Why Do People Abuse Gabapentin? The Unseen Risks

Gabapentin gets abused primarily because, at high enough doses or in combination with other substances, it produces a euphoria that users describe as similar to an opioid high, along with deep relaxation and increased sociability. Originally approved for epilepsy and nerve pain, gabapentin was long considered to have virtually no abuse potential. That assumption has unraveled over the past decade as prescribing surged, misuse reports climbed, and forensic investigators started finding the drug in overdose deaths. The risks that come with gabapentin misuse are genuinely harder to see than those of classic drugs of abuse, and that invisibility is a large part of the problem.

What People Actually Feel When They Misuse Gabapentin

The most commonly reported experience from gabapentin misuse is a euphoria that users compare to opioids, though typically described as not quite as strong. A systematic review of misuse reports found this effect at doses ranging from roughly 1,500 to 12,000 mg, sometimes taken alone and sometimes alongside other drugs like buprenorphine, methadone, or alcohol.¹ For context, a typical prescribed dose for nerve pain is 900 to 1,800 mg per day, so the amounts people chase for a high often dwarf what a doctor would prescribe.

Beyond euphoria, people report deep sedation, calmness, and improved sociability. Some have described a marijuana-like high, a cocaine-like high, or even an effect reminiscent of MDMA. Others report increased energy and focus or simply better sleep.¹ Interviews with opioid users in South Florida found that gabapentin produces feelings reminiscent of alcohol intoxication or opioid euphoria for some, while others feel nothing beyond pain relief.² That unpredictability matters: the wide range of reported effects means some people are blindsided by how strong the drug feels while others dismiss the risk because they never experienced much themselves.

The Opioid Connection

Gabapentin misuse does not exist in a vacuum. It is tightly entangled with opioid use. In one study of psychiatric outpatients, about 16 percent overall reported having misused gabapentin, but when the researchers looked at people with an opioid use disorder specifically, that number jumped to 26 percent, compared with just 4 percent of those without one.³ This is not a coincidence. People in opioid recovery often discover that gabapentin softens withdrawal symptoms, and there is clinical evidence supporting that observation. Small trials have shown gabapentin can reduce the severity of heroin withdrawal symptoms and help patients complete detoxification.⁴⁵

So a person struggling with opioid dependence has two strong incentives to seek gabapentin: it eases the misery of withdrawal, and it can amplify the high from whatever opioids they are still using. That second point is where the danger escalates sharply. The combination of gabapentin and opioids does not just feel stronger; it creates additive respiratory depression, meaning both drugs are suppressing the brain’s drive to breathe. On top of that, opioids slow down the gut, and because gabapentin is absorbed through a narrow window in the upper small intestine, that slower transit time means more gabapentin gets absorbed than it otherwise would.⁶ It is a feedback loop: the opioid makes the gabapentin hit harder, and the gabapentin deepens the sedation and breathing suppression the opioid is already causing. Older adults are especially vulnerable to these combined sedative effects.⁷

Why Gabapentin’s Pharmacology Encourages Dose Escalation

Gabapentin has an unusual absorption quirk that shapes how people misuse it. It relies on a specific amino acid transporter in the upper small intestine to get into the body, and that transporter becomes saturated at higher doses. The result is that doubling the pill count does not double the amount that reaches the bloodstream.⁸ At therapeutic doses, this is actually a built-in safety feature: you cannot simply swallow more and get proportionally more drug. But people chasing a high find workarounds. Some stagger doses over several hours to avoid overwhelming the transporter. Others combine gabapentin with opioids, which, as noted above, slows the gut and effectively expands the absorption window. Some case reports have even documented nasal insufflation as a route of misuse, bypassing the gut entirely.⁹

At the cellular level, gabapentin works by binding to a part of voltage-gated calcium channels and, over time, reducing the number of those channels at the cell surface, which weakens excitatory signaling in the nervous system.¹⁰ This effect is chronic rather than immediate, meaning the drug does not slam the brakes on nerve signaling the way a benzodiazepine does. That slower onset likely contributes to the perception that gabapentin is harmless, even as the nervous system adapts to its presence over weeks and months.

Tolerance, Dependence, and a Withdrawal That Surprises Clinicians

One of the reasons gabapentin was long considered low-risk is that physical dependence was thought to be rare. The clinical reality has caught up. A qualitative systematic review of people who misuse gabapentinoids found that tolerance develops rapidly and that the withdrawal syndrome can be severe, often featuring psychiatric symptoms like intense anxiety, agitation, and insomnia.¹¹ A case series of people taking ultra-high doses documented dependence that met formal diagnostic criteria, along with physical complications including significant weight gain and edema.¹²

Withdrawal from gabapentin can be medically serious. In one striking case, a man on high-dose gabapentin and opioids developed acute respiratory failure and remained unconscious even after his breathing was stabilized. After other causes were excluded, the clinical team concluded he was experiencing gabapentin withdrawal encephalopathy.¹³ Reports like these are still uncommon enough that many emergency physicians do not have gabapentin withdrawal on their radar, which means it can go unrecognized.

How Gabapentin Became So Available

Gabapentin prescribing in the United States nearly doubled between 2009 and 2016, with increases in every state, some as high as 179 percent.¹⁴ A big driver of this explosion was off-label prescribing. An analysis of outpatient visits between 2011 and 2016 estimated that gabapentin was listed on roughly 130 million visits, but fewer than one percent of those visits involved an FDA-approved indication.¹⁵ Doctors were reaching for gabapentin to treat anxiety, insomnia, migraines, and various other pain conditions, partly because it was seen as a safer alternative to opioids and benzodiazepines. The irony is hard to miss: a drug promoted as a non-addictive option became widely available precisely because of fears about addictive drugs, and that wide availability became a pipeline for misuse.

Why Standard Drug Screens Miss It

If you go to an emergency room or a substance-use treatment center, a standard urine drug screen will not detect gabapentin. The immunoassay panels used in most clinical settings are designed to catch broad drug classes like opioids, benzodiazepines, and amphetamines, using antibodies targeted to the most common drugs in each class. Gabapentin does not belong to any of those classes, and the screening technology is not easily updated to include new drugs of concern.¹⁶ Detecting gabapentin requires a specific test, usually a confirmatory method that labs only run when clinicians specifically request it. This means gabapentin misuse is functionally invisible in the very settings where it is most likely to cause harm. A person in opioid treatment who is co-using gabapentin may pass every routine drug screen while their overdose risk climbs.

The Overdose Picture

Gabapentin is not especially lethal on its own. A poison center case series found that even at very high single doses, people who took gabapentin alone generally developed symptoms like drowsiness and dizziness that resolved within about ten hours, and none required hospital admission.¹⁷ The picture changes entirely when other substances are involved. Forensic studies of gabapentin-related deaths consistently find the same pattern: most fatalities involve multiple intoxicants, typically opioids, alcohol, benzodiazepines, or a combination.¹⁸ An autopsy-based review confirmed that combined substance exposure was the dominant pattern and that isolated gabapentinoid intoxication accounted for a minority of cases.¹⁹

This is what makes gabapentin’s role in overdose deaths so easy to underestimate. It rarely kills alone, but it reliably makes other drugs more dangerous. And because it does not show up on standard toxicology screens, its contribution to a death can go unrecorded unless a medical examiner specifically orders the test.

Gabapentin Versus Pregabalin

Pregabalin, gabapentin’s closely related cousin, is already a Schedule V controlled substance in the United States. A systematic review comparing the two found that pregabalin appeared to carry somewhat higher abuse potential, with more pronounced behavioral dependence, a greater tendency for people to transition from prescribed use to self-directed use, and more persistent self-administration.²⁰ Pregabalin’s absorption is not saturable the way gabapentin’s is, so higher doses translate more predictably into higher blood levels, making it easier to dial up effects. This difference helps explain why regulators moved on pregabalin first, but the growing evidence on gabapentin misuse has narrowed the perceived gap.

The Regulatory Tug-of-War

Several U.S. states have moved to classify gabapentin as a Schedule V controlled substance or to require its inclusion in prescription drug monitoring programs. These policies do reduce prescribing. In states that classified gabapentin as Schedule V, researchers found a reduction of about eight total days of gabapentin prescribed per Medicare enrollee, while monitoring-program requirements produced more modest reductions of about one day.²¹ In West Virginia, scheduling gabapentin as a controlled substance was linked to an immediate drop in the rate of gabapentin-involved fatal overdoses.²²

But the picture is not straightforwardly positive. A comprehensive analysis of scheduling laws across jurisdictions flagged evidence that in Kentucky, after gabapentin was scheduled, self-reported nonmedical use actually went up among people who use drugs. The primary source of gabapentin shifted from doctors to unregulated sellers on the street.²³ This mirrors what has happened with other controlled substances: restricting supply through legitimate channels can inadvertently push people toward riskier, less predictable sources. Meanwhile, patients who genuinely need gabapentin for epilepsy or neuropathic pain face additional hurdles getting their prescriptions filled.

Risks in Older Adults

Gabapentin is prescribed frequently to older adults for pain conditions, and this population faces a specific set of dangers. A study of older adults with cognitive impairment found that starting gabapentin was associated with about two and a half times the odds of falling within two years, compared with matched non-users.²⁴ Falls in this age group are a major cause of fractures, hospitalization, and decline in independence. The same study did not find that gabapentin accelerated cognitive or functional decline over the follow-up period, but an elevated fall risk alone is a serious clinical concern for someone who is already cognitively vulnerable. This is not about misuse; it is about the drug’s baseline sedative and balance-disrupting effects in people whose nervous systems are less resilient.

Neonatal Withdrawal

One of the least visible consequences of gabapentin misuse involves newborns. When a pregnant person takes gabapentin regularly, whether as prescribed or through misuse, the drug crosses the placenta. Neonatal gabapentin withdrawal has been documented in case reports, with symptoms including irritability and signs of neurological distress.²⁵ In pregnancies involving both opioids and gabapentin, the picture is more complicated. A case series identified 19 infants exposed to both drugs in utero, and 15 of them showed a distinctive pattern of symptoms not typical of opioid withdrawal alone: tongue thrusting, wandering eye movements, back arching, and continuous limb movements. Ten of those infants could not be weaned from methadone until gabapentin was added to their treatment, and attempts to taper gabapentin too quickly triggered relapse of the abnormal behaviors.²⁶

A cohort study with a meta-analysis looked at broader pregnancy outcomes. After adjusting for confounding factors, first-trimester gabapentin exposure was not linked to an increased risk of major malformations. However, gabapentin use during any trimester was associated with roughly double the risk of neonatal intensive care admission.²⁷ Because gabapentin is not a standard concern for obstetricians the way opioids are, these neonatal symptoms can catch medical teams off guard, delaying appropriate treatment.