Anatomy of Relapse. Why We Keep Going When We Want to Stop
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Anatomy of Relapse
Why We Keep Going When We Want to Stop
Sergey Kalutskiy
2026
Introduction
This book is divided into two parts: Theory and Practice.
Part I presents a new perspective on the mechanism behind all forms of addictive behavior. Part II examines existing treatment approaches — why they help some people and fail others, and how they can be reinterpreted to become genuinely effective in light of this theory.
The book is built around thought experiments. Each one is simple, intuitive, and requires no specialized knowledge.
Modern psychology often feels inaccessible. Behind complex terminology and professional concepts, the living human meaning is easily lost. My aim is to look behind the curtain of scientific language, set aside the heavy jargon, and reveal the problem in its simplest form. You will find that many seemingly complicated theoretical constructions conceal an elementary truth — one that becomes visible through the framework this book proposes.
You will also find that despite the apparent diversity of treatment methods — from spiritual practices to clinical psychotherapy — they ultimately come down to a small number of fundamental ideas.
There are two distinct questions about addiction that are frequently conflated.
First: why does a person begin using, and why do they continue? The answer involves needs, genetic predisposition, environment, personal history, trauma, and many other factors. This book does not attempt to answer that question comprehensively.
Second: why can a person who sincerely wants to stop fail to do so? That is the central question of this book.
These two questions require different explanations. A person may use substances for years without experiencing any inner conflict — and there is nothing mysterious about that. The mystery emerges the moment a genuine desire to stop appears, only to reveal that desire alone is not enough.
Part I Theory
Chapter 1. A Unified Perspective
This book does not attempt to examine individual forms of addiction separately — drug dependence, overeating, smoking, compulsive shopping, or internet addiction. Its aim is different: to uncover the universal internal mechanism behind all forms of addictive behavior and, on that basis, to propose a general theory — one that explains why some treatment methods prove effective while others do not.
These disorders undoubtedly differ in the harm they cause to the body, in the substances involved, and in their impact on personality. Yet a closer look reveals that all addictions share a striking number of common features. They tend to develop according to the same cyclical pattern: relapse, guilt, and a renewed firm intention to "quit forever."
Five universal characteristics can be identified across any addiction.
1. Loss of Control
Loss of control over one's own behavior is the defining feature of addiction. It is precisely what distinguishes addiction from a merely harmful habit.
Nora Volkow, Director of the U.S. National Institute on Drug Abuse (NIDA), describes addiction as a condition associated with dysfunction in the neural systems responsible for self-control and behavioral regulation (Volkow & Li, 2005).
An addicted person typically recognizes their condition and genuinely wishes to stop. Whether the issue is drugs, smoking, or overeating, the individual wants to stop but cannot follow through on their own decision.
Addiction, then, should be understood not primarily as substance misuse but as an impairment of self-regulatory capacity. If a behavior remains fully subject to voluntary control, it is difficult to call it an addiction.
2. From Reward to Relief
A widespread misconception is that addicted individuals continue using simply because they enjoy it: that people with obesity cannot resist tasty food, drug users seek euphoria, and alcoholics drink for pleasure.
A closer look shows that continued use is not always associated with pleasure. The experience may be neutral or even unpleasant. Philosophical analyses of addiction emphasize that compulsive behavior can persist long after it ceases to provide genuine enjoyment, functioning instead as a way of avoiding discomfort rather than producing positive experience (Kennett, Matthews, & Snoek, 2013).
Empirical data support this shift. The affective processing model shows that once addiction is established, the primary motivation for using becomes the alleviation of negative feelings rather than the pursuit of reward (Baker, Piper, McCarthy, Majeskie, & Fiore, 2004). At the neurobiological level, this corresponds to an allostatic shift: the baseline of the reward system drops, and the substance is required not for pleasure but to restore a neutral state (Koob & Le Moal, 2001).
The urge to use is therefore driven more often by an attempt to relieve intense internal tension than by any desire for pleasure. The symptoms may vary — from irritability and anxiety to nausea and tremor — but they are almost always present. Continued use becomes not a source of pleasure but a means of escaping suffering.
This distinction between seeking pleasure and avoiding suffering is fundamental to everything that follows.
3. Withdrawal Syndrome
Withdrawal is often assumed to occur only in drug addiction or chronic alcoholism. In reality, withdrawal-like states are also observed in behavioral addictions such as gambling, shopping, and overeating.
Stanton Peele, analyzing the phenomenon of romantic addiction, noted that the end of addictive relationships is accompanied by pronounced distress, anxiety, and experiences functionally similar to withdrawal (Peele & Brodsky, 1975).
Contemporary research confirms similar patterns in other behavioral addictions. Pathological gambling, for example, is associated with withdrawal-like symptoms — irritability, restlessness, and sleep disturbances — comparable in structure to withdrawal from substance dependence (Yau & Potenza, 2015).
Withdrawal syndrome, then, is not exclusive to chemical addiction. It is a universal response of the self-regulatory system to the loss of a familiar means of stabilization.
4. Propensity for Relapse
One of the most consistent features of addiction is the high likelihood of returning to previous behavior. As early as the 1970s, researchers showed that relapse curves for alcoholism, smoking, and heroin dependence follow strikingly similar patterns: a sharp decline during the first three months of abstinence, followed by a plateau (Hunt, Barnett, & Branch, 1971).
Clinical data indicate that the risk of relapse remains elevated long after treatment ends. In this respect, addiction resembles other chronic illnesses — diabetes, hypertension, asthma: relapse rates in addiction do not exceed rates of treatment non-adherence in these conditions (McLellan, Lewis, O'Brien, & Kleber, 2000).
5. A Shared Neurobiological Basis
According to the American Society of Addiction Medicine (ASAM), addiction is a chronic brain disease affecting systems of motivation and memory (ASAM, 2019).
Despite differences in pharmacological action, psychoactive substances engage similar neural systems related to reward, motivation, and learning — including the mesolimbic dopamine pathway (Koob & Volkow, 2010). Neuroimaging studies show that comparable circuits are activated in behavioral addictions such as gambling (Potenza, 2006).
Understanding addiction as a brain disorder has important implications. It tells us that addiction is neither a moral failing nor a defect of character, but a disruption of regulatory mechanisms grounded in neurobiology. In this sense, the term brain disease is justified: all forms of addiction rely on similar systems of motivation, reward, and memory.
But this does not imply helplessness. The brain is not an external machine that has malfunctioned independently of the person. Psychological processes and neurobiology are simply two levels of description of the same system.
To say that addiction is a brain disease is about as accurate as saying that a computer virus is a disease of a computer. Yet a virus cannot be eliminated by replacing hardware — it requires changes at the level of software. Likewise, in addiction, neural circuits reshape through experience, decisions, and new modes of self-regulation.
The neurobiological model explains where the disruption occurs, but not how it persists. The task of this book is to describe that mechanism at the psychological level.
All forms of addiction share common features: cyclical progression, loss of behavioral control, the presence of withdrawal, a high probability of relapse, and involvement of the same neural systems.
Taken together, these observations suggest that addiction is a universal disorder of will and motivation — not a specific case of substance misuse.
References
Volkow, N. D., & Li, T.-K. (2005). The neuroscience of addiction. Nature Neuroscience, 8(11), 1429–1430. https://doi.org/10.1038/nn1105-1429
Kennett, J., Matthews, S., & Snoek, A. (2013). Pleasure and addiction. Frontiers in Psychiatry, 4, 117. https://doi.org/10.3389/fpsyt.2013.00117
Baker, T. B., Piper, M. E., McCarthy, D. E., Majeskie, M. R., & Fiore, M. C. (2004). Addiction motivation reformulated: An affective processing model of negative reinforcement. Psychological Review, 111(1), 33–51. https://doi.org/10.1037/0033-295X.111.1.33
Koob, G. F., & Le Moal, M. (2001). Drug addiction, dysregulation of reward, and allostasis. Neuropsychopharmacology, 24(2), 97–129. https://doi.org/10.1016/S0893-133X(00)00195-0
Peele, S., & Brodsky, A. (1975). Love and addiction. Taplinger Publishing Company.
Yau, Y. H. C., & Potenza, M. N. (2015). Gambling disorder and other behavioral addictions: Recognition and treatment. Harvard Review of Psychiatry, 23(2), 134–146. https://doi.org/10.1097/HRP.0000000000000051
Hunt, W. A., Barnett, L. W., & Branch, L. G. (1971). Relapse rates in addiction programs. Journal of Clinical Psychology, 27(4), 455–456. https://pubmed.ncbi.nlm.nih.gov/5115648/
McLellan, A. T., Lewis, D. C., O'Brien, C. P., & Kleber, H. D. (2000). Drug dependence, a chronic medical illness: Implications for treatment, insurance, and outcomes evaluation. JAMA, 284(13), 1689–1695. https://doi.org/10.1001/jama.284.13.1689
American Society of Addiction Medicine. (2019). Public policy statement: Definition of addiction. https://www.asam.org/resources/definition-of-addiction
Koob, G. F., & Volkow, N. D. (2010). Neurocircuitry of addiction. Neuropsychopharmacology, 35(1), 217–238. https://doi.org/10.1038/npp.2009.110
Potenza, M. N. (2006). Should addictive disorders include non-substance-related conditions? Addiction, 101(Suppl 1), 142–151. https://doi.org/10.1111/j.1360-0443.2006.01591.x
Chapter 2. The Drug-as-Disease model
In popular understanding, addiction is seen as a disease caused by the substance itself — one that follows a predictable course.
According to this model, regular drug use gradually produces tolerance: the previous dose no longer generates the desired effect, and the individual must consume increasing amounts to achieve the same level of pleasure.
When use stops, withdrawal emerges — a painful condition explained as the body having "adapted" to the substance and now demanding it again. This discomfort, together with an irresistible craving caused by bodily intoxication and brain adaptation, is believed to trap the person in a lifelong cycle of addiction.
This view, although widespread, does not hold up under careful examination. Contemporary research shows that addiction cannot be reduced to the formula "substance → habituation → disease." Its nature is far more complex.
Consider five major misconceptions underlying the traditional model.
1. The Myth of Tolerance
Tolerance refers to physiological adaptation that requires increased doses to achieve the same effect. It is often assumed that a drug user is inevitably doomed to escalate dosage without limit.
In reality, limitless dose escalation is a myth. For most individuals, this process eventually stabilizes. Moreover, tolerance is not a unique marker of addiction — it also develops with many ordinary medications, such as antidepressants, which do not produce compulsive drug-seeking.
Norman Zinberg's studies of opiate users showed that among participants tracked over time, nearly half maintained stable doses for years, 27% reduced their intake, and only 13% increased it (Zinberg, 1984). Zinberg demonstrated that controlled opiate use is possible when social rituals and rules regulate consumption — in other words, context, not the substance alone, plays the decisive role.
Large epidemiological datasets further indicate that most addicted individuals stop using without formal treatment, typically between the ages of 30 and 40. Addiction appears, then, not as a lifelong sentence but as a disorder with a characteristic natural history — one in which recovery is the norm rather than the exception (Heyman, 2009). From a neurobiological perspective, Marc Lewis makes a similar argument: addiction is not a brain disease but a form of deep learning. The brain reorganizes through repeated experience, yet the same plasticity allows it to reorganize again (Lewis, 2015).
2. The Myth of "Hooked After the First Time"
Popular warnings claim that a single dose is enough to enslave a person. Neither clinical experience nor historical evidence supports this.
Alcohol and nicotine clearly do not produce addiction after first exposure; repeated use is required. The same applies even to so-called "hard" drugs. Before the modern war on drugs, opiates were widely included in common medicines and tonics (Brecher, 1972; Courtwright, 1982). Despite broad availability, addiction rates remained relatively low.
In the United Kingdom, heroin was long prescribed for cough and migraine without triggering a widespread epidemic of addiction (Berridge, 1996).
Systematic analyses of medical opioid prescribing show that dependence develops in roughly 8–12% of patients receiving long-term treatment — significantly lower than commonly assumed, though far from zero (Vowles et al., 2015). These findings challenge both extremes: the myth of instant addiction and the opposite belief that prolonged use is entirely safe.
George Vaillant's decades-long longitudinal research on alcoholism showed that even individuals who later described their addiction as sudden had in fact developed dependence gradually, over many years. The experience of "instant addiction" is often a retrospective distortion of memory (Vaillant, 1983).
3. The Myth of Inevitability with Prolonged Use
Another widespread belief holds that prolonged use inevitably leads to addiction. At first glance this seems intuitive: the longer a substance is used, the stronger physiological and psychological adaptation should become. Reality is more complex.
Consider patients receiving medically supervised postoperative analgesia. They are often allowed to regulate their own opioid dosage — conditions that would appear ideal for addiction to take hold. Yet studies consistently show that once pain subsides, patients discontinue use without difficulty. Addiction does not develop (Schug, Merry, & Acland, 1991).
Perhaps the largest natural experiment in history occurred during the Vietnam War. In the late 1960s and early 1970s, a substantial proportion of American soldiers in combat regularly used heroin, marijuana, and amphetamines. Estimates suggest that more than 35% used opioids at least once and about 20% used them regularly. When the U.S. Department of Defense learned of these figures, widespread panic followed. Experts predicted an epidemic of addiction among returning veterans.
The research led by Lee Robins revealed a dramatically different outcome. Among soldiers who tested positive for drugs before demobilization, only 5% continued using during the first year after returning home. Most stopped on their own, without treatment, detoxification, or rehabilitation programs (Robins, 1993).
Long-term follow-up showed that only about 12% resumed use, and even those cases were typically episodic. Roughly nine out of ten stopped almost immediately upon returning to civilian life.
Why? Researchers emphasized the decisive role of context. Drug use in combat served specific functions — coping with stress, fear, pain, and insomnia. Returning home radically changed circumstances: the sources of tension disappeared, social bonds and values were restored, and the need for the drug lost its meaning. The same individuals, the same physiology, the same substances — but a different environment, and the habit dissolved.
4. The Problem with Animal Experiments
Since the mid-twentieth century, the concept of self-perpetuating addiction has relied heavily on animal experiments. In "Skinner boxes," rats or monkeys could press a lever to self-administer drugs. The results appeared straightforward: animals rapidly escalated intake and sometimes consumed drugs to the point of death.
These findings were long interpreted as direct proof that drugs themselves inevitably produce addiction. Canadian psychologist Bruce Alexander questioned the experimental conditions themselves, proposing that the critical factor was social isolation, not the substance. To test this, he created "Rat Park" — an enriched environment with space, toys, food, and social companions (Alexander, Beyerstein, Hadaway, & Coambs, 1981).
The results were striking. Rats in enriched environments showed little interest in morphine solution, preferring ordinary water. Even previously drug-exposed animals often abandoned drug consumption.
Alexander's findings sparked debate. Replication attempts produced mixed results — some confirming the effect, others finding weaker outcomes (Petrie, 1996). Nevertheless, the central insight — that environment plays a decisive role — received substantial support from later research. Enriched environments significantly reduce cocaine self-administration and drug-seeking behavior even after prolonged exposure (Chauvet, Lardeux, Goldberg, Jaber, & Solinas, 2009).
The issue, then, was not whether Alexander was correct in every detail, but that standard experiments with isolated animals systematically overestimated the addictive power of substances by neglecting context.
5. The Myth of Withdrawal as the Primary Driver
It is often assumed that physiological withdrawal symptoms are what force people to resume using. This belief rests on an unexamined conflation: the entire experience of cessation — restlessness, craving, obsessive thinking, psychological pain, a sense of unbearable pressure — is attributed to the body's chemical reaction to the absence of a substance.
Yet only a narrow subset of withdrawal symptoms is genuinely physiological in origin. Tremor, nausea, sweating, tachycardia, and in severe cases seizures and delirium — these reflect the body's acute response to the removal of a substance to which it has adapted. They are medically serious and, in the case of alcohol and benzodiazepines, potentially life-threatening. Discontinuation should occur under medical supervision.
But the broader phenomenology of withdrawal — the restlessness, the obsessive preoccupation with use, the sense of mounting internal pressure, the psychological pain that people describe as unbearable — cannot be accounted for by chemical deficit alone. These symptoms appear with comparable intensity in behavioral addictions where no substance is involved at all. Pathological gambling produces irritability, restlessness, and sleep disturbance structurally similar to substance withdrawal (Yau & Potenza, 2015). Internet gaming disorder is accompanied by craving and distress upon cessation that activate the same neural systems as drug withdrawal (Dong, Wang, Du, & Potenza, 2017; Grant, Potenza, Weinstein, & Gorelick, 2010). The end of addictive relationships triggers a state neurobiologically comparable to withdrawal syndrome (Fisher, Brown, Aron, Strong, & Mashek, 2010).
Similar symptoms — anxiety, irritability, sleep disturbance — also occur during caffeine cessation and antidepressant discontinuation, neither of which involves substances classified as narcotics (Fava, Gatti, Belaise, Guidi, & Offidani, 2015).
If the full range of withdrawal could be explained by the body's chemical readjustment, these phenomena would not exist. The fact that they do suggests that most of what people experience as "withdrawal" is not physiological in the strict sense — it is psychological, and requires a different explanation.
Moreover, even the genuinely physiological component does not explain addiction. Modern medicine can alleviate physical withdrawal relatively effectively. If withdrawal alone explained addiction, treatment would not be so difficult. Yet relapse often occurs weeks or months after the body is already physiologically free of the substance. The primary triggers are not physical craving but emotional states, interpersonal conflicts, and situational pressures (Marlatt & Gordon, 1985).
Research on craving supports this conclusion from another angle. Craving is not even a necessary condition for use — people often engage in substance use automatically, without conscious desire. Craving intensifies primarily when habitual behavior is blocked (Tiffany, 1990). Experimental studies further demonstrate that craving depends less on physiological state than on perceived availability: it increases when individuals believe use is possible and decreases when they consider it impossible (Wertz & Sayette, 2001). Craving is not a mechanical bodily signal but a response mediated by expectations and context.
Contemporary reviews confirm this: the relationship between subjective craving and actual relapse is considerably weaker than commonly assumed. Craving is an important but insufficient predictor of use; it reflects internal conflict rather than directly causing behavior (Sayette, 2016).
The fact that detoxification alone rarely resolves addiction points to the central conclusion: physiological symptoms, despite their severity, are not the primary driving force. They account for only a fraction of the withdrawal experience, and even that fraction does not explain why people return to use. The full phenomenology of withdrawal — the pain, the obsession, the unbearable pressure — demands an explanation that goes beyond chemistry. That explanation is the subject of the next chapter.
The evidence is clear: a substance by itself does not create addiction without the involvement of psychological and social factors.
Addiction is not a chemical trap into which the brain falls. It is a specific form of relationship between a person and a substance — one that arises only within a particular context and serves a particular function.
References
Zinberg, N. E. (1984). Drug, set, and setting: The basis for controlled intoxicant use. Yale University Press.
Heyman, G. M. (2009). Addiction: A disorder of choice. Harvard University Press.