Healing Psychology, Part J - Runaway Habits, Second Half

The previous episode, “Runaway Habits, First Half,” highlighted something important about human addiction: this KIND of problem is shared by all higher animals. If you put an animal into a cage, you make it more likely that the animal will fall into some unproductive, repetitive, stereotypic, habit – a behavior that looks a lot like an addiction. In this episode, “Runaway Habits, Second Half,” we’ll look at something else that provokes addiction-like behavior in animals: disabled attention. There’s plenty of evidence that disabling our attention leads to out-of-control, repetitive, useless behavior. Why would that be? Here’s why: the capacity we call attention has a lot in common with biological immunity. Just as our biological immune system protects us from biological disease, our capacity for attention protects us from malignancies in our behavior. It makes sense, then, that disabling attention gives the green light to bad habits.

Transcript

This Episode of Healing Psychology concludes the reading of Chapter Eight of my upcoming book, Re-Imagining Psychology. 

Copyright © Thomas O. Whitehead, 2022   All rights reserved

[Introduction]

In the previous episode, we pointed to a connection between human addiction and a strange quirk of animal learning. If you take an animal that can learn - any animal that can learn - and put it in a cage, you make it more likely that it will fall into some repetitive, stereotypic, destructive habit—something that looks a lot like an addiction. 

In the current episode, we’ll introduce another thing that invites this strange kind of behavior. Research shows that disabling attention promotes addiction-like habits. But why? What does attention have to do with addiction? 

Plenty! Our capacity for attention works like biological immunity. Just as our biological immune system protects us from biological disease, our capability to focus our attention protects us from malignancies in our behavior.  There’s plenty of evidence that the ability to “pay attention” helps prevent our falling into unhealthy, repetitive habits – including addictions. So, we might call focal attention our “behavioral immunity.”

[reading]

Problem drinking habit

Beginning in the 1950s behaviorist researchers working with rats stumbled across something quite mysterious—the emergence of completely useless habits. These strange behaviors perplexed them. When they tried to fit them into their understanding of animal learning, they made no sense at all. [1] Unable to explain them, they simply gave them a special name, “adjunctive behaviors,” [2]   a label that meant they were simply an unimportant curiosity. Unimportant? They were quite wrong about that.

The “adjunctive” label implied that understanding this behavior wouldn’t add anything to the researchers’ grasp of the learning process. There is a genuine irony here: what they dismissively labeled “adjunctive” was in fact the most important clue to what was really going on. These weird behaviors appeared only when they thwarted the animal’s natural expression of its drives. If they had come to understand why these dysfunctional habits were cropping up, they would have known why addictions develop predictably under frustrating conditions.

Having read the first part of this chapter, it won’t surprise you to learn what the researchers learned—that “adjunctive behaviors” develop when animals are frustrated. For example, when rats are severely frustrated—as when they are confined to a cage—they might develop repetitive behaviors such as atypical aggression, attempts to escape, wheel running, and air licking. The scientists found that these useless habits appeared when the animal could not instantiate its drives naturally. According to researcher Matthew Ford, 

• By definition, adjunctive behaviors are excessive in nature and are purportedly derived from thwarting conditions (sub optimal food reinforcement rate) that dramatically increase the probability of the animal engaging in other possibilities within the environmental context provided. [3]

One adjunctive habit that was exceptionally well studied was “Schedule-Induced Polydipsia“ or SIP. Polydipsia is a fancy word that means drinking too much water. And “schedule-induced” means it’s caused by the rate at which the animal receives food. 

Here’s what researchers noticed. Suppose they starved a rat to 80 to 90 percent of its normal body weight to “activate its hunger drive.” Then they put it in a cage where it could drink all the water it wanted, but where its food supply was tightly restricted. The rat could only get a little bitty food pellet every once in a while—on a drawn-out schedule. The starving animal had to wait a couple of minutes between tiny bites of food. Horribly frustrating for the rat. 

Under these torturous conditions, rats regularly develop the habit of drinking water in between their receipt of the food pellets. They drink much more than they might otherwise drink—in fact, they drink much more than is good for them. 

The combination of starvation and dribbling the food out in itsy bits keeps a rat’s feeding drive cranked up to maximum, but with no naturally satisfying options for its expression. Drinking water doesn’t address the starving rat’s physiologic need for calories, or its drive to eat actual food. But under these conditions, consuming water (which is readily available) is as close as it can get to the experience of consuming food (mostly unavailable). 

The observation leads us to this remarkable conclusion: under these conditions of severe restriction, the rat’s drive to eat ends up instantiated as the habit of drinking large amounts of water! Schedule-Induced Polydipsia. SIP. [4] As with the hamster endlessly running its wheel, the rat’s circumstances squeeze its hunger drive into a form that’s virtually unrecognizable as an instantiation of its parent drive—the hunger drive. 

If researchers hadn’t been blinded by their behaviorist views, SIP could have given them a valuable insight about the expression of drives. Something very much like this occurs in addiction. It is not uncommon for the addict to develop a stereotypical, repetitive, self-destructive habit that’s an almost unrecognizable instantiation of its parent drive: the human drive for personal fulfillment.

Behaviorist researchers played around with the SIP phenomenon for several years without gaining insight into what they were seeing. Even so, they ran across something else relevant to our discussion. They found that messing up the rat’s brain made it even more likely that polydipsia would develop. 

One way to mess up a rat’s brain is to deny it social interaction during its development. Rats are social animals. Normal development requires that they be with other rats as they mature. This is one reason they are so frustrated in solitary confinement, part of what biases them toward the use of drugs and alcohol. And it explains why returning them to a social environment often restores normal rat behavior. 

Isolating young rats from other rats during their younger months has such a devastating developmental impact that they end up looking mentally ill. As researcher Emily Hawkins and colleagues point out,

• Post-weaning social isolation rearing is a non-pharmacological animal model of schizophrenia-like symptoms. Socially isolating rats from weaning (postnatal day 21) through to sexual maturation leads to impaired sensorimotor gating, social withdrawal and impaired cognitive flexibility. The effects of social isolation show a critical period, where isolation between [postnatal days 25 and 45] followed by a group housing reveals irreversible effects on some behaviors... Social isolation during development has an effect on neurochemistry, mimicking alterations seen in schizophrenia ... [5]

Experimenters noticed that groups of rats with brains trashed through social isolation were much more likely to develop SIP, the abnormal drinking habit. [6] These animals have more difficulty focusing their attention. This disability makes them more vulnerable to emerging rogue habits. As we will see, an animal’s ability to attend to its own behavior, to appreciate the consequences of its own acts, determines its resistance to the emergence of dysfunctional patterns. This is why, within the realm of behavior, attention can be compared to immunity in the biological realm.

Theorist E.A. Salzen has examined the varieties and behavioral signs of emotions in some detail. In his view, emotions arise when natural drives are unfulfilled or thwarted. Salzen has noted that two common adjunctive responses to thwarting are “Displacement Activities” (irrelevant behavior) and “Stereotypic Activities” (repetitive movement patterns). [7]

As examples of displacement activities, Salzen cites “behavior such as eating, drinking, and grooming inappropriate to the situation.” We’ve already looked at one example of a displacement activity—SIP. Stereotypic activities he describes as “repeated but apparently aimless sequences of locomotory movements.” Salzen comments that these acts “do seem to be a breakdown in behavior.” And he says, quite significantly, that they “are probably only seen in extreme circumstances as in captive animals and human pathology.” [8] 

These observations about “adjunctive behavior” fit the rest of the evidence about factors predisposing animals toward repetitive, stereotypical, dysfunctional, addiction-like habits. The lesson to be learned from all this is that when environmental deprivation prevails, animals frequently develop maladaptive, stereotyped habits. As we have seen, these repetitive habits may take on a distinctly abnormal quality—something that’s much more likely when attention is disabled. These surprising facts cast light on aspects of human addiction that would otherwise make no sense at all.

The autistic cage

Another line of evidence independently points to the links between impoverished environment, impaired attention, and repetitive, stereotyped habits. This line comes from research on the developmental disorder we know as autism. 

Repetitive behaviors are typical of autism. They are in fact among the criteria for diagnosis. [9] Autism authority Michelle Turner notes that even when these kids are at play, their activities are “highly repetitive and thematically restricted.” [10] According to Brian Boyd and his colleagues, mental health professionals who see such stereotypical behavior in children immediately think autism.

• A clinician who has little knowledge of a child’s social functioning or communication abilities, when told a child repetitively flaps his arms, spends hours lining up toy cars, will not tolerate changes in routine, and has a peculiar fascination with electric fans—is highly likely to suspect the child has autism. Such restricted and repetitive behaviors are a core diagnostic feature of autism spectrum disorder. [11] 

Other diagnostic criteria include significant social impairment, [12] a fact extensively validated through research. [13] Autistic kids typically can’t figure out what their peers believe, or why peers do what they do. They have trouble knowing what others want, especially when their own desires are different. These deficits move satisfying social interaction beyond the reach of severely autistic kids. Their inability to efficiently instantiate their social drives locks them away from normal social relations. In a sense, the disorder confines them to a cage—a cage of a different sort. 

Scientists now believe that these kids’ social deficits are caused partly by their inability to focus their attention effectively. Researchers Vali Shiri et al. stress that “Attention is one of the most important aspects of cognition known as concentration and awareness... Involvement of the cerebral frontal regions in children with autism could be responsible for the notion that says ‘children with autism have an impaired sustained attention’.” [14] 

Impaired attention is critical for our discussion of addiction. Because one kind of attention deficit, the one called “inattentional blindness,”  is a universal characteristic of addiction. 

In a careful study of autistic behavior reported in 2015, Shiri’s group examined the relationship between attention deficits, problems with social interaction, and stereotypical behavior. Their data reveal that problems with social interaction and stereotypical behavior “will be intensified when deficiency of sustained attention increases.” The greater the impairment in the child’s capacity for ordinary attention, the greater was their social isolation, and the more easily they fell into repetitive and stereotypical behaviors. These investigators made it clear that their findings were consistent with those of other researchers. [15] [16]

Like rats, people are social animals. One of the strongest of our human drives is a need to establish a sense of membership and belonging through social participation. But autistic children can’t easily achieve this kind of fulfillment. Their disability erects a barrier between them and the social world in which other kids live. So, like stalled horses and caged lab rats, autistic kids experience their environment as impoverished—a subjective experience similar to what most of us would feel if locked in a cage. Even though the “cage” is psychological rather than physical, its limitations are real.

It isn’t just studies of autistic children that link impaired attention to repetitive behavior. Studies of various animals confirm that impairment of the specific brain functions that support attention can provoke the same kinds of symptoms. For example, exposing rats before birth to certain chemicals damages brain structures needed to maintain attention. Then the rats exhibit autistic characteristics, including rigidly stereotyped habits. Significantly, moving the animals to an enriched environment reduces this repetitive, dysfunctional behavior. [17] It seems that giving the rats’ more options for fulfillment reduces the influence of the small satisfaction they get from repetitive behavior.

The “autistic cage” hypothesis prompts a question. If we could free autistic children from their social attention deficits—if fulfilling social interaction is brought within their reach—would that expansion of options reduce their tendency toward stereotyped behaviors? One recent study suggests the answer is yes. 

R. Loftin and colleagues wanted to see if providing social skills training to socially disconnected autistic children could increase the number and quality of their social interactions, and whether that would reduce repetitive behaviors. One of their subjects was “Stuart” (not his actual name).

• Repetitive motor behaviors for Stuart took several forms and included: clapping that was unrelated to environmental events (i.e., not following a performance); rubbing palms of hands together; hand movements (touching thumb to index finger, tapping hands with fingertips, rubbing hands together); pumping arms as if running; tapping others when unrelated to social initiation or response; full body rocking from front to back or side to side; twisting body on cafeteria seats; audible self talk (not directed at another child or adult); and squinting, winking, or other exaggerated eye movements. [18]

The researchers aimed to increase Stuart’s capacity for social attention. They trained him to pay closer attention to his own behaviors, and closer attention to the responses those behaviors elicited from his peers. The quality of Stuart’s social interaction did improve with this training. As predicted, as his social interaction became more effective the number of his stereotyped behaviors went down. This result was consistent with the findings of other similar studies. [19]

One would certainly expect that as these kids spent more time interacting with others, there would be less time available for repetitive self-stimulation. But it is also likely that, with their attention restored, it was more satisfying to interact with their peers. Then the minimal pleasure they got from repetitive habits became a weaker influence than the more authentic pleasure of social interaction. 

Sensory deprivation

There’s yet another area of research that’s relevant to this topic: the known effects of sensory deprivation. We are born with drives that support our normal perception. Our perceptual organs and systems have evolved under the influence of a constant inflow of information from the outside world. What happens when that flow is cut off? We find ourselves in a constricted environment, a cage of sorts.

We can compare what happens to us in that environment to what happens in other constricted environments. Deprived of information with which to instantiate normal percepts, individuals often begin to have unreal but vivid perceptual experiences resembling hallucinations. Phrased in the terms we are using here, when blocked from instantiating our perceptual drives normally, we instantiate them abnormally. 

Reviewing the available research, researchers Christina Daniel and Oliver Mason noted that prolonged periods of sensory deprivation produce “a range of quasipsychotic phenomena in many, if not all, participants.” They performed a careful experiment of their own, controlling for factors such as individual proneness to hallucination. They concluded that

• Both high and low hallucination prone groups experienced a significant increase in psychosis-like symptoms from baseline in the sensory deprivation environment, and these remained after controlling for state anxiety, suggestibility, and fantasy proneness. As predicted there were marked group differences: the high hallucination prone group reported more psychosislike experiences at both baseline and in sensory deprivation. These findings are consistent with previous research … that, until now, has not taken these potential confounds into account. [20]

This effect was demonstrated by other researchers who blindfolded a volunteer for an extended period. After three weeks she was having unreal visual experiences. Using fMRI, the researchers compared the associated brain activity with the activity typical of normal visual imagery. The brain was indeed acting as if it were actually perceiving something, confirming the subject's report that the “visual hallucinations were more vivid than mental imagery.” [21]

These findings are remarkable, because they are consistent with everything we have reviewed so far. Subjected to sensory deprivation, the human perceptual system creates hallucination-like experiences by striving to perceive something in the absence of the expected input. As with the behavior of caged animals, products created without adequate input are unlikely to be realistic or useful. 

In total, the evidence points to an important conclusion about the impact of impoverished environments on animal behavior. Inherited drives push animals (including human animals) toward their instantiation even when those drives have very little to work with.

Self-sustaining dysfunction

Learning is best understood as a kind of speeded-up evolutionary process. Early in the development of life on earth, the epoch before there were animals that learn, a dysfunctional behavior would have had to develop in the same way as any other evolved behavior—slowly and painfully through natural selection, and across the entire species. Because dysfunctional behavior makes survival less certain, the evolution of such maladaptive behaviors is self-limiting. But the speeded-up evolutionary process within drive/habit animals can spawn malignant behaviors in the blink of an eye. 

A malignancy begins as some behavior pattern that happens to acquire a feature prompting the pattern’s repetition. If executing a bad habit can somehow bias an animal to repeat it, that bad habit has gained a measure of control over its own replication. At this early stage the label “rogue habit” is descriptive. Do rogue habits actually happen? Can habits mindlessly arrange for their own repetition? The answer is yes. To understand how it happens, it will be useful to compare biological viruses and virus-like patterns in behavior. 

Consider the mayhem that goes on inside bacteria. These single-celled organisms accumulate plasmids within themselves, autonomously reproducing strings of genetic material. Simpler types of cells are often littered with these self-reproducing forms. [22]

The best explanation for the proliferation of plasmids is that normal cellular products, strings of DNA or RNA, have mutated into forms able to reproduce themselves using the same nucleotide production machinery that created them. This happens more easily within prokaryotic bacteria and archaea, because these cells have no nuclear membrane isolating cellular products from the production machinery. Only the more advanced eukaryotic cells have a nuclear membrane. 

Because a simple cell has no nuclear membrane, a renegade nucleotide strand may reproduce itself within the intracellular medium by exploiting the resources of the cell. In this way, a mutant string can operate as a sort of proto-virus. It is at this point only a rogue, not yet a full virus. But it has the potential to become one. To evolve into a full virus, the plasmid must divorce itself from the cell. It must gain a protein-based “escape pod” 

Eukaryotic cells, which are considerably more sophisticated than prokaryotes, do have a nuclear membrane. Presumably, the membrane evolved because there was survival value in isolating the cell’s RNA and DNA products from the machinery that produced them. Consequently, all but the simplest eukaryotic cells are free of proto-viral plasmids.

Most plasmids are not harmful, simply because it isn’t in their interest to harm their host. In fact, because their fate is still yoked to that of the host cell, many of them actually develop ways to benefit their cellular host. But what happens when these neutral strings somehow manage to separate their interests completely from the interests of the host? Then they are free to evolve in their own interest, and perhaps to turn malignant. They are free to become actual viruses.

That’s viral development in the biological sphere. Turning our attention to the behavioral sphere, we can see that rogue habits might crop up in a similar way. As we have just documented, self-reproducing habits emerge predictably within impoverished environments. The repetitive, stereotypical habits that develop under such circumstances are often simply useless, rather than directly harmful. But like the plasmids, they have the potential to turn malignant. A normal habit can become a virus-like habit if it accumulates characteristics that compel us to repeat it. Alcoholism, for example, is a habit that creates depression, anxiety, and personal chaos, all of which fuel the alcoholic’s yearning to find relief through drink. 

Summary

• Evidence from animal research suggests that exposure to addictive substances alone is not enough to create substance addiction. Rather, the animals most susceptible to addiction are those denied the satisfaction of instantiating their natural drives. 
• Every drive/habit animal studied develops repetitive, nonproductive, stereotypic habits under conditions of environmental constriction, settings that minimize opportunities for natural fulfillment.
• Impoverishment of the environment makes it more likely that habits will spontaneously begin to promote themselves, escaping the control of the behaving animal. 
• The sequence of events arising within impoverished environment is predictable, providing a way to comprehend the gradual emergence of addictions. 
• Unfortunately, psychology bases much of what we think we know about animal behavior on experiments with animals housed in exactly this kind of barren laboratory environment.
• The abnormal habits of caged animals are likely the result of a corrective feedback process that does not work well under conditions of severe habitat restriction. 

[Post Episode]

Thank you for your interest in Part J of Healing Psychology: Runaway Habits (second half). The Healing Psychology series will continue with readings of additional chapters of the book. The title of the next part is, “The Self and its Defense.” There we’ll talk about the self – one of the core concepts of biology. It’s important because a self is what allows the countless parts of every living thing to stick together. An organism’s self is the foundation of its immunity. And the idea of self is just as important to psychology as it is to biology. Additional information is available on the website, Whiteheadbooks dot com. 

Please join us!

[Music Credits]

“Pianocello-4102” –  ReverieNow

“Soft-rain-delicate-piano-music-3979” – JuliusH

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[1] The researchers were perplexed in large part because they had decided in advance that animals’ subjective experience was not relevant to their learning. This error denied them clarity about the psychological or experiential component of drives.
[2] The word “adjunctive” literally means “added to something else as a supplement rather than an essential part.”
[3] Ford MM. Applications of schedule-induced polydipsia in rodents for the study of an excessive ethanol intake phenotype. Alcohol. 2014, 48, 3, 265-276. Page 266. Available online at http://www.ncbi.nlm.nih.gov/pmc/articles/pmc4016177/pdf/nihms571518.pdf
[4] The application of latin-based terms can lend a “sciencey” aura to an observation. Acronyms like SIP serve a similar purpose. But giving something a sciencey name is not a substitute for understanding it. Neither is collecting massive amounts of data, as the behaviorists did. Indeed, as Douglas Hofstadter remarked, “Sometimes being mired down in gobs of detailed knowledge is the exact thing that blocks deep understanding.” [Hofstadter D. I am a Strange Loop. Basic books, New York, 2007.  Page 205.]
[5] Hawken ER, Delda NJ, Beninger RJ. Increased drinking following social isolation rearing: implications for polydipsia associated with schizophrenia. PLOS One, 2013, 8, 2.  Page 2. Available online at http://www.ncbi.nlm.nih.gov/pmc/articles/pmc3575417/pdf/pone.0056105.pdf
[6] Hawken ER et al, 2013. Page 2.
[7] Salzen EA. On the nature of emotion. International Journal of Comparative Psychology, 1991, 05, 2, 47-88. Page 53.
[8] Salzen EA, 1991. Pages 57-59.
[9] American Psychiatric Association. Desk Reference to the Diagnostic Criteria from DSM-5, 2013. Page 28.
[10] Turner M. Towards an executive dysfunction account of repetitive behavior in autism. Chapter in Autism as an Executive Disorder (James Russell, editor), Oxford University Press, 1997. Page 89.
[11] Boyd B, McDonough S, and Bodfish J. Evidence-Based Behavioral Interventions for Repetitive Behaviors in Autism. Journal of Autism and Developmental Disorders, 2012, 42, 6, 1236-1248. Page 1236.
[12] American Psychiatric Association, 2013. Page 27.
[13] Research on social impairment is summarized in an article by Elisabeth Pacherie. [Pacherie E. Motor-images, self-consciousness, and autism. Chapter in Autism as an Executive Disorder (James Russell, editor), Oxford University Press, 1997. Page 216.]
[14] Shiri V, Hosseini AS, Tahmasebi A, Pishyareh E, Shiri E, and Emami M.  Relationship between sustained, selective, and shifting attention and behavioral symptoms in children with high-functioning autism. Archives of Neuroscience, 2015, 2, 4, e25066. Page 1.
[15] Shiri V et al, 2015. Page 5.
[16] The observed link between attention deficits and repetitive behavior is highly significant.  That's because attention is our primary means of preventing the emergence of self-sustaining, repetitive behavioral patterns of all types. We will detail this link in a later chapter.
[17] Lewis M, et al. Animal models of restricted repetitive behavior in autism. Behavioural Brain Research, 2000, 176, 66-74. Page 67.
[18] Loftin R, Odom S, and Lantz J. Social interaction and repetitive motor behaviors. Journal of Autism and Developmental Disorders, 2008, 38, 1124-1135. Page 1127.
[19] Loftin R et al, 2008. Page 1133.
[20] Daniel C and Mason OJ. Predicting psychotic-Like experiences during sensory deprivation. BioMed Research International (Hindawi Publishing Corporation), Volume 2015, Article ID 439379, 10 pages. Page 6. Available online at https://discovery.ucl.ac.uk/id/eprint/1468060/1/Mason_439379.pdf
[21] Sireteanu R, Oertel V, Mohr H, Linden D, Singer W. Graphical illustration and functional neuroimaging of visual hallucinations during prolonged blindfolding: A comparison to visual imagery. Perception, 2008, 37, 12, 1805–1821. Page 1805.
[22] It is mainly prokaryotic and archaeal cells that develop plasmids.