Sedatives, Phenibut and Kratom

Most of the products on this site’s Dangerous Supplements pages are dangerous because of something hidden in them — a steroid, a stimulant, a heavy metal. The two on this page are different: what is on the label is the problem. Phenibut is a prescription sedative from the former Soviet Union, sold in the United States in bottles labelled “relaxation,” “sleep” or “focus.” Kratom is a Southeast Asian tree whose leaves contain compounds that act on the same receptors as morphine, sold in gas stations and smoke shops as powder, capsules, shots and gummies. Neither is a vitamin, a mineral, a food or a nutrient. The FDA says neither can lawfully be sold as a dietary supplement, and both can produce physical dependence and a withdrawal syndrome when stopped. This page explains what each one is, what the regulators have actually written, what the poison-centre and death-certificate data do and do not show, why an older adult is at particular risk from a “sleep supplement” that is really a sedative, and — because the kratom story is genuinely two-sided — what many users say they get from it and how thin the evidence is in both directions.

Table of Contents

  1. 1. Phenibut: What It Is and How It Reaches US Buyers
  2. 2. What the FDA Says About Phenibut
  3. 3. Tolerance, Dependence and the Withdrawal Syndrome
  4. 4. Sedation, Unsteadiness and Falls in Older Adults
  5. 5. Phenibut With Alcohol, Benzodiazepines and Opioids
  6. 6. Kratom: The Plant and Its Alkaloids
  7. 7. How Kratom Is Sold, and What the FDA Says
  8. 8. Concentrated 7-OH: A Different Product (2025–2026)
  9. 9. What the Death Counts Do and Do Not Show
  10. 10. Kratom Dependence, Withdrawal and the Liver
  11. 11. The Fair Note: Why People Take Kratom, and How Thin the Evidence Is
  12. 12. Interactions, and Who Must Avoid Both
  13. 13. What to Do
  14. 14. The Honest Bottom Line
  15. Research Papers
  16. Connections
  17. Featured Videos

1. Phenibut: What It Is and How It Reaches US Buyers

Phenibut (β-phenyl-γ-aminobutyric acid) is GABA — the brain’s main calming neurotransmitter — with a phenyl ring attached so that it can cross from the blood into the brain, which plain GABA does poorly. It was discovered and brought into clinical practice in Russia in the 1960s, where it is a prescription medicine for anxiety, tension, fear and poor sleep, and where it is also given before and after surgery. Pharmacologically it is a close relative of baclofen, the muscle relaxant; both act mainly on the GABA-B receptor, with a lesser effect on GABA-A, the receptor that benzodiazepines and alcohol act on (Lapin, 2001). It has never been approved as a medicine in the United States, the European Union, the United Kingdom, Canada or Australia.

It reaches American buyers through the internet and through “nootropic” and sleep-and-relaxation product lines. A 2015 survey of English-language online sellers found 48 unrelated suppliers offering phenibut in quantities from a 5-gram sachet to a 1,000-kilogram order, and capsules of 200–500 mg in packs of 6 to 360. The users describing their experiences on drug forums took it for its anti-anxiety and euphoric effects, at an average dose of about 2.4 grams, and the adverse effects they reported most often were tolerance and withdrawal (Owen et al., 2016). The CDC’s summary of US poison-centre calls describes the products as “advertised for anxiety, relaxation, and sleep” and notes that phenibut “is uncontrolled and legal to possess in the United States” while “not approved as a licensed pharmaceutical drug” (Graves et al., 2020).

The practical point for a reader is that a capsule sold as a sleep aid can contain a full pharmacological dose of a prescription-strength sedative, with no prescriber, no pharmacist and no dosing instructions written by anyone accountable for them. On a label it may appear as phenibut, fenibut, phenigam, PhGABA, β-phenyl-GABA, or 4-amino-3-phenylbutanoic acid — the FDA lists these aliases on its phenibut page.

2. What the FDA Says About Phenibut

A dietary supplement may only contain “dietary ingredients” as the law defines them: vitamins, minerals, herbs and other botanicals, amino acids, substances that supplement the diet, and their concentrates, extracts and combinations. Phenibut is none of those. On April 10, 2019 the FDA issued 12 warning letters to supplement companies in a single action; nine concerned the stimulant DMHA and three concerned phenibut. The three phenibut letters went to Atomixx (for a product called Limitless), Evol Nutrition Associates, Inc., doing business as Red Dawn Energy, and NeuroScience Solutions, Inc., doing business as NeuroScience. The letter to Atomixx states the agency’s reasoning in one sentence:

“Because phenibut does not fit in any of the dietary ingredient categories under section 201(ff)(1) of the Act, it is not a dietary ingredient as defined in the Act.”

The FDA’s standing page on phenibut puts the consequence the same way: “Because phenibut does not fit any of the categories of dietary ingredients under the FD&C Act, any dietary supplements that declare phenibut as a dietary ingredient are misbranded.” A misbranded product is one whose labelling is false or misleading, and the companies were given 15 business days to say how they would bring their products into compliance. Both documents are linked under Regulatory Records below.

What this does not mean is also worth stating plainly. The FDA did not ban phenibut; it is not a controlled substance; possessing it is legal, and it is still easy to buy. What the record establishes is narrower and, for a shopper, more useful: any bottle that calls phenibut a dietary ingredient is, in the agency’s own words, misbranded, and no amount of “natural,” “nootropic” or “relaxation” language on the front changes that.

3. Tolerance, Dependence and the Withdrawal Syndrome

The two adverse effects users themselves report most often are tolerance — needing more to get the same effect — and withdrawal when they stop (Owen et al., 2016). That is exactly what one would expect from a drug that acts on GABA receptors, because it is the same pattern seen with benzodiazepines, alcohol and baclofen: the brain adapts to a constant calming signal by turning its own down, and when the drug is removed the nervous system runs hot.

A review by anaesthesiologists at the Mayo Clinic gathered the 22 published cases of acute phenibut withdrawal. The consistent picture was severe psychomotor agitation, often needing physical restraint and several sedating drugs at once, along with psychosis, hallucinations, delirium and seizures; nausea, vomiting and a racing heart; and in some cases rigidity, exaggerated reflexes, unstable blood pressure, fever and muscle jerking — a picture the authors note “may mimic serotonin or neuroleptic malignant syndrome,” two emergencies that an emergency physician might think of first if nobody mentions the supplement. Patients were typically young, and many were also using other drugs (Hardman, Sprung & Weingarten, 2019). The CDC’s poison-centre summary describes the same syndrome in fewer words: “withdrawal symptoms including anxiety, agitation, and acute psychosis” (Graves et al., 2020). At the Minnesota poison centre, about one call in ten about phenibut was a withdrawal call rather than an overdose (McCabe et al., 2019).

The daily intakes in the published cases are measured in grams, not milligrams, and the withdrawal syndrome is a consequence of weeks of regular use rather than a single dose. That is the trap: a product sold as a sleep aid is taken nightly, precisely the pattern that produces dependence, and the person who then decides to stop it “because it’s only a supplement” can walk into the syndrome above. The treatments the Mayo review lists — benzodiazepines, phenobarbital, dexmedetomidine and antipsychotics in the acute phase, then baclofen, gabapentin, pregabalin or clonidine for a taper — are all prescription drugs given in hospital. Section 13 explains what to do instead of stopping abruptly.

4. Sedation, Unsteadiness and Falls in Older Adults

Everything above concerns mostly young men: in the national poison-centre series, 58% of phenibut exposures were in adults aged 18–34 and three-quarters were male (Graves et al., 2020). But phenibut is marketed for sleep, and the people who buy sleep aids are disproportionately older. Their risk is different in kind. In the national series, drowsiness or lethargy was reported in 29% of cases, confusion in 21%, and coma in 6% — 80 people — and the CDC describes “sedation, respiratory depression, and reduced levels of consciousness” as characteristic effects (Graves et al., 2020). For an older adult the relevant outcome is not usually the coma; it is the fall on the way to the bathroom at 3 a.m.

Falls are the leading cause of injury and injury death in Americans aged 65 and over. In 2014, 28.7% of older adults reported falling; the estimated 29 million falls produced 7 million injuries, 2.8 million emergency-department visits, roughly 800,000 hospital admissions and about 27,000 deaths (Bergen, Stevens & Burns, 2016). Sedating medicines are one of the best-established modifiable causes. A meta-analysis of 22 studies covering 79,081 older people found that sedatives and hypnotics raised the odds of falling by 47% and benzodiazepines by 57%, with antidepressants and antipsychotics in the same range (Woolcott et al., 2009). Phenibut is not in those studies because it is not a prescribed drug in the countries where they were done, but it is a GABA-receptor sedative with a longer duration of action than most of them, and there is no pharmacological reason to expect it to be gentler.

The reason a supplement version is arguably worse than the prescription it imitates is the missing conversation. When a physician prescribes a sleeping pill to a 75-year-old, the guidelines push back, the pharmacist counsels about night-time falls, the dose is the lowest that works, and the medicine appears on the medication list that every other doctor sees. A bottle bought online carries none of that. The CDC’s recommended fall-prevention steps include a medication review specifically to find and reduce sedating drugs (Bergen et al., 2016); a phenibut product will only be reviewed if the person mentions it. If you or a parent take anything for sleep that comes from a supplement shelf, put it on the medication list by name.

5. Phenibut With Alcohol, Benzodiazepines and Opioids

Two sedatives add up. Phenibut acts on GABA-B and, to a lesser extent, GABA-A; alcohol, benzodiazepines (alprazolam, diazepam, lorazepam, clonazepam), the “Z-drugs” for sleep (zolpidem and relatives), gabapentin and pregabalin, baclofen and the sedating antihistamines in over-the-counter “PM” products all depress the same system by overlapping routes, and opioids depress breathing by a separate one. Together they push toward the outcome the Minnesota series documented: of 56 phenibut calls to that one poison centre, 11 patients (19.6%) needed a breathing tube (McCabe et al., 2019). Nationally, co-ingestants were present in 40% of adult phenibut cases, one case in eight was classified as a major, life-threatening effect, and three deaths were recorded over the eleven years — one with phenibut as the only agent (Graves et al., 2020).

Those numbers describe a drug that rarely kills on its own and becomes considerably more dangerous in company. The combination that matters most for the sleep-aid buyer is the ordinary one: a glass or two of wine in the evening and a “relaxation” capsule at bedtime. Both are GABA sedatives; the wine makes the capsule stronger and the capsule makes the wine stronger, and neither the wine bottle nor the capsule bottle says so. The rule is simple: phenibut is never combined with alcohol, a benzodiazepine, a sleeping pill, an opioid or a muscle relaxant — and anyone already prescribed one of those has no safe place for phenibut at all.

6. Kratom: The Plant and Its Alkaloids

Kratom is the leaf of Mitragyna speciosa, a tree in the coffee family native to Thailand, Malaysia and Indonesia, where labourers have chewed the leaves or brewed them as tea for generations for stimulation at low doses and pain relief and calm at higher ones. The leaf contains dozens of alkaloids. Two matter pharmacologically: mitragynine, the most abundant, and 7-hydroxymitragynine (7-OH), a minor constituent that is far more potent. Both are partial agonists at the mu-opioid receptor — the receptor morphine, oxycodone and fentanyl act on — and antagonists at the kappa and delta opioid receptors. They are also “G-protein-biased,” a signalling pattern that in laboratory work is associated with less suppression of breathing than classical opioids produce, and they act on adrenergic, serotonin and dopamine receptors as well, which is why raw kratom does not feel or behave quite like a conventional opioid (Kruegel & Grundmann, 2018).

“Partial agonist” is the key phrase, and it cuts both ways. It means the compounds turn the receptor on less fully than morphine does, which is the plausible reason kratom alone rarely stops someone breathing. It does not mean the receptor is not being activated: tolerance, dependence, withdrawal and the reinforcing pull that leads to daily use all follow from mu-opioid activation whether it is partial or full. A traditional Malaysian kratom drink delivers about 79 mg of mitragynine per glass, and regular users there average roughly three glasses a day (Singh, Müller & Vicknasingam, 2014). American users of powdered leaf most often take 1–3 grams per dose (Garcia-Romeu et al., 2020), but there is no standardisation: the alkaloid content of a bag of “kratom” depends on the strain, the age of the leaf, the drying and any concentration step, and nothing on the package is required to tell you.

7. How Kratom Is Sold, and What the FDA Says

Kratom is sold as loose powder, capsules, teas, liquid “shots,” extracts and, increasingly, tablets and gummies, at smoke shops, vape shops, gas stations, convenience stores and online, usually with no dose on the label beyond a serving size and often with a “not for human consumption” disclaimer that exists for legal rather than safety reasons. It is not a scheduled controlled substance under federal law (a handful of states and cities restrict or ban it), which is why it can sit on a counter next to the energy drinks.

The FDA’s position is on its “FDA and Kratom” page, updated December 2025 and linked below: “Kratom is not lawfully marketed in the U.S. as a drug product, a dietary supplement, or a food additive in conventional food.” The agency says it has “warned consumers not to use kratom because of the risk of serious adverse events, including liver toxicity, seizures, and substance use disorder,” that “in rare cases, deaths have been associated with kratom use, as confirmed by a medical examiner or toxicology reports,” and that newborns exposed during pregnancy have shown withdrawal signs. On February 6, 2018, Commissioner Scott Gottlieb published the scientific basis for that stance: a computational model “predicted that 22 (including mitragynine) of the 25 compounds in kratom bind to mu-opioid receptors,” the agency had “44 reported deaths associated with the use of kratom,” and “there is no evidence to indicate that kratom is safe or effective for any medical use.” His summary sentence was that “compounds in kratom make it so it isn’t just a plant — it’s an opioid.” That statement has since been removed from fda.gov; the link below goes to the FDA’s own archive copy.

The FDA has also acted against the claims, which is where the record is most concrete. In June 2019 it sent warning letters to two kratom sellers for marketing their products as treatments for opioid addiction and withdrawal, pain, depression, anxiety and even cancer. The letter to Cali Botanicals, LLC (June 11, 2019) quotes the company’s own website — “Kratom has essential uses in combating opiate addiction and the harrowing withdrawal that comes with trying to kick the habit” — and concludes that such claims make the products unapproved new drugs. That is the pattern to recognise on any kratom package or website: the moment it promises to treat withdrawal, pain or anxiety, it is making a drug claim that no kratom product has ever been permitted to make.

8. Concentrated 7-OH: A Different Product (2025–2026)

Since about 2023 a new category has appeared in the same gas-station display: tablets, gummies, drink mixes, shots and dissolving films sold as “7” or “7-OH,” containing 7-hydroxymitragynine that has been concentrated or made semi-synthetically from mitragynine. This is not kratom leaf in a different shape. In the natural leaf, 7-OH is a trace alkaloid — less than two per cent of the total alkaloid content, as the DEA’s 2026 notice puts it — and the FDA states that it “demonstrates substantially greater mu-opioid receptor potency than kratom’s primary alkaloid constituent mitragynine, as well as other classical opioids such as morphine.” In animal studies, 7-OH is self-administered the way morphine is and increases subsequent morphine intake, whereas mitragynine is not self-administered and reduces it (Hemby et al., 2019). In plain terms: a leaf-kratom tea is a weak partial opioid with a mixed profile; a 7-OH tablet is a potent opioid in a candy wrapper.

The regulatory response was fast by the standards of this field. On July 15, 2025 the FDA sent warning letters to seven companies selling 7-OH tablets, gummies, drink mixes and shots, stating that “7-OH is not lawful in dietary supplements and cannot be lawfully added to conventional foods” and that “there are no FDA-approved drugs containing 7-OH.” On July 29, 2025 the Commissioner announced that the FDA was “recommending a scheduling action to control certain 7-hydroxymitragynine (also known as 7-OH) products under the Controlled Substances Act,” describing 7-OH as “an opioid that can be more potent than morphine” sold “online and in gas stations, corner stores and vape shops,” and stating explicitly that the agency was “not focused on natural kratom leaf products.” On July 6, 2026 the DEA published in the Federal Register a notice of intent to place 7-OH temporarily in Schedule I above a threshold: kratom plant material containing more than 0.050% 7-OH on a dry-weight basis, or any other article containing more than 0.050% or more than 1.00 mg of 7-OH. The notice describes the products as sold at “gas stations and smoke shops, in various forms, including powders, tablets, gummies, and sublingual films designed for rapid absorption,” states that “no controlled clinical trials have been conducted to establish safe consumption limits or standardized dosing,” and that “fatal overdoses involving 7-hydroxymitragynine have been reported.” The FDA’s 7-OH page adds that the action is not intended to apply to natural kratom leaf containing only naturally occurring trace levels. As of this writing the temporary order was still working through the Federal Register process; the primary documents are linked below and will show its current status.

For a reader the lesson is a label-reading one. “Kratom” on a package no longer tells you what is inside. A product that names 7-hydroxymitragynine, “7-OH,” or a milligram amount of it, or that describes itself as an “enhanced,” “extract” or “super” tablet, should be treated as an opioid of unknown strength — and, once the DEA order takes effect, very likely as a Schedule I controlled substance.

9. What the Death Counts Do and Do Not Show

The most-quoted kratom statistic is the CDC’s, and it deserves to be quoted exactly. Using the State Unintentional Drug Overdose Reporting System, the CDC examined 27,338 overdose deaths in 27 states between July 2016 and December 2017. Kratom was detected on post-mortem toxicology in 152 of them (0.56%). Medical examiners or coroners listed kratom as a cause of death in 91 of the 152. In seven of the 152, kratom was the only substance that tested positive — with the report’s own caveat that “the presence of additional substances cannot be ruled out.” Among the kratom-positive deaths, fentanyl or fentanyl analogues were also listed as a cause in 65%, heroin in 33%, benzodiazepines in 22%, prescription opioids in 20% and cocaine in 18%. About 80% of the decedents had a history of substance misuse and roughly 90% had no evidence of current medically supervised treatment (Olsen et al., 2019).

What those numbers prove: kratom is present in a small fraction of overdose deaths, overwhelmingly alongside fentanyl, heroin or benzodiazepines, in people already living with a substance use disorder. What they do not prove: that kratom alone caused those deaths. “Kratom-positive” and “kratom-caused” are different claims, and the seven single-substance cases are too few, and too incompletely characterised, to settle the second one either way. The poison-centre data point the same direction: of 1,807 kratom exposures reported to US poison centres from 2011 to 2017, there were 11 deaths, two after exposure to kratom only, and exposures involving more than one substance had nearly three times the odds of hospital admission (Post et al., 2019). The pharmacology review that preceded these reports concluded that “kratom exposure alone has not been causally associated with human fatalities to date” (Kruegel & Grundmann, 2018), a statement that was fair when written and is now harder to make, given the 7-OH products and the FDA’s medical-examiner-confirmed cases.

So neither slogan is honest. “Kratom kills” overstates a record in which nearly every death involved fentanyl or a sedative. “Nobody has ever died from kratom” ignores the single-substance cases, the concentrated products, and the plain fact that a partial opioid taken with a full one makes the full one more dangerous. The defensible reading is that leaf kratom alone rarely causes fatal overdose, and kratom in combination with opioids, benzodiazepines or alcohol is where the deaths are.

10. Kratom Dependence, Withdrawal and the Liver

Dependence is not rare, and it is dose-related. In the first systematic study of regular kratom users, 293 people in northern Malaysia who had used it for more than six months were assessed with standard dependence and withdrawal questionnaires: more than half met criteria for severe dependence and 45% for moderate dependence. The physical withdrawal symptoms they described were muscle spasms and pain, difficulty sleeping, watery eyes and nose, hot flashes, fever, loss of appetite and diarrhoea; the psychological ones were restlessness, tension, anger, sadness and nervousness — recognisably the opioid withdrawal syndrome in a milder key. People drinking three or more glasses a day had higher odds of all of it (Singh et al., 2014). Among 2,798 mostly American survey respondents, 59% used kratom daily, about a third reported adverse effects (mostly mild and lasting under a day), 0.6% had sought treatment for them, and 2% met DSM-5 criteria for a moderate or severe kratom use disorder in the past year (Garcia-Romeu et al., 2020). Those two studies describe different populations — heavy traditional users versus self-selected online respondents — and the truth for any individual depends on dose and duration, exactly as it does with prescription opioids. Newborns can be affected too: seven neonatal kratom exposures were reported to poison centres in 2011–2017, five with withdrawal (Post et al., 2019).

The liver is a separate, less common harm. The US Drug-Induced Liver Injury Network identified eleven cases of liver injury attributed to kratom, with a recent increase; all were jaundiced, the median time from starting kratom to illness was 14 days, most needed hospital admission, and all eventually recovered (Ahmad et al., 2021). Supplement-related liver injury as a whole — how it presents, which products are most often responsible, and what to ask for at the lab — is the subject of the sibling page Liver Injury from Supplements.

11. The Fair Note: Why People Take Kratom, and How Thin the Evidence Is

Any honest page has to say why millions of Americans use kratom, because the answer is not recklessness. In the largest survey, respondents used it for pain (91%), anxiety (67%) and depression (65%), and 1,144 of the 2,798 — 41% — used it to stop or reduce prescription or illicit opioid use, reporting less withdrawal and craving; 411 of them attributed more than a year of continuous abstinence from opioids to it (Garcia-Romeu et al., 2020). Many of these people were prescribed opioids for years and then cut off; some could not get or afford buprenorphine or methadone; some find that kratom lets them work. Telling them it is “just an opioid” misses that they know, and that it is the least bad option they have found. The pharmacology is at least consistent with their account: a partial agonist that blunts withdrawal while producing less respiratory depression is exactly what a substitution therapy is, and buprenorphine is one.

And yet the evidence for that use is almost entirely what users say about themselves. Surveys recruited through kratom-advocacy channels cannot measure the people for whom it went badly, cannot separate the plant’s effect from the expectation of it, and cannot tell a chronically painful back that improved from one that would have improved anyway. There are no adequately sized controlled trials showing that kratom treats opioid withdrawal or chronic pain, and no product with a known, consistent dose to run them on. The evidence for harm has the mirror-image weakness: case reports, poison-centre calls and death certificates, which record the people who came to attention and nothing about the far larger number who did not. The FDA’s sentence — no evidence that kratom is safe or effective for any medical use — is literally true, and it is equally true that no one has done the studies that would produce such evidence. A reader deserves to know that both sides of this argument are standing on thin ice, and that the thinnest ice of all is under the concentrated 7-OH products, for which no human safety data exist at all.

12. Interactions, and Who Must Avoid Both

Kratom and prescription medicines. Mitragynine inhibits two of the liver enzymes that clear a large share of common drugs. It is a strong competitive inhibitor of CYP2D6 and a time-dependent inhibitor of CYP3A in both the liver and the gut wall, meaning the block deepens with repeated dosing; modelling a 2-gram kratom dose predicted a 5.7-fold rise in blood levels of midazolam, a CYP3A test drug (Tanna et al., 2021). CYP3A handles many benzodiazepines (alprazolam, midazolam, triazolam), several opioids (oxycodone, fentanyl, methadone), many statins, calcium-channel blockers and immunosuppressants; CYP2D6 handles codeine, tramadol, many antidepressants and beta-blockers. Raising the level of a sedative or an opioid you are already taking is the same danger as adding a second one. The deaths in section 9 are consistent with this: a partial opioid that also raises the blood level of a full one.

Phenibut and other sedatives is section 5; the rule there needs no repeating. Who should not take either substance at all:

13. What to Do

If you have been taking phenibut regularly for weeks, do not stop abruptly. The withdrawal syndrome in section 3 — agitation, insomnia, hallucinations, psychosis, seizures — is a medical emergency, and it is precisely the people who took it every night for sleep who are at risk. Tell a physician what you have been taking, how much and for how long, and ask for a supervised taper. The agents clinicians use for that purpose are baclofen (phenibut’s closest prescription relative), gabapentin or pregabalin, clonidine and, where needed, a benzodiazepine, brought down over weeks (Hardman et al., 2019). Do not attempt a taper with more phenibut bought online; the dose in a scoop of powder is unknown. If withdrawal has already begun — severe agitation, confusion, hallucinations, a seizure — go to an emergency department and make sure the word “phenibut” is said out loud and written down, because the picture mimics other emergencies.

If you have been taking kratom daily, stopping is safer than stopping phenibut but not pleasant, and relapse is common. Tapering the daily dose works for many people. If you were using kratom to stay off opioids, an addiction-medicine clinician can offer buprenorphine, which does the same pharmacological job with a known dose, a known safety record and a prescriber; if the reason was pain, say so, because untreated pain is what sent most users to the gas station in the first place. A liver panel is reasonable for anyone who has used kratom for months, and essential if there is dark urine, pale stools, itching or yellow eyes.

If someone has taken either substance and is hard to wake, breathing slowly, or has had a seizure, call 911. For any other question about an exposure — a child who got into a bag of powder, an older relative who took a “relaxation” capsule with wine, a dose that seems far too large — call Poison Control at 1-800-222-1222, free and staffed around the clock. And whatever you take, put it on your medication list by its real name. Phenibut and kratom are only invisible to your doctor and pharmacist if you leave them off.

14. The Honest Bottom Line

Phenibut is a prescription sedative sold without a prescription. The FDA has said in writing that it is not a dietary ingredient and that any supplement declaring it is misbranded. It works for anxiety and sleep the way any GABA sedative does, and it produces tolerance, dependence and a withdrawal syndrome severe enough to need hospital care the way any GABA sedative does — with the difference that no one who sells it will tell you so. For an older adult it carries the fall risk of a sleeping pill without the safeguards that come with one. There is no dose at which it is a “supplement.”

Kratom is a mild partial opioid from a plant, sold without a dose. On its own it rarely causes fatal overdose; combined with opioids, benzodiazepines or alcohol it is part of a real, if small, death toll; taken daily it produces dependence in a substantial share of users; and in rare cases it injures the liver. Many people use it to manage pain or stay off stronger opioids, and their reports deserve respect that the evidence base cannot yet back up in either direction. The concentrated 7-OH tablets and gummies that now share its shelf are a different product — a potent opioid the FDA and DEA are moving to schedule — and should be treated as one. If a package promises to cure withdrawal, treat pain or ease anxiety, the promise is the warning sign: it is the claim the FDA has already acted against, and it tells you the seller knows what they are really selling.

Back to Table of Contents

Research Papers

  1. Lapin I. Phenibut (β-phenyl-GABA): a tranquilizer and nootropic drug. CNS Drug Rev. 2001;7(4):471-481. doi:10.1111/j.1527-3458.2001.tb00211.x — the pharmacology and Russian clinical history: introduced in the 1960s, GABA-B agonist with lesser GABA-A activity, a close relative of baclofen.
  2. Owen DR, Wood DM, Archer JRH, Dargan PI. Phenibut (4-amino-3-phenyl-butyric acid): availability, prevalence of use, desired effects and acute toxicity. Drug Alcohol Rev. 2016;35(5):591-596. doi:10.1111/dar.12356 — 48 online suppliers, 200–500 mg capsules, average dose 2.4 g; tolerance and withdrawal the most commonly reported adverse effects.
  3. Graves JM, Dilley J, Kubsad S, Liebelt E. Notes from the field: phenibut exposures reported to poison centers — United States, 2009–2019. MMWR Morb Mortal Wkly Rep. 2020;69(35):1227-1228. doi:10.15585/mmwr.mm6935a5 — 1,320 exposures, rising sharply since 2015; agitation 30%, drowsiness 29%, coma 6%; major effects 12.6%; three deaths, one with phenibut alone.
  4. McCabe DJ, Bangh SA, Arens AM, Cole JB. Phenibut exposures and clinical effects reported to a regional poison center. Am J Emerg Med. 2019;37(11):2066-2071. doi:10.1016/j.ajem.2019.02.044 — 56 Minnesota calls over 19 years, 86% in the last five; 19.6% intubated; 10.7% withdrawal calls; co-ingestants in 36%.
  5. Hardman MI, Sprung J, Weingarten TN. Acute phenibut withdrawal: a comprehensive literature review and illustrative case report. Bosn J Basic Med Sci. 2019;19(2):125-129. doi:10.17305/bjbms.2018.4008 — 22 published withdrawal cases: severe psychomotor agitation, psychosis, hallucinations, delirium, seizures, autonomic instability; may mimic serotonin or neuroleptic malignant syndrome; the drugs used to treat it.
  6. Bergen G, Stevens MR, Burns ER. Falls and fall injuries among adults aged ≥65 years — United States, 2014. MMWR Morb Mortal Wkly Rep. 2016;65(37):993-998. doi:10.15585/mmwr.mm6537a2 — 28.7% of older adults fell in 2014; 29 million falls, 7 million injuries, 2.8 million ED visits, ~800,000 admissions, ~27,000 deaths; medication review is a core prevention step.
  7. Woolcott JC, Richardson KJ, Wiens MO, et al. Meta-analysis of the impact of 9 medication classes on falls in elderly persons. Arch Intern Med. 2009;169(21):1952-1960. doi:10.1001/archinternmed.2009.357 — 22 studies, 79,081 people: sedatives/hypnotics OR 1.47, benzodiazepines OR 1.57 for falls.
  8. Kruegel AC, Grundmann O. The medicinal chemistry and neuropharmacology of kratom: a preliminary discussion of a promising medicinal plant and analysis of its potential for abuse. Neuropharmacology. 2018;134(Pt A):108-120. doi:10.1016/j.neuropharm.2017.08.026 — mitragynine and 7-OH are G-protein-biased partial mu-opioid agonists and kappa/delta antagonists; as of 2017 kratom alone had not been causally linked to a death.
  9. Hemby SE, McIntosh S, Leon F, Cutler SJ, McCurdy CR. Abuse liability and therapeutic potential of the Mitragyna speciosa (kratom) alkaloids mitragynine and 7-hydroxymitragynine. Addict Biol. 2019;24(5):874-885. doi:10.1111/adb.12639 — in rats, 7-OH is self-administered and increases later morphine intake; mitragynine is not, and reduces it.
  10. Olsen EO, O’Donnell J, Mattson CL, Schier JG, Wilson N. Notes from the field: unintentional drug overdose deaths with kratom detected — 27 states, July 2016–December 2017. MMWR Morb Mortal Wkly Rep. 2019;68(14):326-327. doi:10.15585/mmwr.mm6814a2 — kratom detected in 152 of 27,338 overdose deaths (0.56%); listed as a cause in 91; the only substance detected in 7; fentanyl in 65%.
  11. Post S, Spiller HA, Chounthirath T, Smith GA. Kratom exposures reported to United States poison control centers: 2011–2017. Clin Toxicol (Phila). 2019;57(10):847-854. doi:10.1080/15563650.2019.1569236 — 1,807 exposures, two-thirds in 2016–2017; 11 deaths, 2 kratom-only; multi-substance exposures OR 2.80 for admission; 7 neonatal exposures, 5 with withdrawal.
  12. Singh D, Müller CP, Vicknasingam BK. Kratom (Mitragyna speciosa) dependence, withdrawal symptoms and craving in regular users. Drug Alcohol Depend. 2014;139:132-137. doi:10.1016/j.drugalcdep.2014.03.017 — 293 Malaysian regular users: over half severely dependent, 45% moderately; the physical and psychological withdrawal syndrome; ~79 mg mitragynine per glass.
  13. Garcia-Romeu A, Cox DJ, Smith KE, Dunn KE, Griffiths RR. Kratom (Mitragyna speciosa): user demographics, use patterns, and implications for the opioid epidemic. Drug Alcohol Depend. 2020;208:107849. doi:10.1016/j.drugalcdep.2020.107849 — 2,798 users: pain 91%, anxiety 67%, depression 65%; 41% used it to reduce or stop opioids; 2% met criteria for a kratom use disorder.
  14. Ahmad J, Odin JA, Hayashi PH, et al.; Drug-Induced Liver Injury Network. Liver injury associated with kratom, a popular opioid-like product: experience from the U.S. Drug Induced Liver Injury Network and a review of the literature. Drug Alcohol Depend. 2021;218:108426. doi:10.1016/j.drugalcdep.2020.108426 — 11 cases, all jaundiced, median latency 14 days, most hospitalised, all recovered.
  15. Tanna RS, Tian DD, Cech NB, et al. Refined prediction of pharmacokinetic kratom-drug interactions: time-dependent inhibition considerations. J Pharmacol Exp Ther. 2021;376(1):64-73. doi:10.1124/jpet.120.000270 — mitragynine is a strong CYP2D6 inhibitor and a time-dependent CYP3A inhibitor; a 2 g dose predicted to raise midazolam exposure 5.7-fold.

Regulatory Records

  1. FDA. Phenibut in Dietary Supplements — the agency’s standing page: not a dietary ingredient, products declaring it are misbranded; label aliases; the three April 2019 warning letters. fda.gov
  2. FDA. FDA Acts on Dietary Supplements Containing DMHA and Phenibut, constituent update, 10 April 2019 — 12 warning letters, three for phenibut (Atomixx; Evol Nutrition Associates d/b/a Red Dawn Energy; NeuroScience Solutions d/b/a NeuroScience). fda.gov
  3. FDA. Warning letter to Atomixx, 10 April 2019 — the sentence quoted in section 2 on why phenibut is not a dietary ingredient under section 201(ff)(1). fda.gov
  4. FDA. FDA and Kratom — the agency’s current position (updated December 2025): not lawfully marketed as a drug, dietary supplement or food additive; liver toxicity, seizures, substance use disorder; medical-examiner-confirmed deaths; neonatal withdrawal; 7-OH potency. fda.gov
  5. FDA. Statement from FDA Commissioner Scott Gottlieb, M.D., on the agency’s scientific evidence on the presence of opioid compounds in kratom, 6 February 2018 — the 22-of-25 compounds model, 44 reported deaths, “it’s an opioid.” Removed from the live site; this is the FDA Archive’s capture. FDA Archive (archive-it.org)
  6. FDA. Warning letter to Cali Botanicals, LLC, 11 June 2019 — opioid-addiction, withdrawal, pain and cancer claims make the kratom products unapproved new drugs. fda.gov
  7. FDA. FDA Issues Warning Letters to Firms Marketing Products Containing 7-Hydroxymitragynine, 15 July 2025 — seven companies; tablets, gummies, drink mixes and shots; “7-OH is not lawful in dietary supplements.” fda.gov
  8. FDA. FDA Takes Steps to Restrict 7-OH Opioid Products Threatening American Consumers, 29 July 2025 — the scheduling recommendation; “more potent than morphine”; “not focused on natural kratom leaf products.” fda.gov
  9. FDA. Hiding in Plain Sight: 7-OH Products — the agency’s 7-OH page (updated July 2026), including the DEA’s 1 July 2026 announcement and the note that natural leaf with trace 7-OH is not the target. fda.gov
  10. DEA. Schedules of Controlled Substances: Temporary Placement of 7-Hydroxymitragynine Above a Specified Threshold in Schedule I — notice of intent, Federal Register, 6 July 2026 (FR Doc. 2026-13580): the 0.050% dry-weight and 1.00 mg thresholds, the retail description, and “fatal overdoses involving 7-hydroxymitragynine have been reported.” federalregister.gov · govinfo.gov (PDF)

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