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Is addiction adaptive?

Is addiction adaptive?



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Addiction and addictive traits seem common amongst animals. A pubmed query shows it's been studied in everything from humans to worms.

  • My personal favorite of these is: "Individual Consistency of Feather Pecking Behavior in Laying Hens: Once a Feather Pecker Always a Feather Pecker?"

Is there/was there something adaptive about addictive behaviour?

Alternatively, how it is that addictive behaviour survived/persists if it is not adaptive?


Albeit used in the keywords of the paper, feather pecking is not an addiction, but normal behavior turned pathological in artificial (overcrowded) environments.

Addiction typically arises through overstimulation of reward centers in the brain, most notably the dopaminergic pathways involving the nucleus accumbens. Massive dopamine release, e.g. through cocaïne or meth intake, results in euphoria (Wise & Bozarth, 1985). When the drug's effects wear off it is followed by the 'crash', characterized by dysphoria and a longing for more drugs (CSAT, 1999). Gambling addiction works much in the same way.

Addiction develops because of an interplay of dependence and tolerance. Dependence is caused by downregulation of dopaminergic responses in the reward centers. Notably, dopamine receptors are downregulated when dopamine agonists like stimulant drugs of abuse are chronically administered. Downregulation of dopaminergic responses causes the physiology of the reward pathway to adapt to the presence of dopamine agonists. While the drug is in the system, everything is OK. However, once the levels of the dopamine agonist wears off, the body enters a state of lack of dopaminergic responses, causing dysphoria and depression. Tolerance develops as the liver and other tissues start breaking down the drug more efficiently due to upregulation of the necessary catabolic enzymes. Hence, more of the drug is needed, and the user becomes more and more tolerant. The interplay of dependence and tolerance form the dreaded vicious, downward spiral of addiction.

The reward centers have been crucial in evolution, as they provide motivation to vital acts of life, including eating and sex (University of Colorado, Boulder). Without a proper reward system, why eat or reproduce? However, drugs and other addictive acts such as gambling also activate the reward system.

Highly purified drugs such as crystal meth and cocaïne result in massive dopamine release that is unparalleled by normal physiologic processes such as eating. Before the occurrence of stimulants and things like gambling, the reward system was nothing but essential to life and evolution. Now, things are different and man needs to adapt to these novel, artificial pleasures in life.

References
- Treatment Improvement Protocol (TIP) Series, No. 33. Center for Substance Abuse Treatment. Rockville (MD); 1999
- Wise & Bozarth, Psychiatr Med (1985); 3(4): 445-60


Although addiction as a coping mechanism may help in the short term. Ie.preventing a depressed person from killing themselves through temporary relief of symptoms. In the long run addiction causes many more problems then it solves. The type of addiction also needs to be considered. Many alcoholics can go years before health and financial problems begin to cause trouble. Enough time to raise a family. Possibly the reason addiction genes haven't been removed from the pool. If you look at possibility the most extreme form of addiction, wires directly into the pleasure center of the brain. You see how completely maladaptive it can be. The monkeys will sit and press the button over and over. They neglect grooming behavior, other external stimulation,food and water. Loosing interest in anything beyond the pleasure button. Eventually succumbing to exhaustion. If allowed they will continue pushing the button and die as a result. This is an extreme case because with electronic stimulation the regular negative feedback that results from overstimulation of the pleasure centers appears to be absent. chemical stimulation of the pleasure centers causes tolerance and the feeling becomes harder to obtain the more one uses. Although many addicts chase the high until it kills them as well.


Biological Factors that Influence Addiction

There are various factors that contribute to addiction. Some are genetic, others environmental, or learned, and some biological. For this article, we will be focusing on the biological factors that influence addiction. Addiction is a serious disease that can impair, delay, or stunt brain development.

Imaging studies of the brain in drug-addicted participants, have shown neurochemical and functional changes [1]. Neurochemical studies show that large and fast increases in dopamine are associated with the reinforcing effects of drug abuse, but also continue after drug abuse and withdrawal. These images show that dopamine in the brain is markedly decreased and typically are associated with dysfunction in the prefrontal regions of the brain [1].


How Does Addiction Affect the Brain?

The brain is the most dynamic and complex organ in our bodies. The brain's proper functioning ensures our very survival. When our brains function well, we are constantly adapting to our environment (our surroundings). Ironically, it is the brain's ability to be so adaptive that contributes to the formation of addiction. Addiction causes changes to the brain in at least four fundamental ways:

1. Addiction causes changes to the brain's natural balance (homeostasis).

1. Addiction changes the brain's natural balance (homeostasis).

Addiction interferes with an important biological process called homeostasis. Scientists consider the human body a biological system. All biological systems attempt to maintain a "normal" balance, known as homeostasis. The brain functions as the "overseer" of this balance. It makes various adjustments to maintain a balanced, well-functioning, biological system. Each person's "normal" balance is individually determined. Drugs of abuse and activity addictions lead to changes in this normal balance.

Chronic over-stimulation of the brain (like that which occurs in addiction) interferes with the maintenance of this balance (homeostasis). When the brain has difficulty maintaining homeostatic balance, the wonderfully adaptive brain makes adjustments. It does this by creating a new balanced set-point. The creation of a new balance is called allostasis.

These concepts are easier to understand if we use example more familiar to most people. Suppose I gain 10 lbs. At first, I will just keep trying to fit into my clothing. However, tight clothing is uncomfortable. At some point, I must adapt to the change in my body size. I will eventually acknowledge I need to buy larger clothing. Once I buy larger clothing, I am more comfortable. I've come to accept that my clothing size is now size Large, whereas before it was size Medium. In effect, I changed my "homeostatic balance" from size Medium to size Large. Having reset my size to "Large" I am now more comfortable. Keep in mind, if I lose those 10 lbs. to achieve greater health, I will again have to readjust my clothing size. So, even though I am now healthier, I still have to make an unpleasant and costly adjustment i.e., buying all new clothes in a smaller size. This is very similar to the unpleasant adjustment the brain must go through when people try to give up their addiction. Although this is a positive change, we will be uncomfortable while the brain readjustments itself.

Ironically, the brain's wonderful ability to be so adaptive (via allostasis) causes significant changes to the brain's functioning. These changes account for many behaviors associated with addiction such as: 1) the powerful need to obtain drugs or continue harmful activities despite the harm to self or loved ones, 2) the difficulty of quitting an addictive drug or activity, and 3) the obsessive, all-consuming nature of addictions such that little else in life matters. This is because addiction caused the brain's balance to change to accommodate the addiction. Once changed, the brain requires the addictive substance or activity in order to maintain this new homeostatic balance.


Early Trauma Can Cause Addiction

Traumatic adverse experiences during one’s childhood is one of the biggest underlying causes of addiction. Adverse childhood experiences may include physical abuse, emotional abuse, neglect, parental discord, and sexual abuse.

According to a report by the Substance Abuse and Mental Health Services Administration:

“When children are exposed to chronic stressful events, their neurodevelopment can be disrupted. As a result, the child’s cognitive functioning and/or ability to cope with negative or disruptive emotions may be impaired. Over time, and often during adolescence, the child may adopt unhealthy coping mechanisms…”

A 2008 study confirms that substances are a key aspect of this unhealthy coping, early on in life:

“…children with particular adverse childhood experiences may initiate drinking earlier than their peers and that they may be more likely to drink to cope with problems (rather than for pleasure or to be social).”

The anti-drug campaigns focused on inducing fear of substances neglects the fact that the most at-risk youth are not primarily using it for pleasure. Rather, they are using substances to escape from pain.

Another study on childhood abuse, neglect, and household dysfunction found that those who had more than five adverse childhood experiences were seven to ten times more likely to report substance use problems. The authors state:

“Because adverse childhood experiences seem to account for one half to two-thirds of serious problems with drug use, progress in meeting the national goals for reducing drug use will necessitate serious attention to these types of common, stressful, and disturbing childhood experiences.”

These findings reinforce the need to redirect public funds away from anti-drug campaigns, focusing on the root of the problem: adverse childhood experiences.

A recent 2019 study summarizing two decades of research on adverse childhood experiences argues:

“Adverse childhood experiences and rearing may generate a public health burden that could rival or exceed all other root causes.”

These early experiences affect the brain differently from experiences in adulthood, resulting in long-lasting neurological changes. Beyond the brain, these changes impact parental attachment, resulting in changes in one’s ability to gain secure attachment in one’s relationships later on in life.

Beyond using substances to cope with these early experiences, a recent 2020 study found that adverse childhood experiences also contribute to mobile phone addiction. Other common behavioral addictions among youth might include internet use, gaming, and various forms of gambling within online games.

The recent recognition of behavioral addiction in the DSM-V further emphasizes that substances are not necessary for an addiction to develop. Although substances are often involved in addiction, they are are not the primary cause.


Contents

Adaptation is an observable fact of life accepted by philosophers and natural historians from ancient times, independently of their views on evolution, but their explanations differed. Empedocles did not believe that adaptation required a final cause (a purpose), but thought that it "came about naturally, since such things survived." Aristotle did believe in final causes, but assumed that species were fixed. [1]

In natural theology, adaptation was interpreted as the work of a deity and as evidence for the existence of God. [2] William Paley believed that organisms were perfectly adapted to the lives they led, an argument that shadowed Gottfried Wilhelm Leibniz, who had argued that God had brought about "the best of all possible worlds." Voltaire's satire Dr. Pangloss [3] is a parody of this optimistic idea, and David Hume also argued against design. [4] The Bridgewater Treatises are a product of natural theology, though some of the authors managed to present their work in a fairly neutral manner. The series was lampooned by Robert Knox, who held quasi-evolutionary views, as the Bilgewater Treatises. Charles Darwin broke with the tradition by emphasising the flaws and limitations which occurred in the animal and plant worlds. [5]

Jean-Baptiste Lamarck proposed a tendency for organisms to become more complex, moving up a ladder of progress, plus "the influence of circumstances," usually expressed as use and disuse. [6] This second, subsidiary element of his theory is what is now called Lamarckism, a proto-evolutionary hypothesis of the inheritance of acquired characteristics, intended to explain adaptations by natural means. [7]

Other natural historians, such as Buffon, accepted adaptation, and some also accepted evolution, without voicing their opinions as to the mechanism. This illustrates the real merit of Darwin and Alfred Russel Wallace, and secondary figures such as Henry Walter Bates, for putting forward a mechanism whose significance had only been glimpsed previously. A century later, experimental field studies and breeding experiments by people such as E. B. Ford and Theodosius Dobzhansky produced evidence that natural selection was not only the 'engine' behind adaptation, but was a much stronger force than had previously been thought. [8] [9] [10]

The significance of an adaptation can only be understood in relation to the total biology of the species.

What adaptation is Edit

Adaptation is primarily a process rather than a physical form or part of a body. [12] An internal parasite (such as a liver fluke) can illustrate the distinction: such a parasite may have a very simple bodily structure, but nevertheless the organism is highly adapted to its specific environment. From this we see that adaptation is not just a matter of visible traits: in such parasites critical adaptations take place in the life cycle, which is often quite complex. [13] However, as a practical term, "adaptation" often refers to a product: those features of a species which result from the process. Many aspects of an animal or plant can be correctly called adaptations, though there are always some features whose function remains in doubt. By using the term adaptation for the evolutionary process, and adaptive trait for the bodily part or function (the product), one may distinguish the two different senses of the word. [14] [15] [16] [17]

Adaptation is one of the two main processes that explain the observed diversity of species, such as the different species of Darwin's finches. The other process is speciation, in which new species arise, typically through reproductive isolation. [18] [19] An example widely used today to study the interplay of adaptation and speciation is the evolution of cichlid fish in African lakes, where the question of reproductive isolation is complex. [20] [21]

Adaptation is not always a simple matter where the ideal phenotype evolves for a given environment. An organism must be viable at all stages of its development and at all stages of its evolution. This places constraints on the evolution of development, behaviour, and structure of organisms. The main constraint, over which there has been much debate, is the requirement that each genetic and phenotypic change during evolution should be relatively small, because developmental systems are so complex and interlinked. However, it is not clear what "relatively small" should mean, for example polyploidy in plants is a reasonably common large genetic change. [22] The origin of eukaryotic endosymbiosis is a more dramatic example. [23]

All adaptations help organisms survive in their ecological niches. The adaptive traits may be structural, behavioural or physiological. Structural adaptations are physical features of an organism, such as shape, body covering, armament, and internal organization. Behavioural adaptations are inherited systems of behaviour, whether inherited in detail as instincts, or as a neuropsychological capacity for learning. Examples include searching for food, mating, and vocalizations. Physiological adaptations permit the organism to perform special functions such as making venom, secreting slime, and phototropism), but also involve more general functions such as growth and development, temperature regulation, ionic balance and other aspects of homeostasis. Adaptation affects all aspects of the life of an organism. [24]

The following definitions are given by the evolutionary biologist Theodosius Dobzhansky:

1. Adaptation is the evolutionary process whereby an organism becomes better able to live in its habitat or habitats. [25] [26] [27] 2. Adaptedness is the state of being adapted: the degree to which an organism is able to live and reproduce in a given set of habitats. [28] 3. An adaptive trait is an aspect of the developmental pattern of the organism which enables or enhances the probability of that organism surviving and reproducing. [29]

What adaptation is not Edit

Adaptation differs from flexibility, acclimatization, and learning, all of which are changes during life which are not inherited. Flexibility deals with the relative capacity of an organism to maintain itself in different habitats: its degree of specialization. Acclimatization describes automatic physiological adjustments during life [30] learning means improvement in behavioural performance during life. [31]

Flexibility stems from phenotypic plasticity, the ability of an organism with a given genotype (genetic type) to change its phenotype (observable characteristics) in response to changes in its habitat, or to move to a different habitat. [32] [33] The degree of flexibility is inherited, and varies between individuals. A highly specialized animal or plant lives only in a well-defined habitat, eats a specific type of food, and cannot survive if its needs are not met. Many herbivores are like this extreme examples are koalas which depend on Eucalyptus, and giant pandas which require bamboo. A generalist, on the other hand, eats a range of food, and can survive in many different conditions. Examples are humans, rats, crabs and many carnivores. The tendency to behave in a specialized or exploratory manner is inherited—it is an adaptation. Rather different is developmental flexibility: "An animal or plant is developmentally flexible if when it is raised in or transferred to new conditions, it changes in structure so that it is better fitted to survive in the new environment," writes evolutionary biologist John Maynard Smith. [34]

If humans move to a higher altitude, respiration and physical exertion become a problem, but after spending time in high altitude conditions they acclimatize to the reduced partial pressure of oxygen, such as by producing more red blood cells. The ability to acclimatize is an adaptation, but the acclimatization itself is not. The reproductive rate declines, but deaths from some tropical diseases also go down. Over a longer period of time, some people are better able to reproduce at high altitudes than others. They contribute more heavily to later generations, and gradually by natural selection the whole population becomes adapted to the new conditions. This has demonstrably occurred, as the observed performance of long-term communities at higher altitude is significantly better than the performance of new arrivals, even when the new arrivals have had time to acclimatize. [35]

Adaptedness and fitness Edit

There is a relationship between adaptedness and the concept of fitness used in population genetics. Differences in fitness between genotypes predict the rate of evolution by natural selection. Natural selection changes the relative frequencies of alternative phenotypes, insofar as they are heritable. [36] However, a phenotype with high adaptedness may not have high fitness. Dobzhansky mentioned the example of the Californian redwood, which is highly adapted, but a relict species in danger of extinction. [25] Elliott Sober commented that adaptation was a retrospective concept since it implied something about the history of a trait, whereas fitness predicts a trait's future. [37]

1. Relative fitness. The average contribution to the next generation by a genotype or a class of genotypes, relative to the contributions of other genotypes in the population. [38] This is also known as Darwinian fitness, selection coefficient, and other terms. 2. Absolute fitness. The absolute contribution to the next generation by a genotype or a class of genotypes. Also known as the Malthusian parameter when applied to the population as a whole. [36] [39] 3. Adaptedness. The extent to which a phenotype fits its local ecological niche. Researchers can sometimes test this through a reciprocal transplant. [40]

Sewall Wright proposed that populations occupy adaptive peaks on a fitness landscape. To evolve to another, higher peak, a population would first have to pass through a valley of maladaptive intermediate stages, and might be "trapped" on a peak that is not optimally adapted. [41]

Adaptation is the heart and soul of evolution.

Changes in habitat Edit

Before Darwin, adaptation was seen as a fixed relationship between an organism and its habitat. It was not appreciated that as the climate changed, so did the habitat and as the habitat changed, so did the biota. Also, habitats are subject to changes in their biota: for example, invasions of species from other areas. The relative numbers of species in a given habitat are always changing. Change is the rule, though much depends on the speed and degree of the change. When the habitat changes, three main things may happen to a resident population: habitat tracking, genetic change or extinction. In fact, all three things may occur in sequence. Of these three effects only genetic change brings about adaptation. When a habitat changes, the resident population typically moves to more suitable places this is the typical response of flying insects or oceanic organisms, which have wide (though not unlimited) opportunity for movement. [43] This common response is called habitat tracking. It is one explanation put forward for the periods of apparent stasis in the fossil record (the punctuated equilibrium theory). [44]

Genetic change Edit

Genetic change occurs in a population when natural selection and mutations act on its genetic variability. [45] The first pathways of enzyme-based metabolism may have been parts of purine nucleotide metabolism, with previous metabolic pathways being part of the ancient RNA world. By this means, the population adapts genetically to its circumstances. [10] Genetic changes may result in visible structures, or may adjust physiological activity in a way that suits the habitat. The varying shapes of the beaks of Darwin's finches, for example, are driven by differences in the ALX1 gene. [46]

Habitats and biota do frequently change. Therefore, it follows that the process of adaptation is never finally complete. [47] Over time, it may happen that the environment changes little, and the species comes to fit its surroundings better and better. On the other hand, it may happen that changes in the environment occur relatively rapidly, and then the species becomes less and less well adapted. Seen like this, adaptation is a genetic tracking process, which goes on all the time to some extent, but especially when the population cannot or does not move to another, less hostile area. Given enough genetic change, as well as specific demographic conditions, an adaptation may be enough to bring a population back from the brink of extinction in a process called evolutionary rescue. Adaptation does affect, to some extent, every species in a particular ecosystem. [48] [49]

Leigh Van Valen thought that even in a stable environment, competing species constantly had to adapt to maintain their relative standing. This became known as the Red Queen hypothesis, as seen in host-parasite interaction. [50]

Existing genetic variation and mutation were the traditional sources of material on which natural selection could act. In addition, horizontal gene transfer is possible between organisms in different species, using mechanisms as varied as gene cassettes, plasmids, transposons and viruses such as bacteriophages. [51] [52] [53]

Co-adaptation Edit

In coevolution, where the existence of one species is tightly bound up with the life of another species, new or 'improved' adaptations which occur in one species are often followed by the appearance and spread of corresponding features in the other species. These co-adaptational relationships are intrinsically dynamic, and may continue on a trajectory for millions of years, as has occurred in the relationship between flowering plants and pollinating insects. [54] [55]

Mimicry Edit

Bates' work on Amazonian butterflies led him to develop the first scientific account of mimicry, especially the kind of mimicry which bears his name: Batesian mimicry. [56] This is the mimicry by a palatable species of an unpalatable or noxious species (the model), gaining a selective advantage as predators avoid the model and therefore also the mimic. Mimicry is thus an anti-predator adaptation. A common example seen in temperate gardens is the hoverfly, many of which—though bearing no sting—mimic the warning coloration of hymenoptera (wasps and bees). Such mimicry does not need to be perfect to improve the survival of the palatable species. [57]

Bates, Wallace and Fritz Müller believed that Batesian and Müllerian mimicry provided evidence for the action of natural selection, a view which is now standard amongst biologists. [58] [59] [60]

Trade-offs Edit

It is a profound truth that Nature does not know best that genetical evolution. is a story of waste, makeshift, compromise and blunder.

All adaptations have a downside: horse legs are great for running on grass, but they can't scratch their backs mammals' hair helps temperature, but offers a niche for ectoparasites the only flying penguins do is under water. Adaptations serving different functions may be mutually destructive. Compromise and makeshift occur widely, not perfection. Selection pressures pull in different directions, and the adaptation that results is some kind of compromise. [62]

Since the phenotype as a whole is the target of selection, it is impossible to improve simultaneously all aspects of the phenotype to the same degree.

Consider the antlers of the Irish elk, (often supposed to be far too large in deer antler size has an allometric relationship to body size). Obviously, antlers serve positively for defence against predators, and to score victories in the annual rut. But they are costly in terms of resource. Their size during the last glacial period presumably depended on the relative gain and loss of reproductive capacity in the population of elks during that time. [64] As another example, camouflage to avoid detection is destroyed when vivid coloration is displayed at mating time. Here the risk to life is counterbalanced by the necessity for reproduction. [65]

Stream-dwelling salamanders, such as Caucasian salamander or Gold-striped salamander have very slender, long bodies, perfectly adapted to life at the banks of fast small rivers and mountain brooks. Elongated body protects their larvae from being washed out by current. However, elongated body increases risk of desiccation and decreases dispersal ability of the salamanders it also negatively affects their fecundity. As a result, fire salamander, less perfectly adapted to the mountain brook habitats, is in general more successful, have a higher fecundity and broader geographic range. [66]

The peacock's ornamental train (grown anew in time for each mating season) is a famous adaptation. It must reduce his maneuverability and flight, and is hugely conspicuous also, its growth costs food resources. Darwin's explanation of its advantage was in terms of sexual selection: "This depends on the advantage which certain individuals have over other individuals of the same sex and species, in exclusive relation to reproduction." [67] The kind of sexual selection represented by the peacock is called 'mate choice,' with an implication that the process selects the more fit over the less fit, and so has survival value. [68] The recognition of sexual selection was for a long time in abeyance, but has been rehabilitated. [69]

The conflict between the size of the human foetal brain at birth, (which cannot be larger than about 400 cm 3 , else it will not get through the mother's pelvis) and the size needed for an adult brain (about 1400 cm 3 ), means the brain of a newborn child is quite immature. The most vital things in human life (locomotion, speech) just have to wait while the brain grows and matures. That is the result of the birth compromise. Much of the problem comes from our upright bipedal stance, without which our pelvis could be shaped more suitably for birth. Neanderthals had a similar problem. [70] [71] [72]

As another example, the long neck of a giraffe brings benefits but at a cost. The neck of a giraffe can be up to 2 m (6 ft 7 in) in length. [73] The benefits are that it can be used for inter-species competition or for foraging on tall trees where shorter herbivores cannot reach. The cost is that a long neck is heavy and adds to the animal's body mass, requiring additional energy to build the neck and to carry its weight around. [74]

Adaptation and function are two aspects of one problem.

Pre-adaptation Edit

Pre-adaptation occurs when a population has characteristics which by chance are suited for a set of conditions not previously experienced. For example, the polyploid cordgrass Spartina townsendii is better adapted than either of its parent species to their own habitat of saline marsh and mud-flats. [76] Among domestic animals, the White Leghorn chicken is markedly more resistant to vitamin B1 deficiency than other breeds on a plentiful diet this makes no difference, but on a restricted diet this preadaptation could be decisive. [77]

Pre-adaptation may arise because a natural population carries a huge quantity of genetic variability. [78] In diploid eukaryotes, this is a consequence of the system of sexual reproduction, where mutant alleles get partially shielded, for example, by genetic dominance. [79] Microorganisms, with their huge populations, also carry a great deal of genetic variability. The first experimental evidence of the pre-adaptive nature of genetic variants in microorganisms was provided by Salvador Luria and Max Delbrück who developed the Fluctuation Test, a method to show the random fluctuation of pre-existing genetic changes that conferred resistance to bacteriophages in Escherichia coli. [80]

Co-option of existing traits: exaptation Edit

Features that now appear as adaptations sometimes arose by co-option of existing traits, evolved for some other purpose. The classic example is the ear ossicles of mammals, which we know from paleontological and embryological evidence originated in the upper and lower jaws and the hyoid bone of their synapsid ancestors, and further back still were part of the gill arches of early fish. [81] [82] The word exaptation was coined to cover these common evolutionary shifts in function. [83] The flight feathers of birds evolved from the much earlier feathers of dinosaurs, [84] which might have been used for insulation or for display. [85] [86]

Animals including earthworms, beavers and humans use some of their adaptations to modify their surroundings, so as to maximize their chances of surviving and reproducing. Beavers create dams and lodges, changing the ecosystems of the valleys around them. Earthworms, as Darwin noted, improve the topsoil in which they live by incorporating organic matter. Humans have constructed extensive civilizations with cities in environments as varied as the Arctic and hot deserts. In all three cases, the construction and maintenance of ecological niches helps drive the continued selection of the genes of these animals, in an environment that the animals have modified. [87]

Some traits do not appear to be adaptive as they have a neutral or deleterious effect on fitness in the current environment. Because genes often have pleiotropic effects, not all traits may be functional: they may be what Stephen Jay Gould and Richard Lewontin called spandrels, features brought about by neighbouring adaptations, on the analogy with the often highly decorated triangular areas between pairs of arches in architecture, which began as functionless features. [88]

Another possibility is that a trait may have been adaptive at some point in an organism's evolutionary history, but a change in habitats caused what used to be an adaptation to become unnecessary or even maladapted. Such adaptations are termed vestigial. Many organisms have vestigial organs, which are the remnants of fully functional structures in their ancestors. As a result of changes in lifestyle the organs became redundant, and are either not functional or reduced in functionality. Since any structure represents some kind of cost to the general economy of the body, an advantage may accrue from their elimination once they are not functional. Examples: wisdom teeth in humans the loss of pigment and functional eyes in cave fauna the loss of structure in endoparasites. [89]

If a population cannot move or change sufficiently to preserve its long-term viability, then obviously, it will become extinct, at least in that locale. The species may or may not survive in other locales. Species extinction occurs when the death rate over the entire species exceeds the birth rate for a long enough period for the species to disappear. It was an observation of Van Valen that groups of species tend to have a characteristic and fairly regular rate of extinction. [90]

Just as there is co-adaptation, there is also coextinction, the loss of a species due to the extinction of another with which it is coadapted, as with the extinction of a parasitic insect following the loss of its host, or when a flowering plant loses its pollinator, or when a food chain is disrupted. [91] [92]

Adaptation raises philosophical issues concerning how biologists speak of function and purpose, as this carries implications of evolutionary history – that a feature evolved by natural selection for a specific reason – and potentially of supernatural intervention – that features and organisms exist because of a deity's conscious intentions. [95] [96] In his biology, Aristotle introduced teleology to describe the adaptedness of organisms, but without accepting the supernatural intention built into Plato's thinking, which Aristotle rejected. [97] [98] Modern biologists continue to face the same difficulty. [99] [100] [101] [102] [103] On the one hand, adaptation is obviously purposeful: natural selection chooses what works and eliminates what does not. On the other hand, biologists by and large reject conscious purpose in evolution. The dilemma gave rise to a famous joke by the evolutionary biologist Haldane: "Teleology is like a mistress to a biologist: he cannot live without her but he's unwilling to be seen with her in public.'" David Hull commented that Haldane's mistress "has become a lawfully wedded wife. Biologists no longer feel obligated to apologize for their use of teleological language they flaunt it." [104] Ernst Mayr stated that "adaptedness. is a posteriori result rather than an a priori goal-seeking", meaning that the question of whether something is an adaptation can only be determined after the event. [105]


The broad view: love as addiction

There is a broader understanding of addiction that has been gaining steam in recent years. As two of us have argued, addiction should be considered to be a spectrum of motivation that emerges from the repeated application of any type of reward, including drug rewards, gambling rewards, food rewards, and sexual rewards (Foddy and Savulescu 2006, 2010 Foddy 2011). These appetite-motivations arise in response to reward conditioning, and are, indeed, the evolved mechanism by which we humans and other animals learn to behave in survival- and reproduction-enhancing ways. At the same time, such appetites do not always lead directly to these 𠇎volutionary” outcomes, especially in humans, and even more so in the modern environment we have created for ourselves (see Earp, Sandberg, and Savulescu 2012). Our appetite for food, for example, is not strictly genetically controlled: we are weaned onto it during gestation, and it can wax and wane over the course of our lives, often in ways that run contrary to our real nutritive needs (Foddy 2011). By the same token, we may develop appetites for any rewarding behavior, and these appetites may exceed or fall beneath a level that suits our biological needs, our conscious values, or our personal preferences.

On a broad view, then, addictions are simply appetites: they are felt needs that can be temporarily satisfied, but which become urgent and distracting if one abstains from fulfilling them for too long. Conversely, and perhaps counterintuitively, appetites are simply weak addictions. At least on this account, then, everyone is �icted’ to food, to sex, and to other ordinary substances and behaviors, although most of us are not ‘hooked’ on them to such a degree as to cause us any major harm or distress or to merit the application of a psychiatric diagnosis or treatment (see Foddy and Savulescu 2010, for a sustained defence of this view).

A similar broad approach can be applied to the concept of love addiction. This approach would claim that to love someone is literally to be addicted to them, though perhaps only weakly. In line with this view, James Burkett and Larry Young (2012) have recently argued that romantic relationships experienced universally𠅏rom �lling in love” to ultimate separation and subsequent withdrawal—may be considered a form of addiction. To prime the reader for their thesis, they open their seminal paper on this subject with the following vignette:

At first, each encounter was accompanied by a rush of euphoria—new experiences, new pleasures, each more exciting than the last. Every detail became associated with those intense feelings: places, times, objects, faces. Other interests suddenly became less important as more time was spent pursuing the next joyful encounter. Gradually, the euphoria during these encounters waned, replaced imperceptibly by feelings of contentment, calm, and happiness. The moments between encounters seemed to grow longer, even as they stayed the same, and separation came to be filled with painful longing and desire. When everything was brought to an abrupt end, desperation and grief followed, leading slowly into depression. (Burkett and Young 2012, 1)

Does this story describe falling in love or becoming addicted to a drug? Burkett and Young’s point, of course, is that it could equally describe both. Drawing on evidence from animal models along with parallel research in human attachment and the neurobiology of substance abuse, they conclude that there is 𠇊 deep and systematic concordance … between the brain regions and neurochemicals involved in both addiction and social attachment” (Burkett and Young 2012, 2).

In other words, substance dependence and everyday romantic bonding have much more in common than their outward psychological profiles. At the level of the brain, the mechanisms underlying pair-bonding in socially monogamous or quasi-monogamous species (such as humans) overlap quite substantially with those involved in reward learning and addiction (see, e.g., Wise 1996). The greatest overlap occurs in neurochemical regions involved in the processing of dopamine (Kelley and Berridge 2002 Burkett and Young 2012) oxytocin (Insel 2003 McGregor, Callagham and Hunt 2008), and other neurotransmitters such as serotonin. As Margolis (2005, x) states: “… through sex [with our partner], orgasm’s serotonin rush and momentary muscular relaxation comprise the most potent and popular drug we have.”

With respect to dopamine, both mating and addictions elicit very similar neurochemical activity, concentrated in the reward circuitry of the brain: sex, orgasm, and all known drugs of abuse stimulate high levels dopamine release in the nucleus accumbens (see Burkett and Young 2012, Kirsch et al. 2006, and Di Chiara et al. 2004 for more information). In fact, the role of dopamine extends far beyond addiction and is linked to a wide range of other processes associated with reward-learning—including eating, drinking, having sexual intercourse, and love (see Burkett and Young 2012, for a review). Some scientists have suggested that this dopaminergic overlap may explain why experiencing love or engaging in sexual activity can feel like a cocaine rush (Blum, Wernel, et al. 2012 Bartels and Zeki 2000).

Finally, neuroimaging support for an overlap between love-addiction and drug-addiction comes from studies in which participants have been exposed to images of their romantic partners during scanning. These images evoke not only self-reported feelings of love and positive affect but also show heavy activation in brain’s reward regions (Aron et al. 2005 Bartels and Zeki 2000 Young 2009 Fisher et al. 2006).

These are just a few of the neurochemical and functional similarities between “normal” love attachment and drug addiction that have been noted by Burkett and Young as well as by other researchers who argue for the 𠇋roader” view of love addiction. There are many others as well. But what about differences between love and addiction? Surely the numerous “parallels” between these phenomena𠅊t both the behavioral and neural levels—should not be taken to mean that they are strictly equivalent. In the following section, we examine some of these differences, and assess their implications for the 𠇋road” vs. “narrow” debate.


Biological Magic/Adaptive Biology magic

So from out of nowhere i got a wild idea for something:

For magic users, their powers also diretly affect their Biology. So far ive only come up with obvious "Fire Proficients grow resilient skinlayers against heat" or Magicians who use speed enhancing magic will become fast on biologial scale (reaction times, nerves and in general Metabolism or in rare cases even be able to run faster) and Mages who use Magic to Fly grow means of Flight, (prominently Wings). All these things are at first dependent on the use of Magic but with time the Wings would become strong enough to sustain flight, the Mage can and will run faster and the Fire Mage can walk right through a Burning Forest.

This all is just a wild idea but i like it, what else could be expressed with magic? Like If i got a Mind- Mage what biological change would happen to him/her? Do you think this system could be viable ? Also what would be a sustaining power for this? (Mana, Life Power, small kitten tears etc.)

I think a Mind Mage could develop something like a "telepathy gland" for passive mind reading or at the very least lie detection or something.

As for "mana", Iɽ treat it like a vitamin or supplement that kinda just helps you use magic, like a Fire Pill that helps your body bind fire mana or something. A Rage Pill that allows you to turn into a demon. An Aviator Pill that helps you morph your body into a bird like physiology.

Maybe some Energy Capsules would help replenish stamina or Dragon Syrup could eventually allow you to firebreathe.

No joke, nothing mean here, but I recommend looking up how trans people transition or how bodybuilders go from scrawny to swol to get a picture for how such a transformation might happen. How would the characters feel, what made them opt for this change, how would they change during the process, would they give up, would there be people who discourage them?

The supplements also add an extra theme of addiction.

I recommend looking up athlete movies, workout vlogs, drug essays, drug rehab interviews, trans people vlogs and so on to get a good grasp on your themes.

I know this is more writing advice, but with me it's a mixed package.

A system like this does have immense potential and if used right can even build a massive following on its premise alone. It's really up to your skill as a writer now, so good luck. Hope I helped.

Well my skill as writer is nonexistent XD. but yes I think I can take a look at that and work with it if i like it. Addiction is indeed a really good point tho I don't really know how to utilize this. Prolly after I've checked on your mentioned Info sources.

Well actually I'm partaking in a collaborative World building sub and I'm designing my Civilisation so I might be able to pull this off.

This is one of my favorite types of systems. It's like the Mutant idea in the X-Men, but with a lot more choice and sacrifice behind it.

One similar system is the concept of "Savants" in Brandon Sanderson's Cosmere. A savant is someone who has used a magic system so much that they're bodies have become dependent on them. Sometimes, the changes are good, but most of the time, they can be neutral or even negative.

For example, there is one minor character who used the ability to turn things into smoke too much their body is slowly becoming smoke, and they are working to restore it. Or another character used a magic that amplified their senses so much that they could see through a blindfold and even the most minor stimulation was blinding to their senses but at the same time, if they ran out of the material fueling that magic, they wouldn't be able to cope with the lack of sensation.

Savantism is especially nice from our perspective because it is based on other magic systems - the idea itself is only unique because of the base system it gets attached to. But this also means that basically anyone can make a variation of the idea without copying someone else.

Interesting yea. I'll take a look at that Brandon. It sounds like the thing I'm going for, I'm sure it can help me. Tho my idea includes that the biological changes surpass the need for magic sustain at one point. You see at the beginning the wings need to be sustained to remain working and the further they use Flight the stronger the Biology adapts untill it is truly a part of their body. The combinations of changes if someone starts using another type of magic after one change completes are interesting

I use a very similar kind of magic in the book I am writing. ɻiomancy'. Users can make themselves faster and stronger, grow different appendages, heal.wounds ect. The flip side is, if you 'grow' something too quickly you get all kinds of nasty cancers. Most mages end up looking really fucking weird since through healing their cells with Biomancy they are effectively immortal. After a while they get bored of the overtly human form. Most have wings, horns, odd coloured skin, ect ect.

This sounds really interesting. I hope I can read that book when it's finished.

Yaaa im not going down that road. I want to have it like a side effect that at first people where like "The fuck is happening" but then see the advantages. Tho I haven't spend a thought about possible downsides yet.

Perhaps a good source of power for the system could be the wizard eating or exposing themselves to the things that they wish to adapt to or emulate.

If someone wishes to gain a bird's flight, for example, heɽ have to obtain birds of some kind and devour with almost ritualistic fervour their bones and feathers to gain their aviary characteristics. (Or their talons if they want to make digging for worms and the like easier.)

Or resistance to fire by gradually exposing themselves to higher and higher temperatures until a protective carapace starts growing over their skin.

You could complicate the process by adding extra steps so that not every Joe, Bill and Stephen suddenly ends up with cow hooves and broccoli hair, but the simplicity could allow for creativity.

(Depending on how many mutations a person can stack up, the end result could be anything at all from eldritch to fantastic. From an amalgamation of limbs and tumors to the noble dragon, each opposite extremes of the same system that pursued vastly different goals, the former psychic might over the strange and peculiar and the latter unparalleled prowess and indestructibility.)

I think those rituals can be a boost. I really like the idea of using a drug like substance as main power source described by someone else in the comments but I think I can use rituals as some kind of boost or inhibition to some effects.

The 'speed of thought' is often used to mean instantaneous, but it isn't. The rate at which thought travels between neurons depends on where we're looking at in the body, with thoughts in the brain traveling at around 270-280mph, but as we get further away from the brain or spinal cord, thoughts get slower. They flow along nervous structures called axons, which at their thinnest transmit thoughts at 1-3mph.

I imagine that mental mages or speed mages would have reinforced axons, allowing for swifter reaction times.

I'm also picturing mental mages or creation mages distributing their nervous system like an octopus. For example, a purpose-built brain in the arm that they're only distantly aware of the vague thoughts of, which causes the arm to near-instantly react to things without the higher thought processes of the brain.

Death or decay mages would probably have more efficient and lethal digestive systems, or would kill any invading diseases or parasites.

Water mages could have high blood pressure and immunity to its negative effects, leading to effective circulation, resistance to blood loss, and improved healing.

Earth mages could have ablative layers of skin. Get hit by a blow, the outer layer of skin shatters, dispersing most of the force, leaving several layers of skin beneath it.

Air mages could have more and more of their body serve dual purposes as increased lung capacity and its original purpose, becoming lighter and lighter as they do so, making it easier and easier to be acrobatic, athletic, and generally aerobic.


Piaget's Theory of Child Development

1 The Epistemology of Piaget

Piaget, who trained as a biologist, had as a primary objective to understand the development of knowledge in the human species, rather than to understand why and how children develop. His first originality was to address philosophical questions (such as the origin or the development of knowledge) by empirical means, in particular by relying on the study of child development (supposed to be, at the beginning of his career, a mere ‘detour’ of some years). He established the discipline of genetic epistemology (the term ‘genetic’ referring to the concept of genesis or evolution, as proposed by Baldwin), with the aim ‘to study the roots of the various sorts of knowledge from their most elementary forms on and to follow their development in ulterior levels including scientific thinking,’ and by grounding it in both historico-critical and psychogenetic approaches. Piaget's epistemology is constructivist, in the sense that knowledge is neither a mere reflection of the external world (realism), nor a projection of pre-existing structures of the mind (nativism), and the origins of knowledge are to be found in the practical and cognitive activity of the subject. Piaget's epistemology is also fundamentally interdisciplinary.

His primary hypothesis was that intelligence is a form of biological adaptation (e.g., Piaget 1967 ), that is, intellectual or cognitive behaviors are the products of an organism, in interaction with its environment, and the end point of biological evolution. This is not to say that psychological phenomena can be reduced to biological ones, as Piaget always opposed biological reductionism intelligence is an organizing activity whose functioning transcends biological organization, by elaborating new structures. The main characteristic common to knowledge and to living organisms is their adaptive character. Adaptation itself, whether biological or cognitive, relies on two mechanisms, defined very early in Piaget's work, namely assimilation (incorporation of new information into an existing system) and accommodation (modification of existing schemes or structures by newly assimilated elements, so as to respond to the demands of the environment). By so doing, actions and operations become coordinated with one another such coordinations define a new entity, which in turn constitutes a new object for thought and action. This is the process that Piaget labeled equilibration. Contrarily to frequent, but too simplistic interpretations, equilibration does not correspond to a stable (even if only temporary) state of equilibrium, but is the process of coordination in itself.

As a consequence of the functional continuity that Piaget postulated between biological and psychological entities, a given level of knowledge is always considered to result from a reorganization of the preceding one. Reconstruction means more than a mere addition of elements of a lower type in order to attain a higher level, but implies a total reorganization and a change in scale. One direct consequence of a constructivist perspective is that an epistemologist or a psychologist studying any level of development will ask what characterized the preceding level and will stress developmental progression towards higher levels. An essential mechanism for this reconstruction is reflecting abstraction, that is, a process by which the subject extracts characteristics or coordinations from actions or operations it is called ‘reflecting’ both because it consists of a mental reorganization and because it implies a reflection or a transfer onto a higher level of what was established at a lower level. Reflecting abstraction is contrasted with empirical or simple abstraction, which bears mainly on observable characteristics of objects or classes of objects.


Theories of Addiction – A Detailed Analysis

In many cases, addiction theorists have now progressed beyond stereotyped disease conceptions of alcoholism or the idea that narcotics are inherently addictive to anyone who uses them.

The two major areas of addiction theory—those concerning alcohol and narcotics—have had a chance to merge, along with theorizing about overeating, smoking, and even running and interpersonal addictions.

Yet this new theoretical synthesis is less than meets the eye: It mainly recycles discredited notions while including piecemeal modifications that make the theories marginally more realistic in their descriptions of addictive behavior.

These theories are described and evaluated in this section as they apply to all kinds of addictions. They are organized into sections on genetic theories (inherited mechanisms that cause or predispose people to be addicted), metabolic theories (biological, cellular adaptation to chronic exposure to drugs), conditioning theories (built on the idea of the cumulative reinforcement from drugs or other activities), and adaptation theories (those exploring the social and psychological functions performed by drug effects).

While most addiction theorizing has been too unidimensional and mechanistic to begin to account for addictive behavior, adaptation theories have typically had a different limitation.

They do often correctly focus on the way in which the addict’s experience of a drug’s effects fits into the person’s psychological and environmental ecology. In this way drugs are seen as a way to cope, however dysfunctionally, with personal and social needs and changing situational demands. Yet these adaptation models, while pointing in the right direction, fail because they do not directly explain the pharmacological role the substance plays in addiction.

They are often considered—even by those who formulate them—as adjuncts to biological models, as in the suggestion that the addict uses a substance to gain a specific effect until, inexorably and irrevocably, physiological processes take hold of the individual.

At the same time their purview is not ambitious enough (not nearly so ambitious as that of some biological and conditioning models) to incorporate non-narcotic or non-drug involvements. They also miss the opportunity, readily available at the social-psychological level of analysis, to integrate individual and cultural experiences.

Genetic Theories

How Is Alcoholism Inherited?

Cigarette smoking, alcoholism, and overweight—like divorce, child abuse and religion—run in families. This addictive inheritance has been most studied in the case of alcoholism.

Studies endeavoring to separate genetic from environmental factors, such as those in which adopted-away offspring of alcoholics were compared to adopted children with nonalcoholic biological parents, have claimed a three to four times greater alcoholism rate for those whose biologic parents were alcoholic (Goodwin et al. 1973). Vaillant (l983) approvingly cited the Goodwin et al. and other research indicating genetic causality in alcoholism (see especially Vaillant and Milofsky 1982), but his own research did not support this conclusion.

In the inner-city sample that formed the basis for Vaillant’s primary analysis, those with alcoholic relatives were between three and four times as likely to be alcoholic as those without alcoholic relatives. Since these subjects were reared by their natural families, however, this finding does not distinguish effects of alcoholic environment from inherited dispositions. Vaillant did find that subjects with alcoholic relatives they did not live with were twice as likely to become alcoholic as subjects who had no alcoholic relatives at all.

Yet further nongenetic influences remain to be partialed out of Vaillant’s results.

The chief of these is ethnicity: Irish Americans in this Boston sample were seven times as likely to be alcohol dependent as were those of Mediterranean descent. Controlling for such large ethnicity effects would surely reduce the 2 to 1 ratio (for subjects with alcoholic relatives compared to those without) in alcoholism substantially even as other potential environmental factors that lead to alcoholism (besides ethnicity) would still remain to be controlled for.

Vaillant reported two other tests of genetic causality in his sample. He disconfirmed Goodwin’s (1979) hypothesis that alcoholics with alcoholic relatives—and hence a presumed inherited predisposition to alcoholism—inevitably develop problems with drinking earlier than do others. Finally, Vaillant found no tendency for the choice of moderate drinking versus abstinence as a resolution for drinking problems to be related to number of alcoholic relatives, although it was associated with the drinker’s ethnic group.

Proposing genetic mechanisms in alcoholism on the basis of concordance rates does not provide a model of addiction. What are these mechanisms through which alcoholism is inherited and translated into alcoholic behavior?

Not only has no biological mechanism been found to date to underlie alcoholism, but research on alcoholics’ behavior indicates that one cannot be found in the case of the loss of control of drinking that defines alcoholism. Even the most severely alcoholic individuals “clearly demonstrate positive sources of control over drinking behavior” so that “extreme drunkenness cannot be accounted for on the basis of some internally located inability to stop” (Heather and Robertson 1981: 122). Intriguingly, controlled-drinking theorists like Heather and Robertson (1983) propose exceptions to their own analyses: Perhaps “some problem drinkers are born with a physiological abnormality, either genetically transmitted or as a result of intrauterine factors, which makes them react abnormally to alcohol from their first experience of it” (Heather and Robertson 1983: 141).

While it is certainly a fascinating possibility, no research of any type supports this suggestion. Vaillant (1983) found that self-reports by AA members that they immediately succumbed to alcoholism the first time they drank were false and that severe drinking problems developed over periods of years and decades.

The exceptions to this generalization were psychopaths whose drinking problems were components of overall abnormal lifestyles and behavior patterns from an early age.

owever, these kinds of alcoholics showed a greater tendency to outgrow alcoholism by moderating their drinking (Goodwin et al. 1971), indicating they also do not conform to a putative biological model. Prospective studies of those from alcoholic families also have failed to reveal early alcoholic drinking (Knop et al.1984).

Findings like these have led genetic theorists and researchers instead to propose that the inherited vulnerability to alcoholism takes the form of some probabilistically greater risk of developing drinking problems.

In this view a genetic tendency—such as one that dictates a drinker will have an overwhelming response to alcohol—does not cause alcoholism. The emphasis is instead on such biological abnormalities as the inability to discriminate blood alcohol level (BAL), which leads alcoholics to show less effect from drinking and to drink more without sensing their condition (Goodwin 1980 Schuckit 1984).

Alternately, Schuckit (1984) proposed that alcoholics inherit a different style of metabolizing alcohol, such as producing higher levels of acetaldehyde due to drinking. Finally, Begleiter and other theorists have proposed that alcoholics have abnormal brain waves prior to ever having drunk or that drinking creates unusual brain activity for them (Pollock et al. 1984 Porjesz and Begleiter 1982).

All these theorists have indicated that their results are preliminary and require replication, particularly through prospective studies of people who become alcoholics.

Negative evidence, however, is already available. Several studies have found that sensitivity to BAL, peak BAL after drinking, and elimination of blood alcohol are unrelated to family histories of alcoholism (Lipscomb and Nathan 1980 Pollock et al. 1984). Other negative evidence for both BAL discrimination and metabolic hypotheses is provided by the case of American Indians and Eskimos. These groups are hyperresponsive to alcohol’s effects (that is, they respond immediately and intensely to the alcohol in their systems) and yet have the highest alcoholism rates in the United States.

The claim of inheritance of alcoholism from the opposite theoretical direction—that these groups succumb to alcoholism so readily because they metabolize alcohol so quickly—likewise does not succeed. Groups that share the hypermetabolism of alcohol that Eskimos and Indians display (called Oriental flush), such as the Chinese and Japanese, have among the lowest alcoholism rates in America. The disjunctive connection between obvious metabolic characteristics and drinking habits actually contraindicates significant biological determinism in alcoholism (Mendelson and Mello 1979a).

The basic problem with genetic models of alcoholism is the absence of a reasonable link to the drinking behaviors in question. Why do any of the proposed genetic mechanisms lead people to become compulsive imbibers? For example, in the case of an insensitivity to alcohol’s effects, why wouldn’t an individual who can’t reliably detect that he has drunk too much simply learn from experience (in the absence of any proposed genetic compulsion to drink) to limit himself to a safer number of drinks?

Do such drinkers simply choose to drink at unhealthy levels and to experience the extreme negative consequences of drinking that, after years, may lead to alcoholism (Vaillant 1983)? If so, why? That is the question.

On the other hand, the proposed differences in metabolizing alcohol and changes in brain functioning due to drinking are extremely subtle when compared with the gross effects of Oriental flush. Yet even groups characterized by Oriental flush, like the Indians and the Chinese, can show diametrically opposite responses to the same intense physiological changes.

If a given individual did indeed have an extreme reaction to alcohol, why would he not become the type of drinker who announces, “I only have a drink or two because otherwise I become giddy and make a fool of myself”? For those drinkers for whom alcohol might produce a desirable change in brain waves, why does the person prefer this state over others or other ways of gaining the same effect? The variation in behavior that is left unaccounted for in the most optimistic of these models is such as to discount the potential gain from the pursuit of as yet unestablished links between genetically inherited reactions to alcohol and alcoholic behavior.

Finally, since all studies have found that it is sons and not daughters who most often inherit the risk of alcoholism (Cloninger et al. 1978), in what comprehensible ways can any of the genetic mechanisms thus far suggested for alcoholism be sex-linked?

The Endorphin-Deficiency Explanation of Narcotic Addiction

Since the primary assumption about narcotics has been that the drugs are equally and inevitably addictive for everyone, pharmacological theories of narcotic addiction have rarely stressed individual biological proclivities to be addicted. It was only a matter of time, however, before pharmacological and biological theorists began to hypothesize inherited mechanisms to account for differences in addictive susceptibility.

When Dole and Nyswander (1967) introduced the ideas that narcotic addiction was a “metabolic disease” and that the tendency to become addicted outlived the actual dependence on a drug, the way was opened to suggest that “metabolic disorder could precede as well as be precipitated by opiate use” (Goldstein, cited in Harding et al. 1980: 57). That is, not only might habitual narcotic use cause a chronic and residual need for drugs, but people conceivably might already have had such a need when they started taking drugs and came to rely on them.

The discovery that the body produces its own opiates, called endorphins, presented a plausible version of this mechanism. Endorphin theorists like Goldstein (1976b) and Snyder (1977) speculated that addicts may be characterized by an inbred endorphin deficiency that leaves them unusually sensitive to pain. Such people would then especially welcome—and might even require—the elevation of their pain threshold brought on by narcotics. Heroin addicts have not yet been demonstrated to show unusual levels of endorphins. Moreover, this type of theorizing is badly strained—as are all metabolic theories of addiction—by the commonplace observations of drug abuse and addiction that were noted in chapter 1. Addicts do not in fact indicate a chronic, habitual need for narcotics. They regularly alter the type and amount of drug they use, sometimes abstaining or quitting altogether as they age. Most of the Vietnam veterans who were addicted in Asia and who then used narcotics in the United States did not become readdicted. Noting that almost none of the patients introduced to a narcotic in the hospital indicate a prolonged desire for the drug, we may wonder why so small a percentage of the general population displays this endorphin deficiency.

Endorphin deficiency and other metabolic models suggest a course of progressive and irreversible reliance on narcotics that actually occurs in only exceptional and abnormal cases of addiction. Those with inbred metabolic defects could conceivably account for only a small percentage of those who become addicted over their lifetimes. Why would the narcotic addiction that disappeared for most Vietnam veterans (or for the many other addicts who outgrow it) differ fundamentally from all other kinds of addiction, such as the kind that persists for some people? To accept this dichotomous view of addiction violates the basic principle of scientific parsimony, by which we should assume that the mechanisms at work in a large portion of cases are present in all cases. This is the same error made by psychologists who concede (without empirical provocation) that some alcoholics may indeed have constitutional traits that cause them to be alcoholic from their first drink even as research shows all alcoholics to be responsive to situational rewards and to subjective beliefs and expectations.

Preprogrammed Obesity

In his influential internal-external model of obesity, Schachter (1968) proposed that fat people had a different style of eating, one that depended on external cues to tell them when to eat or not. Unlike those of normal weight, Schachter’s overweight subjects apparently could not rely on internal physiological signs to decide whether they were hungry. As a social psychologist, Schachter originally emphasized cognitive and environmental stimuli that encouraged the obese to eat. However, his model left open the question of the source of this insensitivity to somatic cues, suggesting the probability that this was an inherited trait. Schachter’s (1971) view of the sources of overeating became increasingly physiological in nature when he began comparing the behavior of ventromedial-lesioned rats with obese humans. Several of Schachter’s prominent students followed his lead in this direction.

For example, Rodin (1981) eventually rejected the internal-external model (as most researchers have by now) with an eye toward locating a neurological basis for overeating. Meanwhile Nisbett (1972), another Schachter student, proposed an extremely popular model of body weight based on an internal regulatory mechanism, called set-point, which is inherited or determined by prenatal or early childhood eating habits.

Peele (1983b) analyzed Schachter’s evolution into a purely biological theoretician in terms of biases Schachter and his students had shown all along against personality dynamics against group, social, and cultural mechanisms and against the role of values and complex cognitions in the choice of behavior. As a result, the Schachter group consistently failed to pick up discrepant indicators in their obesity research, some of which led eventually to the jettisoning of the internal-external model. For example Schachter (1968) noted that normal-weight subjects did not eat more when they were hungry (as predicted) because they found the type of food and the time of day inappropriate for eating. In another study that had important implications, Nisbett (1968) discovered that formerly overweight subjects who were no longer obese behaved similarly to obese subjects in an eating experiment. That is, they ate more after having been forced to eat earlier than when they had not eaten before. Nisbett interpreted these results as showing that these subjects were unable to control their impulses to overeat and could therefore not be expected to keep excess weight off.

This line of thinking was solidified in Nisbett’s set-point hypothesis, which held that the hypothalamus was set to defend a specific body weight and that going below this weight stimulated a greater desire to eat. The idea that obese people could not lose weight, based on laboratory studies and the performance of clients in weight-loss programs, had been the central tenet in all of the Schachter group’s work on obesity (cf. Schachter and Rodin 1974 Rodin 1981). Yet such pessimism seems an unlikely deduction from a study like Nisbett’s (1968), in which subjects who had been obese and who continued to display an external eating style had indeed lost weight. When Schachter (1982) actually questioned people in the field about their weight-loss histories, he found remission was quite common in obesity: of all those interviewed who had ever been obese and who had tried to lose weight, 62.5 percent were currently at normal weight.

Schachter’s serendipitous finding disputed the entire thrust of over a decade’s research—namely, that people were locked into obesity by biological forces. The idea would not die easily, however. Another Schachter student and his colleague recorded Schachter’s (1982) finding but dismissed its significance by indicating it was probably only those obese subjects who were above their set-points who had been able to lose weight in this study (Polivy and Herman 1983: 195-96). Polivy and Herman based this calculation on the estimate that from 60 to 70 percent of obese people were not obese in childhood. Their assertion requires that we believe that nearly all of the people in the Schachter study who have been overweight for reasons other than biological inheritance (and only these) had lost weight. Yet undoubtedly many in this category would remain fat for whatever presumably nonset-point reasons had caused them to become obese in the first place. Rather than being the underlying source of obesity its adherents had painted it to be, set-point now seemed not to be a major factor in most cases of overweight.

Polivy and Herman’s (1983) description of their outlook did not reflect this understanding about set-point and obesity. Instead, they argued that “for the foreseeable future, we must resign ourselves to the fact that we have no reliable way to change the natural weight that an individual is blessed or cursed with” although “perhaps, as research progresses, we will be able to imagine such biological interventions—including even genetic manipulations” that will enable people to lose weight (p. 52). Polivy and Herman furthermore attributed binge overeating—the extreme of which is bulimia—to people’s attempts to restrain their eating in the effort to go below their natural weight (see chapter 5). These researchers’ work agrees with that of popular writers (Bennett and Gurin 1982) and the dominant research approaches in the field (Stunkard 1980) in maintaining a view of human eating and overeating that is essentially the same as that held by biological theorists of alcoholism and drug addiction toward drinking and drug consumption. In all cases, people are seen to be under the sway of invariant forces that, in the long run, they cannot hope to contravene.

Meanwhile, Garn and his coworkers (1979) have shown that similarities in weight levels among people who live together are a result of similar eating habits and energy expenditure. This “cohabitational effect” holds for husbands and wives and is the largest factor in weight similarities between parents and adopted offspring. People who live together who become fat do so together (Garn et al. 1979). The longer parents and their children live together (even when the children are age 40) the more they resemble each other in fatness. The longer parents and children live separately, the less pronounced such similarities become until they approach 0 at the extremes of separation (Garn, LaVelle, and Pilkington 1984). Garn, Pilkington, and LaVelle (l984), observing 2,500 people over two decades, found “those . . . who were lean to begin with generally increased in fatness level. Those who were obese to begin with generally decreased in fatness level” (pp. 90-91). “Natural weight” may be a very variable thing, influenced by the same social values and personal coping strategies that affect all behavior (Peele 1984).

Interpersonal Addiction

The enormity of the implications of the genetic transmission of addictive impulses is driven home by several theories claiming that people are compelled by chemical imbalances to form unhealthy, compulsive, and self-destructive interpersonal relationships. Tennov (1979) maintained that such “limerent” people, who are in every other way indistinguishable from other people, have a biological propensity to fall head-over-heels in love and create disastrous romantic attachments. Liebowitz (1983) proposed that a failure in neurochemical regulation—similar to that hypothesized to cause manic-depressive reactions leads people (almost exclusively women) to fall heatedly in love, often with inappropriate partners, and to become inordinately depressed when the relationships fail. These theories illustrate mainly the temptation to believe that compelling motivations must have a biological source and the desire to mechanize human differences, imperfections, and mysteries.

Biological Theories of Addiction

Peele and Brodsky (1975), in the book Love and Addiction, also described interpersonal relationships as having addictive potential. The thrust of their version of interpersonal addiction, however, was exactly the opposite of that in Liebowitz (1983) and Tennov (1979): Peele and Brodsky’s aim was to show that any powerful experience can form the object of an addiction for people predisposed by combinations of social and psychological factors. Their approach was antireductionist and rejected the deterministic force of inbred, biological, or other factors outside the realm of human consciousness and experience. Their work signaled a burst of addiction theorizing in areas other than substance abuse, the bulk of which—paradoxically—sought to analyze these phenomena at a biological level. The result has been the proliferation of biologic theories to account both for the range of compulsive involvements people form and for the tendency some people show to be addicted to a host of substances.

Smith (1981), a medical clinician, has posited the existence of an “addictive disease” to account for why so many of those who become addicted to one substance have prior histories of addiction to dissimilar substances (cf. “The Collision of Prevention and Treatment” 1984). It is impossible to explain—as Smith attempts to do—how innate, predetermined reactions could cause the same person to become excessively involved with substances as disparate as cocaine, alcohol, and Valium. In examining the generally strong positive correlations among tobacco, alcohol, and caffeine use, Istvan and Matarazzo (1984) explored the possibilities both that these substances are “linked by reciprocal activation mechanisms” and that they may be linked by their “pharmacologically antagonistic . . . effects” (p. 322). The evidence here is rather that substance abuse exceeds biological predictability. The fact of multiple addictions to myriad substances and nonsubstance-related involvements is primary evidence against genetic and biological interpretations of addiction.

Nonetheless, neuroscientists put forward biological theories of just this degree of universality. One researcher (Dunwiddie 1983: 17) noted that

drugs of abuse such as opiates, amphetamine, and cocaine can pharmacologically stimulate many of the brain centers identified as reward centers…. On the other hand, there is considerable evidence that certain individuals have an enhanced liability for drug abuse, and frequently misuse a variety of seemingly unrelated drugs. It is interesting to speculate that for various reasons, perhaps genetic, perhaps developmental or environmental, the normal inputs to these hypothetical “reward pathways” function inadequately in such individuals. If this were the case, there may be a biological defect underlying poly-drug abuse.

While piling hypothesis upon hypothesis, Dunwiddie’s description presents no actual research findings about drug abusers, nor does it present a specific hypothetical link between deficient “reward pathways” and “polydrug abuse.” It would seem the author thinks people who get less reward from drugs are more likely to abuse them.

Milkman and Sunderwirth’s (1983) neurological model of addiction is not limited to drug abuse (as nothing in Dunwiddie’s account would so limit it). These authors believe that addiction can result from any “self-induced changes in neurotransmission,” where the more neurotransmitters that are involved “the faster the rate of firing,” leading to the “elevated mood sought by cocaine users, for example” (p. 36). This account is actually a social-psychological one masquerading as neurological explanation, in which the writers introduce social and psychological factors such as peer influence and low self-esteem into their analysis by suggesting “that the enzyme produced by a given gene might influence hormones and neurotransmitters in a way that contributes to the development of a personality potentially more susceptible to . . . peer group pressure” (p. 44). Both Dunwiddie’s and Milkman and Sunderwirth’s analyses cloak experiential events in neurological terminology without reference to any actual research that connects biological functioning to addictive behavior. These models represent almost ritualistic conceptions of scientific enterprise, and while their analyses are caricatures of contemporary scientific model building, they come unfortunately close to mainstream assumptions about how the nature of addiction is to be interpreted.

Exposure Theories: Biological Models

The Inevitability of Narcotic Addiction

Alexander and Hadaway (1982) referred to the prevailing conception of narcotic addiction among both lay and scientific audiences—that it is the inevitable consequence of regular narcotics use—as the exposure orientation. So entrenched is this viewpoint that Berridge and Edwards (1981)—while arguing that “Addiction is now defined as a disease because doctors have categorized it thus” (p. 150)—refer readers to an appendix in which Griffith Edwards declared “anyone who takes an opiate for a long enough period of time and in sufficient dose will become addicted” (p. 278). This view contrasts with conventional beliefs about alcohol that would reject the same statement with the word “alcohol” substituted for “an opiate.”

Underlying the exposure model is the assumption that the introduction of a narcotic into the body causes metabolic adjustments that require continued and increasing dosages of the drug in order to avoid withdrawal. No alteration in cell metabolism has yet been linked with addiction, however. The most prominent name in metabolic research and theory, Maurice Seevers, characterized efforts during the first sixty-five years of this century to create a model of addictive narcotic metabolism to be “exercises in semantics, or plain flights of imagination” (cited in Keller 1969: 5). Dole and Nyswander (1967 cf. Dole 1980) are the modem champions of heroin addiction as a metabolic disease, although they have provided no explicit metabolic mechanism to account for it. Endorphin theorists have suggested that regular use of narcotics reduces the body’s natural endorphin production, thus bringing about a reliance on the external chemical agent for ordinary pain relief (Goldstein 1976b Snyder 1977).

This version of the relationship between endorphin production and addiction—like the one suggesting addicts inherit an endorphin deficiency (see above)—does not fit the data reviewed in chapter 1. Put baldly, exposure to narcotics does not lead to addiction, and addiction does not require the metabolic adjustments claimed for it. Those given the most reliable and purest supplies of narcotics, hospital patients, display—rather than an escalating need for the drug—a reduced desire for it. In an experimental trial of self-administration of morphine by hospitalized postoperative patients, subjects in the self-administration condition employed moderate, progressively declining doses of the drug (Bennett et al. 1982). That even infants and animals do not manifest an acquired hunger for opiates is the subject of chapter 4. On the other hand, compulsive street users of narcotics often do not show the expected hallmarks of addiction, such as withdrawal.

Endorphins and Nonnarcotic Addiction

Although unsubstantiated in the case of narcotic addiction, endorphin-related explanations have proved irresistible to those considering other addictive behavior. In particular, discoveries that food and alcohol—as well as narcotics—can affect endorphin levels have prompted speculation that these substances create self-perpetuating physical needs along the lines of those the narcotics supposedly produce. Weisz and Thompson (1983) summarized these theories while noting that “At this time there is not sufficient evidence to conclude that endogenous opioids mediate the addictive process of even one substance of abuse” (p. 314). Harold Kalant (1982), a distinguished neuroscientist, was more conclusive in his rejection of the idea that alcohol and narcotics could act according to the same neurological principles. “How do you explain . . . in pharmacological terms,” he queried, that cross-tolerance occurs “between alcohol, which does not have specific receptors, and opiates, which do” (p. 12)?

To date, the most active speculation by clinicians about the role of endorphins has been in the area of compulsive running and exercising (cf. Sacks and Pargman 1984). If running stimulates endorphin production (Pargman and Baker 1980 Riggs 1981), then compulsive runners are presumed to undergo narcotic-like physical states to which they become addicted. Research on the relationship between endorphin levels, mood swings, and running motivation has failed to turn up regular relationships (Appenzeller et al. 1980 Colt et al. 1981 Hawley and Butterfield 1981). Markoff et al. (1982) and McMurray and his colleagues (1984) reported that exercising subjects treated with the narcotic-blocking agent naloxone reported no differences in perceived exertion and other physiological measures from those not treated. Addicted running—defined by inflexibility and insensitivity to internal and external conditions, running until the point of harming oneself, and being unable to quit without experiencing withdrawal—is no better explained by endorphin levels than is the self-destructiveness of the heroin addict (Peele 1981).

Cigarette Addiction

Schachter (1977, 1978) has been the most vigorous proponent of the case that cigarette smokers are physically dependent on nicotine. They continue to smoke, in Schachter’s view, in order to maintain habitual levels of cellular nicotine and to avoid withdrawal. Interestingly, Schachter (1971, 1977, 1978 Schachter and Rodin 1974) has proposed that different types of factors determine obesity and smoking: the former is due to an inbred predilection while the latter is due to an acquired constraint (avoidance of withdrawal). This is the same distinction drawn in traditional theories of alcohol and narcotic addiction. The distinction is necessary in order to defend biological causality in the case of excessiveness both in activities that are common to most people (eating and drinking alcohol) and activities that only some indulge in (smoking and narcotics use).

As with alcohol and narcotic use (see below), there is no prima facie reason why destructive eating and smoking habits need necessarily be dictated by separate classes of factors. Indeed, studies Schachter (1978) and his students conducted with cigarette smokers replicated results of Schachter and Rodin’s (1974) work with the obese. For example, both smokers (while not smoking) and the obese were more distractible and more sensitive to negative stimuli like pain than were nonsmokers or normal-weight people. Both smokers and the obese apparently found their habits allayed anxieties and cushioned them against unpleasant stimulation (see Peele 1983b for further discussion.) Furthermore, the apparent uniformity in the addictive use of cigarettes that Schachter’s model suggests is illusory. Different smokers consume different amounts of tobacco and inhale different levels of nicotine Best and Hakstian (1978) found such variations to reflect different motivations and settings for smoking and to suggest different circumstances under which smokers can quit.

Leventhal and Cleary (1980) have pointed out how inexact the regulation of nicotine intake is in Schachter’s studies: Schachter (1977) found that a 77 percent reduction in nicotine level produced only a 17 to 25 percent increase in cigarette consumption. More tellingly, these authors reflected, “Schachter’s model and studies … assume a direct and automatic step from changes in plasma nicotine level to craving and [separately] smoking and say nothing about the mechanisms and experience that give rise to either” (p. 390). For example, Schachter (1978) himself noted that Orthodox Jews regularly withstood withdrawal to give up smoking during the sabbath. People’s values do not cease to operate in the face of physiological forces. Later, in the same study in which he detected a high remission rate for obesity, Schachter (1982) discovered that over 60 percent of those in two communities who had tried to quit smoking had succeeded. They had ceased smoking on the average for 7.4 years. Heavier smokers—those consuming three or more packs of cigarettes a day—showed the same remission rate as lighter smokers. It would seem that Schachter’s nicotine regulation model, which he designed primarily to explain why habitual smokers cannot quit, does not take the measure of the behavior in question. Whereas his formulation of nicotine addiction had emphasized the ineluctable, overwhelming nature of withdrawal from cigarettes, he now found the ability to overcome such withdrawal “to be relatively common” (p. 436). In other words, there needs to be some additional level of explanation for why people persist in smoking as well as for why they can give it up (Peele 1984).

Alcohol Dependence

As narcotic addiction theorists have been forced by the recognition of individual variations in addiction to postulate innate neurochemical differences among people, alcoholism specialists have increasingly put forward the claim that alcohol problems are simply a function of excessive drinking. It might be said that conceptions of alcoholism and narcotic addiction not only are meeting on common ground but are passing each other going in opposite directions.

The change in emphasis in alcoholism is in good part a result of the desire of psychologists and others to achieve rapprochement with disease theories (see chapter 2). It has led controlled-drinking clinicians to assert that a return to moderate drinking is impossible for the physically dependent alcoholic. Intriguingly, behaviorists have thus adopted Jellinek’s (1960) formulation of the disease theory of alcoholism, in which he claimed that true (gamma) alcoholics could not control their drinking due to their physical dependence. (In his 1960 volume Jellinek was ambiguous about the extent to which this disability was inbred and irreversible, the traditional claims made by AA.)

The concept of alcohol dependence has been elaborated by a group of British researchers (Edwards and Gross 1976 Hodgson et al. 1978). In the same breath, it attempts to replace the disease theory (whose defects are more broadly agreed upon in Great Britain than in the United States) while rescuing important disease notions (see critique by Shaw 1979). The alcohol-dependence syndrome resembles the disease of alcoholism in conceiving of drinking problems as a condition that can be identified in isolation from the drinkers psychological state and situation and as one that endures beyond the alcoholic’s active drinking. Severity of dependence is assessed purely in terms of how much people habitually drink and the physical consequences of this drinking (Hodgson et al. 1978), without regard for their reasons for drinking or cultural, social, and other environmental factors. Thus, those who are heavily dependent are thought to have a stable condition that makes their return to moderate drinking unlikely.

The alcohol-dependence syndrome suffers from the tension of acknowledging the complexity of alcoholic behavior. As its supporters note, “the control of drinking, like any other behavior, is a function of cues and consequences, of set and setting, of psychological and social variables in short, control, or loss of it, is a function of the way in which the alcoholic construes his situation” (Hodgson et al. 1979: 380). Within this framework, Hodgson et al. regard withdrawal symptoms to be a strong cue for alcoholics to return to heavy drinking. However, the appearance of withdrawal in alcoholism is itself variable and subject to drinkers’ subjective constructions. Moreover, such symptoms are regularly overcome by alcoholics in their drinking careers and in any case are limited in duration. Avoidance of withdrawal simply cannot account for continued drinking (see Mello and Mendelson 1977). There is a more basic objection yet to the alcohol dependence concept. In his critique of “the concept of drug dependence as a state of chronic exposure to a drug,” Kalant (1982) remonstrated that dependence concepts have “ignored the most fundamental question—why a person having experienced the effect of a drug would want to go back again and again to reproduce that chronic state” (p.12).

Whereas speculation about human drug dependence has been influenced greatly by generalizations from animal research (generalizations that are largely incorrect, see chapter 4), the alcohol-dependence syndrome has had to fly in the face of animal research. It is difficult to get rats to drink alcohol in the laboratory. In his seminal research, Falk (1981) was able to induce such drinking through the imposition of intermittent feeding schedules that the animals find highly uncomfortable. In this condition, the rats drink heavily but also indulge in excessive and self-destructive behavior of many kinds. All such behavior—including drinking—depends strictly on the continuation of this feeding schedule and disappears as soon as normal feeding opportunities are restored. Thus, for rats that had been alcohol-dependent, Tang et al. (1982) reported “a history of ethanol overindulgence was not a sufficient condition for the maintenance of overdrinking” (p.155).

On the basis of animal research, at least, alcohol dependence seems to be strongly state-dependent rather than a persistent characteristic of the organism. Rather than being contradicted by human behavior, this phenomenon may be even more pronounced for humans. The supposed biological basis of drinking behavior in the alcohol dependence model is thus unable to deal with major aspects of alcoholism. As one of the authors (Gross 1977: 121) of the alcohol-dependence syndrome observed:

The foundation is set for the progression of the alcohol dependence syndrome by virtue of its biologically intensifying itself. One would think that, once caught up in the process, the individual could not be extricated. However, and for reasons poorly understood, the reality is otherwise. Many, perhaps most, do free themselves.

Control of Alcohol Supply

Sociological theory and research has been the main counterpoint to disease theories of alcoholism (Room 1983) and has made decisive contributions in depicting alcoholism as a social construction, in discrediting the idea that drinking problems can be organized into medical entities, and in disproving empirical claims regarding such bedrock disease notions as inevitable loss of control and reliable stages in the progress of alcoholism (see chapter 2). Yet some sociologists have also been uncomfortable with the idea that social beliefs and cultural customs affect levels of drinking problems (Room 1976). In place of such sociocultural interpretations of alcoholism, sociology as a field has now largely adopted a supply-of-alcohol perspective based on findings that alcohol consumption in a society is distributed in a unimodal, lognormal curve (Room 1984).

Since a large proportion of the alcohol available is drunk by those at the extreme end of this skewed curve, increases or decreases in alcohol availability are believed to push many drinkers above or below what might be considered a heavy and dangerous drinking level. Alcohol supply policy recommendations thus include raising taxes on liquor to lower overall consumption. The alcohol supply model is most certainly not a biological theory and does not itself lead to theoretical derivations about alcohol metabolism. Yet as Room (1984: 304) has pointed out, it can be rationalized with the disease-theory view that those at the extreme of the curve have lost control of their drinking. In fact, the model fits best with the alcohol-dependence syndrome, where alcoholic behavior is conceived principally to be the result of excessive consumption.

At the same time, the alcohol-supply view violates a number of sociologically based findings. Beauchamp (1980), for example, propounded the alcohol-supply argument while reporting that Americans consumed from two to three or more times as much alcohol per capita in the late eighteenth century as they do today and yet had fewer alcohol problems in the colonial period. Nor does the supply model make good sense of discontinuities in consumption within a given region.

Alcohol problems in France are centered in the nonwinegrowing regions that must import more expensive alcoholic beverages (Prial 1984). In the United States, fundamentalist Protestant sects consume less alcohol per capita because many of these groups abstain. However, these groups—and the relatively dry regions of the South and Midwest—also have higher alcoholism rates and incidences of binge drinking (Armor et al. 1978 Cahalan and Room 1974).

How also do the Jews, located principally in the highest consumption areas in the country (urban and Eastern), maintain an alcoholism rate one-tenth or less than the nationwide rate (Glassner and Berg 1980)? On the policy side, Room (1984) noted that efforts to curtail supplies have often backfired and led to greater binges in consumption.

At a psychological level, the idea that people incur the costs of alcoholism simply because they have more alcohol available to them makes little sense. For example, what exactly is the impact on the alcoholic of making supplies harder to obtain?

The result of limiting the ready medical supply of narcotics was to turn many men into alcoholics (O’Donnell 1969). Vaillant (1983) found that abstaining alcoholics were highly prone to abuse other substances or to form alternate compulsive involvements. Here the sociological level of analysis, like the metabolic, suffers from a lack of a grasp of the individual’s overall addictive ecology. The popularity of alcohol-supply ideas within a community noted for its opposition to disease ideas may make one pessimistic about whether there still can remain any intellectual resistance to metabolic theories of alcoholism and addiction.

Exposure Theories: Conditioning Models

Conditioning theories hold that addiction is the cumulative result of the reinforcement of drug administration. The central tenet of conditioning theories is that (Donegan et al. 1983: 112):

To say that a substance is used at a level considered to be excessive by the standards of the individual or society and that reducing the level of use is difficult is one way of saying that the substance has gained considerable control over the individual’s behavior. In the language of behavior theory the substance acts as a powerful reinforcer: behaviors instrumental in obtaining the substance become more frequent, vigorous, or persistent.

Conditioning theories offer the potential for considering all excessive activities along with drug abuse within a single framework, that of highly rewarding behavior. Originally developed to explain narcotic addiction (cf. Woods and Schuster 1971), reinforcement models have been applied to most popular psychoactive drugs and to nondrug addictions like gambling and overeating (Donegan et al. 1983). Solomon (1980), in a broadly influential approach he calls the opponent-process model of motivation, has extended conditioning principles to every pleasurable and compulsive activity.

The complex processes that characterize learning also allow increased flexibility in describing addictive behavior. In classical conditioning, previously neutral stimuli become associated with reactions brought on in their presence by a primary reinforcer. Thus an addict who relapses can be conceived to have had his craving for the addiction reinstated by exposure to the settings in which he previously used drugs (Wikler 1973 S. Siegel 1979, 1983).

The Myth of the Universal Reinforcer: The Inherent Pleasurableness of Narcotics

Conditioning theories leave open one critical question: What is a reinforcing activity? The assumption in narcotic addiction is usually that the drug provides an inherent, biologic reward and/or that it has strong reinforcement value due to its prevention of withdrawal pain (Wikler 1973).

This assumption is part of a wide range of theories of addiction (cf. Bejerot 1980 Dole 1972 Goldstein 1976a McAuliffe and Gordon 1974 Wikler 1973). Indeed, the belief that narcotics are irresistible to any organism that, once having tried them, has free access to drugs is the epitome of the exposure model of addiction. The body of work thought best to demonstrate the truth of this belief is the observation that laboratory animals can readily be induced to ingest narcotics and other drugs. Chapter 4 shows this view to be unfounded: drug use is no more self-perpetuating for animals than it is for humans.

No less a biological determinist than Dole (1980) has now declared that “most animals cannot be made into addicts…. Although the pharmacological effects of addictive substances injected into animals are quite similar to those seen in human beings, animals generally avoid such drugs when they are given a choice” (p. 142).

If the behavior of laboratory animals is not locked in by drug action, how is it possible for human beings to become addicted and lose the possibility of choice? One proposal to account for the feverish pursuit of drugs and other human involvements has been that these experiences bring in ordinate pleasure, or euphoria. The idea that pleasure is the primary reinforcement in addiction is present in several theories (Bejerot 1980 Hatterer 1980 McAuliffe and Gordon 1974) and most especially has a central role in Solomon’s (1980) opponent-process model. The ultimate source of this idea has been the supposedly intense euphoria that narcotics, particularly heroin, produce, a euphoria for which normal experience offers no near counterpart. In the popular image of heroin use and its effects, euphoria seems the only possible inducement for using a drug that is the ultimate symbol of self-destructiveness.

Some users describe euphoric experiences from taking heroin, and McAuliffe and Gordon’s (1974) interviews with addicts revealed this to be a primary motivation for continuing to use the drug. Other research contests this notion vigorously. Zinberg and his colleagues have interviewed a large number of addicts and other heroin users over several decades and have found the McAuliffe and Gordon work to be extremely naive. “Our interviews have revealed that after prolonged heroin use the subjects experience a ‘desirable’ consciousness change induced by the drug. This change is characterized by increased emotional distance from external stimuli and internal response, but it is a long way from euphoria” (Zinberg et al. 1978: 19). In a survey of British Columbian addicts (cited in Brecher 1972: 12), seventy-one addicts asked to check their mood after taking heroin gave the following responses: Eight found the heroin experience to be “thrilling” and eleven found it “joyful” or “jolly,” while sixty-five reported it “relaxed” them and fifty-three used it to “relieve worry.”

Applying labels such as “pleasurable” or “euphoric” to addictive drugs like alcohol, barbiturates, and narcotics seems paradoxical, since as depressants they lessen intensity of sensation. For example, narcotics are antiaphrodisiacs whose use frequently leads to sexual dysfunction. When naive subjects are exposed to narcotics, usually in the hospital, they react with indifference or actually find the experience unpleasant (Beecher 1959 Jaffe and Martin 1980 Kolb 1962 Lasagna et al. 1955 Smith and Beecher 1962). Chein et al. (1964) noted the very special conditions under which addicts found narcotic effects to be pleasurable: “It is . . . not an enjoyment of anything positive at all, and that it should be thought of as a ‘high’ stands as mute testimony to the utter destitution of the life of the addict with respect to the achievement of positive pleasures and of its repletion with frustration and unresolvable tension” (in Shaffer and Burglass 1981: 99). Alcoholics’ drinking does not conform any better to a pleasure model: “The traditional belief that alcoholism is maintained primarily as a function of its rewarding or euphorigenic consequences is not consistent with the clinical data” as “alcoholics become progressively more dysphoric, anxious, agitated and depressed during chronic intoxication” (Mendelson and Mello 1979b: 12-13).

The opposite picture—the rejection of positive drug rewards by those in a position to pursue more lasting satisfactions—is evident in a study of volunteer subjects’ reactions to amphetamines (Johanson and Uhlenhuth 1981). The subjects originally reported the drug elevated their moods and preferred it to a placebo. After three successive administrations of the drug over several days, however, the subjects’ preference for the amphetamine disappeared even though they noted the same mood changes from its use. “The positive mood effects, which are usually assumed to be the basis of the reinforcing effect of stimulants, . . . were not sufficient for the maintenance of drug taking, probably because during the period of drug action these subjects were continuing their normal, daily activities.” The drug state interfered with the rewards they derived from these activities, and thus, “in their natural habitat these subjects showed by their preference changes that they were uninterested in continuing to savor the mood effects” (Falk 1983: 388).

Chein et al. (1964) noted that when ordinary subjects or patients find narcotics pleasurable they still do not become compulsive drug users and that a percentage of addicts find heroin to be extremely unpleasant at first but nonetheless persist in taking drugs until they became addicted. All these examples make clear that drugs are not inherently rewarding, that their effects depend on the individual’s overall experience and setting, and that the choice of returning to a state—even one experienced as positive—depends on the individual’s values and perceived alternatives. Reductionist models have no hope of accounting for these complexities in addiction, as illustrated by the most widely deployed of such models, Solomon’s (1980) opponent-process view of conditioning.

Solomon’s model draws an elaborate connection between the degree of pleasure a given state produces and its subsequent capacity to inspire withdrawal. The model proposes that any stimulus leading to a distinct mood state eventuates in an opposite reaction, or opponent process. This process is simply the homeostatic function of the nervous system, much the same way that presenting a visual stimulus leads to an after-image of a complementary color. The stronger and the greater the number of repetitions of the initial state, the more powerful the opponent reaction and the more rapid its onset after the first stimulus ceases. Eventually, the opponent reaction comes to dominate the process. With narcotics and other powerful mood-arousing involvements such as love, Solomon proposes, an initial positive mood is replaced as the individual’s primary motivation for re-experiencing the stimulus by the desire to avoid the negative, or withdrawal state.

Solomon and Corbit (1973, 1974) constructed this model from experimental evidence with laboratory animals. As we have seen, neither the positive feelings it posits from narcotics use nor the traumatic withdrawal it imagines can account for human drug taking. Moreover, the model’s mechanistic version of neurological sources of motivation creates a Platonic ideal of pleasure as existing independent of situation, personality, or cultural milieu. The model likewise holds that a person’s response to this objective degree of pleasure (or else equally specifiable withdrawal pain) is a predetermined constant. People in fact display all sorts of differences in how ardently they pursue immediate pleasure or how willing they are to endure discomfort. For example, people vary in their willingness to delay gratification (Mischel 1974). Consider that most people find hot fudge sundaes and devil’s food cake to be extremely enjoyable and yet only a very few people eat such foods without restraint. It simply isn’t plausible that the main difference between compulsive and normal eaters is that the former enjoy the taste of food more or suffer greater withdrawal agony when not stuffing themselves.

Solomon uses the opponent-process model to explain why some lovers cannot tolerate the briefest of partings. Yet this separation anxiety seems less a measure of depth of feeling and length of attachment than of the desperation and insecurity of a relationship, which Peele and Brodsky (1975) called addictive love. For example, Shakespeare’s Romeo and Juliet prefer to die rather than be parted. This state does not result from accumulated intimacies that were eventually replaced by negative sensations, as Solomon’s model predicts. Shakespeare’s lovers cannot bear to part from the start. At the time when they both commit suicide, they have met only a handful of times, with most of their meetings having been brief and without physical contact. The kinds of relationships that lead to the withdrawal extremes of murder and suicide when the relationship is threatened rarely coincide with notions of ideal love affairs. Such couplings usually involve lovers (or at least one lover) who have histories of excessive devotion and self-destructive affairs and whose feeling that life is otherwise bleak and unrewarding has preceded the addictive relationship (Peele and Brodsky 1975).

Associative Learning in Addiction

Classical conditioning principles suggest the possibilities that settings and stimuli associated with drug use either become reinforcing in themselves or can set off withdrawal and craving for the drug that lead to relapse. The first principle, secondary reinforcement, can explain the importance of ritual in addiction, since actions like self-injection acquire some of the reward value of the narcotics they have been used to administer. Conditioned craving leading to relapse would appear when the addict encountered settings or other stimuli that were previously connected with drug use or withdrawal (O’Brien 1975 S. Siegel 1979 Wikler 1973). For example, Siegel (1983) applied conditioning theory to explain why the Vietnam soldier addicts who most often relapsed after their return home were those who had abused drugs or narcotics before going to Asia (Robins et al. 1974). Only these men would be exposed to familiar drug-taking environments when they returned home that set off the withdrawal that in turn required them to self-administer a narcotic (cf. O’Brien et al. 1980 Wikler 1980).

These ingenious conditioning formulations of human drug use have been inspired by laboratory studies of animals and human addicts (O’Brien 1975 O’Brien et al. 1977 Siegel 1975 Wikler and Pescor 1967). For example, Teasdale (1973) demonstrated that addicts showed greater physical and emotional responses to opiate-related pictures than to neutral ones. However, the conditioned craving and withdrawal such studies uncover are by the evidence minor motivations in human relapse. In the laboratory, Solomon has been able to create negative opponent-process states that last for seconds, minutes, or at most days. O’Brien et al. (1977) and Siegel (1975) have found that responses associated with narcotic injections in humans and rats that can be conditioned to neutral stimuli are extinguished almost immediately when the stimuli are presented on unrewarded trials (that is, without a narcotic).

What is more important, these laboratory findings do not appear relevant to addicted street behavior. O’Brien (1975) reported a case of an addict just out of prison who became nauseated in a neighborhood where he frequently had experienced withdrawal symptoms—a reaction that led him to buy and inject some heroin. This case has been described so often that, in its repetition, it seems a typical occurrence (see Hodgson and Miller 1982: 15 Siegel 1983: 228). Yet it is actually a novelty. McAuliffe and Gordon (1974) reported that “We have interviewed 60 addicts concerning their many relapses, and we could find only one who had ever responded to conditioned withdrawal symptoms by relapsing” (p. 803). In their thorough study of the causes of relapse, Marlatt and Gordon (1980) found heroin addicts rarely reported postaddiction withdrawal to be the reason they relapsed. None of the cigarette smokers or alcoholics Marlatt and Gordon interviewed listed withdrawal symptoms as the cause of their relapse.

Conditioned responses are particularly unlikely to account for relapse, since most former addicts do not relapse to addiction after they use a drug again. Schachter (1982) found that former smokers would smoke at a party but not return to regular smoking. Vaillant (1983) noted that “relatively few men with long periods of abstinence had never taken another drink” (p. 184). Half of the addicted Vietnam soldiers used a narcotic at home, but only a minority became readdicted (Robins et al. 1975). Waldorf’s (1983) investigation of heroin addicts who quit on their own found ex-addicts typically injected themselves with heroin after licking the habit to prove to themselves and others that they were no longer hooked. All these data point out that the unconditioned stimulus (actual drug use) is not sufficient provocation for a return to addiction. It is impossible that the weaker conditioned stimuli could provide sufficient motivation.

For Siegel and others who have analyzed the Vietnam remission data in conditioning terms, the crucial variable is simply situational change. All situational changes are equivalent in terms of this model as long as drugs have been taken in one environment and not the other, since then the new environment does not evoke conditioned withdrawal symptoms. This has prompted Siegel et al. to recommend a fresh setting as the best remedy for addiction. Yet it would certainly seem that other features of this new setting would be at least as important as familiarity for affecting addiction. Rats habituated to morphine in a diverse, social environment refused the drug in the same environment when offered a choice, while caged, isolated rats on the same presentation schedule continued to consume the morphine (Alexander et al. 1978). Zinberg and Robertson (1972) reported that addicts’ withdrawal symptoms disappeared in a treatment environment where withdrawal was not accepted, while their withdrawal was exacerbated in other environments, such as prison, where it was expected and tolerated.

The Role of Cognition in Conditioning

Addicts and alcoholics—whether treated or untreated—who achieve remission often do experience important changes in their environments. These changes frequently result, however, from self-initiated attempts to escape the addiction and other life problems. There are also those who modify addictive habits without drastically rearranging their lives. This is especially true for those addicted to less socially disapproved substances like cigarettes but also holds for a distinct minority of former alcoholics and heroin addicts. Modification of the addict’s environmental stimuli appears in these cases to be an entirely internal or psychological process. Siegel (1979) recognized this role for cognitive stimuli when he explained why some Vietnam veterans relapsed without returning to old drug haunts. He cited Teasdale (1973) and O’Brien (1975) to indicate men experienced withdrawal and craving when “talking about drugs in group therapy,” “seeing pictures of drugs and ‘works,”‘ or just “imagining themselves injecting drugs in their customary setting” (p.158).

The conditioned responses that occur with regard to subjective experience and as a result of environmental changes that addicts themselves bring about cast conditioning theories in a whole new light, where these responses seem an adjunct to individual self-control and motivation to change rather than the sources of such change. Moreover, conditioning theories in addiction are limited by their inability to convey the meaning the individual attaches to his or her behavior and environment. As a result, conditioning theories must be made so complex and ad hoc to explain the complexities of human drug taking that they lose the precision and predictive power that are their supposed scientific assets. They seem destined to suffer the same fate as did the U.S. intervention in Vietnam, the event that has prompted so much speculation about the role of conditioning in drug use. In both cases rationales become so cumbersome and counterproductive in the effort to respond to information from the field that they must collapse of their own weight.

Siegel’s utilization of cognitive variables to account for conditioning anomalies observed in heroin use is part of a venerable tradition. The first explicitly cognitive conditioning model in addiction was Lindesmith’s (1968, originally published in 1947), which contended that to be addicted the heroin user must be aware that the withdrawal pain he suffers is due to cessation of drug use and that readministering the drug will alleviate this pain. Thus so many nineteenth century narcotic users may have failed to become addicted because they simply didn’t know that narcotics were addicting! Lindesmith elaborated how cognitions affect addiction in connection with hospital patients. Patients do realize they are taking a narcotic and understand the drug’s effects, but they associate these effects with their illness. When they leave the hospital (or later when their prescription for painkillers runs out) they know any discomfort will be temporary and a necessary part of convalescence and thus they do not become addicted.

We may wonder why Lindesmith reserved the role of cognition in his model for this very limited number of ideas. For example, would not a hospital patient’s belief that continued narcotic use was harmful or that other opportunities outweighed the option of giving in to the drug’s effects be a part of the decision not to continue using narcotics? Such matters as self-conception, perceived alternatives, and values against drug intoxication and illicit activity would naturally seem to influence the individual’s choices. It is not only the decision whether to continue using a drug that cognitions, values, and situational pressures and opportunities determine, however. They also determine how the drug’s effects and withdrawal from these effects will be experienced. Contrary to Lindesmith’s scheme, people who recover from illnesses almost never acknowledge craving narcotics outside the hospital (Zinberg 1974).

Adaptation Theories

Social Learning and Adaptation

Conventional conditioning models cannot make sense of drug behavior because they circumvent the psychological, environmental, and social nexus of which drug use is a part. One branch of conditioning theory, social-learning theory (Bandura 1977), has opened itself to the subjective elements of reinforcement. For example, Bandura described how a psychotic who continued his delusional behavior in order to ward off invisible terrors was acting in line with a reinforcement schedule that was efficacious despite its existing solely in the individual’s mind. The essential insight that reinforcers gain meaning only from a given human context enables us to understand (1) why different people react differently to the same drugs, (2) how people can modify these reactions through their own efforts, and (3) how people’s relationships with their environments determine drug reactions rather than vice versa.

Social-learning theorists have been especially active in alcoholism, where they have analyzed how alcoholics’ expectations and beliefs about what alcohol will do for them influence the rewards and behaviors associated with drinking (Marlatt 1978 Wilson 1981). Yet it has also been social-learning theorists who have launched the alcohol-dependence syndrome and who seem to feel subjective interpretation is far less important than the pharmacological effects of alcohol in causing drinking problems (Hodgson et al. 1978, 1979). This lacuna in their theorizing is most noticeable in the inability of modem social-learning theorists to make sense out of cultural variations in drinking styles and experiences (Shaw 1979). Whereas McClelland et al. (1972) offered an experiential bridge between individual and cultural conceptions about alcohol (see chapter 5), behaviorists have regularly rejected this kind of synthesis in favor of direct observations and objective measurements of alcoholic behavior (embodied by Mendelson and Mello 1979b).

In another area of social-learning theory, Leventhal and Cleary (1980) proposed “that the smoker is regulating emotional states and that nicotine levels are being regulated because certain emotional states have been conditioned to them in a variety of settings” (p. 391). In this way they hoped to “provide a mechanism for integrating and sustaining the combination of external stimulus cues, internal stimulus cues, and a variety of reactions including subjective emotional experience . . . with smoking” (p. 393). In other words, any number of levels of factors, from past experience to current setting to idiosyncratic thoughts, can influence the person’s associations with smoking and subsequent behavior. In creating a conditioning model as complex as this one in order to account for behavior, however, the authors may have been putting the cart before the horse. Instead of conceiving of cognition and experience as components of conditioning, it seems easier to say that addiction involves cognitive and emotional regulation to which past conditioning contributes. In this view, addiction is an effort by an individual to adapt to internal and external needs, an effort in which a drug’s effects (or some other experience) serve a desired function.

Social-Psychological Adaptation

Studies that have questioned users about their reasons for continued drug-taking or that have explored the situations of street users have revealed crucial, self-aware purposes for drug use and a reliance on drug effects as an effort to adapt to internal needs and external pressures. Theoretical developments based on these investigations have focused on the psychodynamics of drug reliance. Such theories describe drug use in terms of its ability to resolve ego deficiencies or other psychological deficits—brought on, for example, by lack of maternal love (Rado 1933). In recent years theorizing of this sort has become broader: less wedded to specific child-rearing deficits, more accepting of a range of psychological functions for drug use, and including other substances besides narcotics (cf. Greaves 1974 Kaplan and Wieder 1974 Khantzian 1975 Krystal and Raskin 1970 Wurmser 1978).

These approaches developed in response to the clearcut finding that very few of those exposed to a drug, even over extended periods, came to rely on it as a life-organizing principle. What they failed to explain adequately is the great variability of reliance on drugs and addiction in the same individuals over situations and life span. If a given personality structure led to the need for an specific kind of drug, why then did the same people wean themselves from the drug? Why did others with comparable personalities not become wedded to the same substances? What was obvious in the case of narcotic addiction was its strong association with certain social groups and lifestyles (Gay et al. 1973 Rubington 1967). Efforts to incorporate this level of social reality led to higher-order theories that went beyond purely psychological dynamics to combine social and psychological factors in drug use (Ausubel 1961 Chein et al. 1964 McClelland et al. 1972 Winick 1962 Zinberg 1981).

Such social-psychological theories addressed the function of drug use in adolescent and postadolescent life stages as a way of preserving childhood and avoiding adult conflicts (Chein et al. 1964 Winick 1962). They also dealt with the availability of drugs in certain cultures and the predisposing social pressures toward their use (Ausubel 1961 Gay et al. 1973). Finally they presented the impact of social ritual on the meaning and style of use that a person in a given setting adopted (Becker 1963 Zinberg et al. 1977). What ultimately limited these theories was their lack of a formulation of the nature of addiction. While nearly all of them minimized the role of physiological adjustments in the craving and response to withdrawal that signify addiction (Ausubel 1961 Chein et al. 1964 Zinberg 1984), they provided little in the way of basic mechanisms to account for the dynamics of addiction.

As a result, the social-psychological literature exists in almost total isolation from the pharmacological and learning literature on addiction. Because they do not confront laboratory-based models directly, social-psychological theorists are forced to rely on biological concepts that their own data and ideas contradict (as illustrated by the discussion, in chapter 1, of Zinberg et al. 1978). This exaggerated deference to pharmacological constructs makes these theorists reluctant to incorporate a cultural dimension as a basic element in addiction or to explore the meaning of nonsubstance addictions—surprisingly so, given that their own emphasis on the socially and psychologically adaptive functions of drugs would seem to apply equally well to other involvements. What may curtail the social and psychological analysis of addiction most is the inappropriate meekness and limited scientific aspirations of those best suited to extend the boundaries of addiction theory in this direction. Such meekness certainly does not characterize modern conditioning and biological theorizing.

The Requirements of a Successful Theory of Addiction

A successful addiction model must synthesize pharmacological, experiential, cultural, situational, and personality components in a fluid and seamless description of addictive motivation. It must account for why a drug is more addictive in one society than another, addictive for one individual and not another, and addictive for the same individual at one time and not another (Peele 1980). The model must make sense out of the essentially similar behavior that takes place with all compulsive involvements. In addition, the model must adequately describe the cycle of increasing yet dysfunctional reliance on an involvement until the involvement overwhelms other reinforcements available to the individual.

Finally, in assaying these already formidable tasks, a satisfactory model must be faithful to lived human experience. Psychodynamic theories of addiction are strongest in their rich explorations of the internal, experiential space of their subject matter. Likewise, disease theories—while seriously misrepresenting the nature and constancy of addictive behavior and feelings—are based on actual human experiences that must be explained. This last requirement may seem the most difficult of all. One may wonder whether models built on social-psychological and experiential dynamics make any sense when confronted with the behavior of laboratory animals or newly born infants.

Dr. Stanton Peele, recognized as one of the world's leading addiction experts, developed the Life Process Program after decades of research, writing, and treatment about and for people with addictions. Dr. Peele is the author of 14 books. His work has been published in leading professional journals and popular publications around the globe.

Comments

Learning the how and why is vital in order to treat all addiction. I see all models as tools that can be applied or not at the goal of treating the disease of addiction.


Addiction from the Bottom Up: A Felt Sense Polyvagal Model of Addiction

Reaching beyond the western, post Descartes view of mind/body duality as distorted and harmful, I have explored alternative ways of experiencing and conceptualizing the body. I think this is critical when working with addiction because our current understanding and treatment of addiction reflect this disembodied view—addiction is seen as a malfunctioning of our computer-like brains. But the current brain disease model is failing us. Rates are soaring. People are dying in the streets. We can and must do better than this.

To approach addiction from a new perspective, I created a model to conceptualize and treat addiction: The Felt Sense Polyvagal Model (FSPM). FSPM addresses addiction where it lives, in the body. Based on over 40 years of client interactions, the model understands addiction as an adaptive attempt to regulate emotional states. Addictive behaviors are self-soothing strategies to survive when we cannot calm ourselves, and they are self-harmful. These behaviors do not come from sickness however, they come from a bodily response to threat and a wired-in survival mechanism.

From an embodied place of experiencing, and through the lens of Polyvagal Theory, we can understand addictive behaviors as the body’s attempt to keep us alive when being in the present moment is too overwhelming. Shifting to a bottom up approach allows us to experience both the wisdom of the body, and the wisdom of addictive responses.

To create the FSPM, I drew from Stephen W. Porges’ Polyvagal theory (2011), which offered a new understanding of the autonomic nervous system. As I began to learn about Polyvagal Theory, I realized that it enhanced my understanding of what I knew intuitively: Clients were using addictive behaviors to propel themselves from a state of sympathetic arousal to a dorsal vagal response of numbing, and vice versa. Through the lens of the autonomic nervous system (ANS), we see these behaviors as adaptive. While they may look bizarre, they have a logic of their own that is oriented towards survival. This understanding is key to appreciating the vital importance of Porges’ discovery.

Why is this so? Because it validates these behaviors as adaptive, and the folks who rely on them as, in a sense, normal. Polyvagal Theory teaches us that we respond to threat in a very elegant and systematic way, first by activating the ventral branch of the vagus nerve, our ‘smart’ vagus. If the situation cannot be resolved in this way, the sympathetic branch kicks in to empower us to mobilize. If mobilizing is not possible, we have a third option available to maximize our potential for survival, the dorsal branch of the vagus nerve that shuts us down, helping us to dissociate, to bear the unbearable.

This is vitally important because we then see traumatic responses in a new light. A paradigm shift is demanded of this new light. A shift that honours the body’s inherent knowing, healing shame and blame, and putting new and more body- informed healing practices into the forefront.

Many other cultures and movements never lost their appreciation for the wisdom of the body. Our culture lost its way post Descarte. We have much to learn and unlearn. My own understanding came from the Feminist movement. We embraced body wisdom, and intuitively understood traumatic responses, including addiction, as inherently helpful. But our female voices were not respected, and we didn’t have a significant piece that Polyvagal theory provides. That is, a sophisticated understanding of the autonomic nervous system that provides a neurophysiological explanation for traumatic/addictive responses, and the power of a scientific language that speaks to, and challenges, our post Descarte era. Porges’ capacity to integrate top down and bottom up ways of knowing is making him a powerful contributor, a change agent in our currently desperate culture of global trauma.

My work is also influenced by Eugene Gendlin (1978), who coined the term felt sense based on a contemplative practice called Focusing. Focusing is a six-step process that helps us find our implicit embodied knowing about an issue in our life. A knowing that is at first vague. Turning attention inwards and listening with compassion allows a felt sense, a whole sense of the situation, to form.

Thoughts, feelings, physical sensations, and memories are different aspects of experience that create a pathway into the Felt Sense. In asking questions about these aspects we help the client to deepen their embodied knowing of the issue. As the felt sense forms we pause and stay with the fullness of experiencing. Sometimes a Felt Shift, a physical release happens as the client integrates a new knowing. This shift is the bodies’ knowing and pointing in the direction of growth and healing. The client feels a relief, a settling. Focusing is a natural process that happens all the time. Gendlin found that clients who were doing well in therapy were connected to their bodies. They had access to a Felt Sense. However, because we live in such a disembodied culture, many clients needed help to connect, so Gendlin created the steps.

I also incorporated Marc Lewis’ s learning model of addiction. Lewis, a neuroscientist, reinterpreted the neuroscientific data on addiction from what he called a disease-free bias. He reframed addiction as the development of coping habits within a social matrix. “According to Lewis, addiction is an extreme outcome of a normally functioning brain” (Snoek and Matthews, 2017).

In addition, I’ve brought an anti-oppressive lens to the understanding of the root causes of addiction. It is from this lens that we have seen the profound impact that oppression has on the development and increasing incidence of addictive behaviors. Experiences of oppression lead to trauma, and trauma is the underbelly of addiction. Consequently, marginalized groups are much more vulnerable. Staci Haines, author of The Politics of Trauma, (2019) puts it so well when she says that trauma robs us of safety, belonging and dignity. Without these basic needs being met, we seek out quick and dirty ways of soothing to help us survive.

My objective was to provide a teaching/clinical model of addiction that offered a radical paradigm shift, challenging our current pathologizing approach. I integrated new neurobiological findings in brain research, supported by an alternative learning model of addiction, as well as subsequent clinical approaches that address embodied trauma therapies.

My goal was for therapists to understand addiction using a sophisticated theoretical framework and treatment strategies that challenged old, disembodied approaches. The model is adaptable to any school of psychotherapy or healing practice.

The Felt Sense/Polyvagal Model

To support FSPM, I created two graphic models. One for clinicians and one for client use. Looking at the graphic depiction of the FSPM Clinician version we can see the overlap with Porges’ work.

First are the three circuits of the ANS, connected via a solid lined, inverted triangular

A) the ventral vagus is in yellow at the bottom of the page,
B) the sympathetic in red on the right, and
C) the dorsal vagus is in grey on the left.

Next are the Intertwining States, connected by the dotted line triangle.
Intertwining states are states in the system that utilize two pathways. The ANS has the capacity to blend states creating a greater range of experiences. The intertwining states are represented in the model in mixed colors.

A) Play is on the bottom right in yellow/red.

B) Stillness is bottom left yellow/grey.

C) And the FSPM proposes a third intertwining state of Addiction, which is at the top of the model, red/grey.

As a state, Addiction is a blending of sympathetic and dorsal. Without the presence of the ventral vagus, the Social Engagement System is offline. When trauma and other states of emotional dis-regulation occur, the capacity to regulate through the ventral vagus are compromised. The ANS shifts into survival mode. People then employ addictive behaviors to seek relief from suffering.

In addition to providing a new map for clinical applications, I created a simple version for clients that uses what I call the ‘Six F’s’ to define the states of the autonomic nervous system: Flight/Fight, Fawn/Freeze, Fixate, Flow, Fun, Flock.

1. Sympathetic Response: Flight is a state of fear and anxiety. In this state the body mobilizes to run and escape. Fight is a mobilizing state of anger.

2. Dorsal Response: Fawn is a state of surrendering to someone with power over you. Freeze is a collapse of the ANS into a dissociative state when sympathetic response is ineffective.

3. Fixate is the intertwining state of addiction that acts as a propeller between Flight/Fight and Fawn/Freeze.

4. Flow is an intertwining state between ventral and dorsal. A state of safety with stillness.

5. Fun is an intertwining state between ventral and sympathetic, a state of playfulness.

6. Flock is the ventral state of grounding and safety.
With time our clients learn how to identify and track the state they are in and to use the tools that we teach them to move more into the ventral vagal state.

Applying the Model

I offer an example starting with Focusing. A client comes in with anxious feelings and a tightening in her throat. She says that she doesn’t know why she feels this way. We begin the process of quietly turning attention inwards, down into the centre of the body. Tears come as she connects the physical sensations with the feelings of sadness and anger. A beginning of the Felt Sense starts to form. I ask, “Can you welcome both feelings?” She pauses and explores where there are no words. She puts a hand on her throat.

“I don’t know how to be with anger,” she says. More sensing into the body.
More tears flow as she feels the physical sensations of the Felt Sense flooding into her throat and now down into her chest. A whole Felt Sense of her situation forms: thoughts, feelings, physical sensations, and memories.

“This goes way back for me. Little girl afraid to be angry, so I cry instead. “And”, she stops, hesitating to say the next sentence, “I eat. A lot. And then I make myself sick to get rid of it. This needs to stop. I need my anger.”

Her whole body moves and relaxes with a Felt Shift. She feels her throat loosening, a new piece has come for her. An explicit knowing that has great meaning for her. A need to connect with her anger. Her Felt Sense carries this meaning forward into her life as she welcomes what came in her Focusing practice session.

Next, we can map the felt sense onto the Felt Sense Polyvagal Model to integrate the autonomic nervous system states. This gives us more information about the client’s journey. In the Clinician version she moves back and forth from chaos/sympathetic meme, over to rigid/dorsal (fawn), a shutting down of anger and surrender of power, then down to Integrated/Ventral meme in her Focusing Oriented Psychotherapy session. Together we look at the Client Version of the model as she maps her journey from Flight/Fight to Fawn to Flock.

In Conclusion: A Call to Action

Polyvagal theory teaches us that we are not safe until all of us are safe, feel a sense of belonging, and have dignity in our lives. Because we coregulate each other, we are designed to live in community. We thrive when we are taking good care of the most vulnerable folks in our culture. Addiction is created and prolonged by states of vulnerability.

At a time like this, with a global pandemic upon us, we need more than ever to learn the lessons of a Polyvagal informed society. We need to learn from folks suffering from addiction. They tell us where we are failing as a culture, and what we must do to bring safety to each and every one of us. If we all need to go home and practice social distancing, then we better make sure that all of us have a safe home to go to. Otherwise, none of us are going to be safe.

“Addiction is our teacher,” says Bruce Alexander (2010), a researcher and author. In his documentary, Addiction: The View from Rat Park, he shows us how we have lost connection with each other and with the natural world. In our disconnected state, we, as a culture, can’t know how to feel into the problem or the solution. We cling to our top down explanations of demon drugs to avoid feeling into the embodied cultural trauma of our times. Like the addicted soul, we delude ourselves. We have lost our way. But only in our heads. The body knows the answer.

Addiction is a political problem, and I invite you to join me in standing up and speaking up to make a difference!

I am currently writing a book about the FSPM model. For information and questions please visit my website: http://www.focusingonborden.com/

Jan Winhall, M.S.W. R.S.W. F.O.T.T. Toronto, Canada. Jan is a psychotherapist in private practice and Director of Focusing on Borden, a centre for teaching Focusing and Focusing-Oriented Therapy. Jan is the author of Understanding and Treating Addiction with the Felt Sense Experience Model. In Emerging Practice in FOT. Jan teaches internationally and is a lecturer in the Faculty of Social Work at the University of Toronto. She is currently writing a book about her new Felt Sense/Polyvagal Model for treating addiction.

Alexander, B. K. (2010). The globalization of addiction: A study in poverty of spirit. Oxford, United Kingdom: Oxford University Press.

Gendlin, E. (1978). Focusing. New York, NY: Everest House Publishing.

Haines, S. (2019). The Politics of Trauma. Berkeley, California: North Atlantic Books.

Lewis, M. (2015). The Biology of Desire. Canada: Penguin Random House Doubleday Canada.

Porges, S. W. (2011). The Polyvagal Theory: Neurophysiological foundations of emotions, attachment, communication, self regulation. New York, NY: W. W. Norton and Company.