memetic stance allows research to proceed with the objective of explaining the spread of non-rational behaviour in terms of the fitness of that behaviour itself. Until recently, such memetic research has been of a largely non-rigorous and anecdotal nature. Despite offering the exciting prospect of being an autonomous social theory that is compatible and coherent with, but not reducible to, our knowledge of the biological world, the emerging discipline of memetics has yet to produce any concrete results. This is essentially because the issue of how to successfully operationalise the emerging paradigm has yet to be addressed; memeticists have yet to exploit their innovative analytical framework to build a body of theoretically informed empirical research. It is here that the body of social contagion research may be of particular use to memetics, offering itself up as a rich source of empirical evidence, whilst offering important methodological lessons and inspiration for future research. For example, the emotional contagion scale developed by Doherty (1997) could be used by memeticists, as could the field studies, correlational and experimental methods that have been exploited by social contagion researchers. More generally, memeticists could develop the social contagion research tradition of using the substrate neutral tools of epidemiology to assist their research programme. These tools could be adapted to provide useful information about differential incidence and prevalence of evolving cultural traits, as well as structure of endemic and epidemic features of society.
The use of epidemiological tools would have the advantage of allowing memetic research to proceed without making any ontological claims as to the nature or status of what exactly is being spread. Epidemiology is not the study of the inheritance of particular diseases or pathologies per se; rather it is the study of the distribution and pattern of the measurable effects of infection. Memetics qua social epidemiology might aspire to a similar goal. In the same way that causal mechanisms in the epidemiology of disease depend on, and vary with, the particular pathology that is being studied, taking the memetic stance does not require that social patterns be reduced to any one particular selective mechanism. Epidemiology may proceed independently of the aetiology of social products being researched; no assumptions about the heterogeneity or homogeneity of causal mechanisms are necessary.
The emerging paradigm of memetics and the established tradition of social contagion research do not simply have much to learn from each other, they are in fact two sides of the same social epidemiological coin, the former a theory-rich version of the latter, and the latter an evidence-rich version of the former. Taking the memetic stance is a radical move, but there are some wheels, particularly of the methodological variety, that just don't need to be reinvented by memeticists, because they can already be found in social contagion research. Equally, memetics brings to the social contagion table an innovative conceptual framework with an important evolutionary component that the latter currently lacks. By integrating social contagion research and the memetic paradigm we would allow for the development a robust body of theoretically informed empirical research. In doing this we will be laying one more foundation for the long overdue Kuhnian paradigm shift that will finally see the integration of social science within a broader evolutionary paradigm.
The author would like to thank members of `Meme Lab', Sue Blackmore, Nick Rose and Derek Gatherer, for discussing and reviewing earlier drafts of this article and for their useful constructive criticism. The usual qualifier of course applies.
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