The Baby in Memetic Bathwater - WHITEHEADBOOKS.com

Summary

Introduced by science writer Richard Dawkins in 1976, the concept of the “meme” was promoted by psychologist Susan Blackmore, philosopher Daniel Dennett, and others. Dawkins held that memes were, like genes, replicating units critical for adaptation. Unlike genes, though, memes were conceived as behavioral replicators – units that propagated by means of imitation. This idea caught the imagination of the public at large. And it provoked a flurry of excitement among behavioral scientists, energy that blossomed briefly into “memetics,” a new area of scientific study. Following a brief run, memetics fell out of favor. But scientists rejected memetics for the wrong reasons. There is a golden nugget of truth embedded within memetics, a concept critical for the understanding of dysfunctional human behavior. That truth: not only are behavioral replicators possible, but they are quite common – as evidenced by the parasitic replicators we know as addictions.

Introduction

In 1976 Richard Dawkins unleashed some powerful ideas into the world. That was the year he published his now-classic book The Selfish Gene. 1 Previously biology, in line with Charles Darwin’s theory of evolution, had regarded the animal as the unit that struggles for survival in the world. The animal, with its many genes, was widely understood to be the unit of natural selection.

But Dawkins flipped things around, shifting the spotlight to the gene itself. In his view, it was the individual gene that was doing its best to persist. The gene was “selfish,” looking out for its own welfare. 2 It is only out of self-interest, he reasoned, that individual genes team up with other genes to form a genome, and so create a living organism. Animals are best understood as “survival machines,” he said, lumbering vehicles transporting their gene operators from one generation to the next. Genes make animals, he argued, simply because those animals perpetuate the actual units of selection – the individual genes within the animal genome.

The birth of a meme

The selfish gene idea was indeed powerful, and it has had a lasting impact upon biological thinking. But in the same book Dawkins introduced another, more controversial idea that has stubbornly refused to go away – that of the meme.

According to Dawkins the individual genes of animals are “replicators,” strings of amino acids – the informational macromolecules DNA and RNA. But there is no reason to assume, argued Dawkins, that replicators necessarily have to be composed of DNA and RNA. Perhaps there are other forms that can perpetuate themselves through natural selection. As a sort of intellectual exercise, he speculated that replicating units might be passed from one person to another not through a biochemical medium, but through a behavioral medium – imitation. He coined the label “meme” to refer to this hypothetical kind of non-biological replicator. “Memes,” he said, “spread through human culture as genes spread through the gene pool. Memes can be good ideas, good tunes, good poems – anything that spreads by imitation as genes spread by bodily reproduction or viral infection.” 3

Over the succeeding decade the meme idea proved astoundingly popular. It made a lot of sense to a lot of people. To some it seemed obvious that memes were not only a possibility, but something real. People could witness, right before their eyes, concepts and strings of behaviors jumping from person to person. Those ideas and behaviors did indeed seem to have a life of their own, spreading like viruses, just as Dawkins had suggested. The meme idea itself became a meme, a way of understanding the spread of ideas that propagated itself like wildfire through the popular imagination.

In The Selfish Gene Dawkins had presented the meme idea as hypothetical, something of a metaphor. He was illustrating his point that there could possibly be replicators in media other than DNA. Later, though, he talked about memes as if they were actual viral processes that could parasitize the human mind as host. In 1991 science writers Douglas Hofstadter and Daniel Dennett edited a collection of musings on the nature of the human mind. 4 An essay by Dawkins was part of that collection. As Dawkins put it this time, “memes should be regarded as living structures, not just metaphorically but technically. When you plant a fertile meme in my mind, you literally parasitize my brain, turning it into a vehicle for the meme’s propagation in just the way that a virus may parasitize the genetic mechanism of a host cell.” 5 The meme was now conceptualized as a behavioral virus.

The next few years saw the appearance of a number of books about “mind viruses” based on the meme replicator. In 1996 writer Aaron Lynch published one entitled Thought Contagion, 6 which described patterns of meme transmission. The same year Richard Brody put out a volume entitled Viruses of the Mind. 7

Thanks in large part to the energy and enthusiasm of respected British psychologist Susan Blackmore, a new focus of scientific study burst into being – memetics. She recognized the potential of the meme idea, and began speaking and writing prolifically on the subject. The Journal of Memetics came to life in 1997. In 1998 Blackmore published in this journal an influential paper that more precisely defined memes and memetics from a scientific perspective. In line with Dawkins’ original characterization, she emphasized that memes were replicators based strictly upon imitation. 8 With interest snowballing, maybe it isn’t surprising that the scientific community began taking a more critical look at the idea of memes.

Flying high

Interest in memetics soared through the 1990s. At the time, few would have predicted that the fledgling science would shortly crash to the ground. But crash it did. The problem, it seems, was that there were two ways of thinking about memes. The first was the informal, very popular idea of some kind of viral process spreading infectiously from brain to brain. The second was the formal scientific hypothesis that there was an actual behavioral replicator based strictly upon imitation. It was the second memetics – the formal scientific proposition – that could not sustain flight.

The scientific version of memetics contains a fatal flaw. Scientists believed that a true replicator must be able to reliably store and transmit information from one generation to the next. DNA qualifies because it is chemically stable. It can store and pass informational sequences rigidly and reliably. By contrast, as the party game “telephone” shows, imitation is a notoriously poor way to pass accurate information. In this game a phrase is whispered from one person to another down a chain of individuals. Invariably, by the time the message reaches the last person it has become unrecognizable. Building a strong replicator out of imitation would be like constructing a freight train out of Jello. A replicator based upon imitation, critics maintained, would be way too flimsy to hold itself together. Such a squishy replicator made no sense to critics.

Dawkins tried to salvage the imitation idea. He pointed out that in the real world learning by imitation usually happens in two phases. The first part is deciding to copy something – for example a dance step you’ve seen. The second part is adjusting your copy so that it works. If your new dance step doesn’t satisfy you, then you change it until you’re happy with it.

There’s no doubt Dawkins’ description of imitation was correct. When we pass ideas and behaviors on through imitation, this second step is always included. But with the addition of that second step meme transmission begins to look more like a mere suggestion. Now it resembles a rough sketch of a new way of acting or thinking. The nitty gritty details are not actually transmitted by the replicator. Instead, the detail is recreated within each individual through his or her own rehearsal, to work within his or her own unique environment. Proponents of memetics had trouble responding to this criticism, so many of them backed away from the meme idea. Sadly, it seemed the party was over.

A double-edged sword

Critics had cut down memetics using the razor-sharp sword of logic. It did seem their criticisms were justified: there’s no way imitation-based replicators could work in exactly the same way they were claiming DNA-based replicators work. And this brings us to the point of this story: the critics’ claims were themselves flawed.

Were they thinking outside the box, critics might have realized that their weaponized logic has a second edge, equally sharp. That second edge cuts not into memetics, but into their notion of DNA-based replication.

Dawkins’ two-step model accurately describes replication-by-imitation. So it seems we have two credible models of replication. It’s just that they operate on different levels. On the biological level it’s transmission through DNA; on the behavioral level it’s transmission by imitation and rehearsal. Each model tells us something about the way replication works. Each casts light upon a larger truth behind them.

The critics had argued that a replicator based on imitation must work the same way a DNA replicator works. But now we can reverse the argument. A DNA replicator must work like an imitation replicator. And if we think it through we find that it’s true. The DNA replicator serves a suggestion or blueprint, the details of which are worked out anew with each generation.

There’s no way a completely efficient DNA replicator could be beneficial in the real world – at least the way it was envisioned by meme critics. The critics temporarily forgot how evolution by natural selection works. It is always and ever a two-step process. Those two steps are (1) variation of forms, and (2) selection of best variants according to the demands of the environment.

DNA replicators are in no way exempt from this two-step requirement. A perfect, 100 percent efficient DNA replicator would create no variation at all. Without variation, there could be no selection. But variation and selection are what keeps the replicator adapted to current conditions. Because environmental conditions change over time, a perfect replicator would quickly fall out of alignment with real-world requirements. So a perfect replicator would replicate itself “perfectly” into extinction.

When it comes to evolution, that second step – adjustment to fit current conditions – is essential. Nature has gone to great lengths to ensure that there is always variation in genetic transmission, no matter how perfect the replicator. Sexual recombination is, among other things, a way to guarantee variation within each successive generation. Multiple alleles of each gene exist within every sexually breeding population. These alleles are shuffled and dealt out like hands in a poker game. Every hand is different. That’s the variation part. And the winning hands are chosen by nature herself – the winners live longer than the losers. That’s the selection part.

Variation and selection apply to the transmission of behaviors too. It’s just that the process is a bit different. Behavioral replication operates on a very different timescale. Learning is like speeded-up evolution. Modifying a DNA or RNA replicator by natural selection takes a very long time, because it requires many successive generations of animals. But in higher animals dramatic changes in behavior can be observed within a single generation, within a single individual.

Let’s revisit the “telephone” party game. On the evolutionary timescale of the biological DNA replicator, we have to imagine a long string of generations rather than a long string of people. Start out with one DNA replicator, and follow it forward a few million generations. Imagine what that replicator will have become. Can we reasonably expect it to be the same as when we started? Not hardly. Chances are that it would be significantly different – just as in the telephone game. And that’s not a bad thing. It’s evolution.

Things are both similar and different within the arena of behavior. Evolution has produced more than one kind of animal behavior. Instinctive behavior is the kind shaped directly by natural selection. This kind is “hard-wired” into the animal. Instinctive acts have a robotic character, like the behavior typical of a jellyfish or a paramecium or a spider. Because instinctive behavior is driven directly by natural selection, it evolves very slowly, over the course of many generations. Those robot-like animals that “act right” get their needs filled within their current environment, because their behavior fits that environment. So they survive to reproduce. Their “right” behavior passes on to the next generation. The runners-up die before the next round begins, and don’t pass on their dysfunction. In this way the instinctive behavioral repertoire of the species is modified over the generations so that it stays relevant.

Replicating habits

The situation is quite different with the second type of behavior – learned habits. In this type the details of the behavior are never spelled out in advance. The animal always works the details out for itself. Imitation-based replicators of this second type are well known to behavioral scientists.

A replicator without any details? This may strike non-psychologists as a strange idea – it might even seem absurd. Nevertheless it’s mainstream science. Replication without specific details is the standard model for all habit development. Behavioral scientists long ago concluded that when it comes to higher animals, each individual inherits not specific behaviors, but general drives that guide the assembly of their specific habits. What’s passed to the individual animal from its ancestors is the drive, an instinctive set of general predispositions – not the details of how the animal will ultimately express that drive. 9 The specifics are always worked out by the animal itself through the process behavioral scientists call learning.

Habit assembly through reinforcement – learning – works something like evolution: it’s a process of variation and selection. More than a hundred years ago psychologist Edward Lee Thorndike formulated his Law of Effect, 10 which says that “behaviors that are followed by a ‘satisfying state of affairs’ tend to be repeated and those that produce an ‘unpleasant state of affairs’ are less likely to be repeated.” 11 In other words, the animal tries out multiple variants of any new behavior, selecting for repetition those variants that bring the most satisfaction. The selecting is done according to the animal’s subjective experience of fulfillment. 12

Habit-based learning was one of evolution’s home runs. It offers a tremendous advantage to higher animals. 13 It provides all the benefits of evolved behavior, but without either the snail-slow development speed or the robotic rigidity. And crucially, a different way of behaving can be worked out “on-the-fly” within a single animal. When it comes to learned behavior, the details are always supplied by the individual, who runs through variants of a new behavior until satisfied with the result. That’s how habit development works – including the habits we are here calling replicators. Dawkins’ characterization of learning-by-imitation was right on target. The details of the transmission are worked out through individual rehearsal.

Because two-stage replicators are already the de facto standard in behavioral science, it isn’t really too much of a stretch to imagine exactly the kind of behavioral replicator Dawkins was talking about.

Save the baby!

In rejecting memetics wholesale we are pitching the baby out with the bathwater. In this case, the “bathwater” is the unsupportable idea that strings of behavior must have the same fidelity as strings of DNA. That murky water should be thrown out. On the other hand, we would do well to strain the precious “baby” out of the mix. That baby is the reality that we can reasonably expect to discover replicators flourishing within non-DNA media. Recall that Dawkins’ rationale for inventing the meme was to press home just this point.

And recent events demonstrate that his point was well taken. In the years since he introduced the meme concept biologists have identified some real-life, non-DNA replicators – the self-reproducing proteins we call prions.

Way back in the 1940s researchers had noticed that certain neurological diseases – for example “scrapie” in sheep and CJD (Creutzfeldt-Jakob Disease) in humans – could be passed on through tissues that had been treated to destroy DNA and RNA. Scientists were perplexed, since at that time every disease organism was assumed to be based on DNA and RNA. They began to suspect that the infectious agent might be some kind of protein structure.

Given the DNA orthodoxy of the time, the idea of a non-DNA replicator struck many biologists as blasphemy. Nevertheless, by the 1980s researchers had succeeded in isolating an infectious protein from diseased animals. Importantly, they were able to inactivate the infectious agent using chemicals known to destroy proteins. There was no longer room for doubt. They had confirmed a non-DNA disease, a non-DNA replicator. 14

Mainstream science now accepts that prions are abnormally folded proteins capable of reproducing themselves. The strangely folded proteins spread by provoking normal proteins around them to refold into the same abnormal shapes. Those newly-created prions, in turn, convert other proteins into prions. And so on. Now that researchers know what they are looking for, they have discovered other kinds of prions reproducing themselves in yeasts. Apparently prions are fairly common.

Given these discoveries within the biological arena, it’s no longer such a stretch to imagine replicators operating within the medium of behavior. We can expect some of these patterns to be pathological, and to share features of the viruses so common within the biological arena. It’s a reasonable assumption that a behavioral virus will behave much like a cellular virus – with allowances for the fact that the hosts of bio-viruses are individual cells, while the hosts of behavioral viruses are behaving animals. The products of cells are proteins. But the behavioral products of higher animals are learned habits. So perhaps we should not be surprised to find, at some point in the near future, a behavioral virus with the following characteristics:

The virus will come in the form of a useless, debilitating, and/or dangerous habit.
The viral habit will replicate itself opportunistically by inducing its own repetition.
The specific mechanisms by which the habit provokes its repetition can vary widely.
The viral habit will stabilize with repetition as the individual host refines its expression.
As the pattern is refined, the host’s behavior will become increasingly stereotypical.
With refinement, more and more of the host’s resources will be consumed by the pattern.
The host will find it increasingly difficult to control the expression of the viral habit.

When we start looking for this kind of maladaptive habit, we immediately turn up a suspect. Certain “bad habits” precisely fit the above criteria. Consider the maladaptive behavioral patterns we currently label “addictions.” Here we are talking about both addictions that involve substances, and those addiction-like processes that are purely behavioral.

Alcoholism, for example, is recognizably disease-like, and has long been called a disease by some. Alcoholism should not be confused with alcohol use. A great many people drink alcohol either occasionally or routinely. But only a small percentage of those drinkers become true alcoholics. Multiple factors – for example genetics, personal and family values, and lack of personal fulfillment – favor the development of the malignant, self-reproducing pattern of alcoholism.

My upcoming book Rogue Habits 15 examines in detail the likelihood that humans have been literally immersed in behavioral viruses even before they evolved from their animal ancestors. It details reasons to interpret several kinds of maladaptive habits as behavioral viruses.

Notes and References

Dawkins R. The Selfish Gene. 1976, Oxford, Oxford University Press.
Here we are speaking of genes as if they were people, with desires and motives. Clearly, they are not. They have no awareness or any motives. Even so, they do have interests, in the same sense that a month-old child can have an “interest” in a property he has inherited from his parent. As Dawkins pointed out, genes have a stake in getting themselves reproduced. Explaining such things in easier if we anthromorphize the genes, for purely didactic reasons.
Partial transcript of a video presentation by Richard Dawkins embedded within an online article: Solon Bolivia. Richard Dawkins on the Internet’s hijacking of the word “meme.” Wired Magazine, June 20, 2013.
Hofstadter DR, and Dennett DC (eds). The Mind’s I: Fantasies and reflections on self and soul. Basic books, 1981.
Dawkins R. Selfish genes and selfish memes. Chapter 10 (pages 124-144) in Hofstadter DR and Dennett DC, 1981, page 143.
Lynch A. Thought Contagion: How Belief Spreads through Society. New York, Basic Books, 1996.
Brody R. Viruses of the Mind: The New Science of the Meme. Integral Press, Seattle, 1996.
Blackmore S. Imitation and the definition of a meme. Journal of memetics – evolutionary models of information transmission, 1998, 2.
Swiss psychiatrist Carl Jung neatly encapsulated this idea in his concept of the “archetype.” In his view, archetypes are inherited predispositions reflecting the way ancestors have gone about making their living in the world. They are, he wrote, “forms of instinct” that remain unconscious until they are expressed as specific thoughts, images, or behaviors. See: Jung CG. Memories, Dreams, Reflections. Vintage books, New York, 1962. Page 168.
Thorndike EL. Animal Intelligence: An experimental study of the associative processes in animals. Psychological Review Monograph Supplements, 1898, 2, 4-160.
Schacter D, Gilbert D, and Wegner D. Psychology. Worth Publishers, New York, page 225.
For a detailed and thoughtful discussion of the central role of satisfaction in learning and the evolution of awareness see: Damasio AR. The Feeling of What Happens: Body and emotion in the making of consciousness. Harcourt Brace and Company, New York, 1999.
The capacity for learning also creates some very serious problems for higher animals. But that’s a topic for another time.
Zabel MD and Reid C. A brief history of prions. FEMS Pathogens and Disease, 2015, 73, ftb087, pages 3-5.
Whitehead T0. Rogue Habits: Understanding out-of-control behavior in disease terms. Currently in late draft, seeking publisher.