It’s not only people addicted to alcohol or drugs who experience significant withdrawal symptoms if they stop using. Antidepressant (AD) withdrawal symptoms are also common, can be severe and prolonged, and may last months or years. For example, with antidepressant discontinuation, feelings resembling electric shocks, often called “brain zaps,” may occur in the head or body, along with nausea, vomiting, dizziness, and other symptoms. In some cases, ending antidepressant use may feel as difficult as stopping heroin. But antidepressants are not addictive.
A recent 2025 study by Mark Horowitz, M.D., Ph.D, a clinical research fellow in psychiatry with the National Health Service (NHS) in London, and his colleagues surveyed 310 patients who had been taking antidepressants. They found 79% experienced withdrawal symptoms upon ending antidepressants, with 45% reporting moderate-to-severe symptoms and about 20% experiencing symptoms lasting three months or longer. Longer duration of use was associated with greater likelihood of severe protracted symptoms and being less likely to be able to stop their ADs. Horowitz has stated his career was influenced by his own experience with severe withdrawal symptoms when trying to stop antidepressants.
People aren’t addicted to ADs; instead, their bodies become used to taking them and react if not receiving them or even taking a lower dosage. Antidepressant withdrawal is common—but distinct from addiction. The Horowitz study underscores the urgent need to distinguish between physiological dependence and addictive use.
For much of the 20th century, medical research and teaching equated physical withdrawal symptoms with addiction, and many people still believe it’s true. A drug was assumed “addictive” if patients experienced a recognizable abstinence syndrome when ending use. This framework was shaped by dramatic and sometimes dangerous withdrawal syndromes seen with ending use of alcohol, barbiturates, and opioids among the addicted. However, this interpretation implied physiological dependence was the disorder, and further, presumed drugs without vivid withdrawal symptoms were non-addictive. Contemporary neuroscience—pioneered in part by my work—corrected this misconception by distinguishing clearly between withdrawal and addiction.
Withdrawal is a physiological adaptation to chronic drug exposure to many different medications, including antidepressants. In contrast, addiction is a motivational pathology—a learned, acquired attachment marked by craving, compulsive use, reinforcement, impaired control, and persistence, despite harm. Thus, experiencing antidepressant withdrawal symptoms is not addiction. The DSM-5, the psychiatric manual, also cautions that withdrawal symptoms alone do not define a substance use disorder.
In fact, antidepressants are not addictive, although data from over 31,000 WHO-reported cases confirmed robust withdrawal signals may occur with multiple antidepressants if their use is ended, particularly with serotonin norepinephrine reuptake inhibitors (SNRIs) and paroxetine. ADs do not cause euphoria, intoxication, reinforcement, or compulsive drug-taking. Patients do not escalate doses or seek multiple prescribers, and they don’t compulsively buy these drugs on the street.
It’s not just antidepressants causing physical reactions when patients stop taking them or take a lower dosage. Many medications cause withdrawal symptoms without being addictive, including anticonvulsants (gabapentin, pregabalin), antipsychotics (quetiapine, risperidone), dopaminergic agents (pramipexole, ropinirole), cardiovascular agents (β-blockers, clonidine), and corticosteroids. In each case, abrupt discontinuation after chronic use may cause significant physiological rebound effects. But in none of these cases are withdrawal symptoms consistent with addiction—with craving, dose escalation, drug-seeking, or compulsive use. Addiction arises when the motivational system—not just the body’s homeostatic system—is dysregulated.
Patients experiencing withdrawal after stopping antidepressants often fear they are “addicted” because of these symptoms. At the same time, some clinicians minimize withdrawal symptoms or even overreact by mislabeling the person experiencing them a substance abuser. Both responses are flawed. An evidence-based model—where withdrawal is a homeostatic disruption, and addiction is a motivational disorder—provides a better foundation for clinical care by reducing stigma, enhancing diagnostic clarity, and guiding AD tapering.
What We Learned from Cocaine
In the 1970s and early 1980s, cocaine was often described in academic and clinical circles as “non-addictive,” solely because it did not produce a withdrawal syndrome like alcohol or opioids. However, this assumption failed to account for cocaine’s compulsive use, cravings, and high relapse rates. In groundbreaking work, Dackis and I proposed the dopamine depletion hypothesis in 1985, arguing that chronic cocaine use caused profound dysregulation in mesolimbic dopamine circuits, leading to anhedonia (extreme lack of emotion or feeling “flat,”) dysphoria (a generalized feeling of unease), and cue-triggered craving during abstinence. Cocaine addiction, we argued, is dominated by dopamine and emotional dysregulation, causing compulsive drug-seeking. These findings led to the reevaluation of cocaine and acknowledgment that physical withdrawal symptoms were not necessary for addiction, and also that cocaine is highly addictive.
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In addition, clonidine use for opioid detoxification illustrated that withdrawal symptoms can be pharmacologically eliminated by taking medication, without ever treating the addiction itself. In studies led by my colleagues and me, clonidine—a hypertension drug—was demonstrated to reverse opioid withdrawal symptoms. Clonidine helped cocaine patients tolerate detoxification with minimal physical distress. However, the underlying addictive processes—relapse, craving, conditioned cues, motivational drive—remained untouched. Clonidine has proven that eliminating withdrawal symptoms is not equivalent to curing addiction.
What Is Addiction?
The psychiatric manuals, the DSM-5 and the newer DSM-5-TR, define substance use disorders using 11 criteria, grouped into four domains: impaired control, social impairment, risky use, and pharmacological criteria (tolerance and withdrawal). Critically, DSM-5 makes it clear that addiction is primarily a disorder of reinforcement and motivation, not a physiologic reaction to discontinuation. Addiction reflects the hijacking of the motivational system—it’s not withdrawal symptoms that cause addiction.
Recognizing this distinction allows more precise tapering strategies for medications like antidepressants or suggesting alternative treatments for depression, like transcranial magnetic stimulation (TMS), Spravato, an esketamine nasal spray for depression, or cognitive behavioral treatment.
Conclusion
Substance use disorders (SUDs) are disorders of pathological attachment—mediated by reinforcement, bad learning, habit, and craving—they are not defined by physical dependence. Antidepressants prove withdrawal symptoms can occur in the absence of addiction. In addition, detox is a treatment easing withdrawal from some medications, but it’s no cure for addiction. Recognizing these distinctions decreases stigma and improves understanding of addiction.
