Why Does Ashwagandha Make Me Feel High?

Ashwagandha activates the same family of brain receptors that anti-anxiety drugs like benzodiazepines target, and it raises levels of serotonin and dopamine in animal models. That combination can produce a floaty, relaxed, mildly euphoric sensation that some people describe as feeling “high.” The effect is not identical to cannabis or alcohol intoxication, but the underlying neurochemistry overlaps enough that the comparison makes sense. Whether the feeling is pleasant or alarming depends on dose, individual metabolism, and what else you are taking.

Ashwagandha Acts on the Same Receptors as Sedatives

The most direct explanation for the altered feeling is GABA. Gamma-aminobutyric acid is the brain’s main inhibitory chemical messenger, the one responsible for calming neural activity. Benzodiazepines, alcohol, and sleep medications all work partly by enhancing GABA signaling, and each of them can make you feel sedated, relaxed, or intoxicated depending on the dose. Ashwagandha does something similar, though less powerfully.

Lab studies using mammalian GABA-A receptors have shown that a water extract of ashwagandha directly activates these receptors, producing measurable ion currents. The effect was blocked by bicuculline, a known GABA-A antagonist, confirming that the activation is genuinely GABAergic rather than some unrelated chemical coincidence. Interestingly, the two most famous individual compounds in ashwagandha, withanolide A and witaferin A, did not activate the receptors on their own, suggesting that the GABA effect comes from other, less-studied constituents in the whole extract.¹ Molecular modeling research has since pointed to smaller alkaloids like hygrine, tropine, and withasomnine as promising GABA-A agonist candidates.²

In a sleep-focused experiment, ashwagandha extract increased gene expression of GABA-A receptors and promoted non-REM sleep with a slow-wave EEG pattern, the kind of deep, restorative sleep that the brain enters when GABA activity is high.³ For someone who takes ashwagandha during the day, especially at a higher dose, that same GABA-boosting action can feel less like restful sleepiness and more like a detached, dreamy, or mildly intoxicated state.

Serotonin and Dopamine Get a Boost Too

GABA alone does not explain the whole picture. Ashwagandha also influences the monoamine neurotransmitters, serotonin and dopamine, that regulate mood, motivation, and reward. In a mouse study using chronic mild stress to model depression, a high-dose ashwagandha root extract raised brain dopamine levels by about 24% and serotonin levels by about 36% compared to stressed controls. It also suppressed MAO-A, the enzyme that breaks down serotonin at synapses, meaning the serotonin that was released stuck around longer.⁴

If you translate that to human subjective experience, a simultaneous uptick in GABA activity (calm, sedated) and serotonin and dopamine levels (brighter mood, mild reward sensation) could easily register as feeling “high.” It is the same general combination that makes alcohol enjoyable in small amounts before the sedation takes over. The difference is that ashwagandha’s effects are typically milder and build over days of use rather than hitting within minutes.

This also helps explain why the experience varies so much between individuals. People who already have robust serotonin and dopamine signaling may barely notice the mood shift. People who are chronically stressed and running low on those neurotransmitters may feel a dramatic lift that, by contrast with their baseline, feels euphoric or altered.

Your Thyroid Could Be Part of the Problem

There is a less obvious explanation that catches some people off guard. Ashwagandha can stimulate thyroid hormone production, and if your thyroid tips into overactivity, the symptoms can feel a lot like a stimulant high: racing heart, restlessness, feeling wired, trouble sleeping, and a jittery sense of heightened energy.

A case report documented a 73-year-old woman who developed full-blown thyrotoxicosis, with a dangerously low TSH level and supraventricular tachycardia, after two years of self-treating her hypothyroidism with ashwagandha. Her symptoms resolved completely once she stopped taking it.⁵ That is an extreme case, but milder thyroid stimulation could contribute to a buzzed or amped-up sensation in people with borderline thyroid function, even at normal supplement doses. If the “high” you feel from ashwagandha leans more toward feeling wired than feeling relaxed, thyroid involvement is worth considering with a blood test.

Blood Sugar Dips Can Feel Strange

Ashwagandha has demonstrated effects on blood sugar regulation. It can inhibit enzymes that break down carbohydrates, increase insulin secretion from the pancreas, and improve insulin sensitivity.⁶ For most people, especially those with insulin resistance, that is a benefit. But if your blood sugar is already normal or you take it on an empty stomach, the glucose-lowering effect could push you into mild hypoglycemia.

Low blood sugar produces its own set of altered-state symptoms: lightheadedness, a spacey or disconnected feeling, mild confusion, and sometimes a giddy or dreamlike quality. Someone unfamiliar with what hypoglycemia feels like could easily describe it as feeling high. This is more likely if you take ashwagandha first thing in the morning without food, or if you combine it with other supplements or medications that also lower blood sugar.

When the Feeling Crosses Into Something More Serious

For most people, the slightly altered feeling is mild and manageable. But there are case reports showing that ashwagandha’s neurological effects can occasionally escalate to something more alarming. A 40-year-old man presented with prolonged sleep, abnormal sleep behaviors, acute confusion, and retrograde amnesia that were temporally linked to ashwagandha use. His doctors attributed the episode to GABAergic modulation by withanolides, noting that individual differences in drug metabolism likely made him more susceptible than average. His symptoms resolved completely after he stopped the supplement.⁷

This is a single case, not a widespread risk. But it illustrates an important point: the same GABAergic mechanism that produces pleasant calm in one person can produce memory gaps, confusion, and excessive sedation in another. The dividing line is mostly genetic, determined by how quickly your liver enzymes process the active compounds. If you are a slow metabolizer, the same dose produces higher blood levels and a stronger brain effect.

Mixing Ashwagandha With Other Substances Amplifies the Effect

Because ashwagandha has genuine GABAergic activity, combining it with other GABA-enhancing substances stacks the effects. A review of adaptogen-drug interactions flagged ashwagandha’s potential for pharmacodynamic interactions with benzodiazepines, z-drugs (like zolpidem), and other central nervous system depressants.⁸ In practical terms, this means that if you take ashwagandha while also drinking alcohol, using a prescription sleep aid, or taking a benzodiazepine for anxiety, you are more likely to feel excessively sedated, high, or impaired than either substance would cause alone.

The same logic applies to cannabis. THC has its own GABAergic and dopaminergic effects, and adding ashwagandha on top of that can deepen the sedation and euphoria beyond what you would expect. Even over-the-counter antihistamines that cause drowsiness (diphenhydramine, for example) could interact, since ashwagandha also modulates histamine receptors.

If you have recently started ashwagandha and suddenly feel significantly more affected by your evening glass of wine or your allergy medication, the supplement is a likely contributor. The solution is straightforward: separate them by several hours, or reduce the ashwagandha dose.

Stopping Suddenly Can Create Its Own Problems

The GABA connection also means that ashwagandha is not entirely consequence-free to stop taking abruptly, at least for some people. A case report described a 20-year-old man who developed tachycardia, insomnia, and anxiety symptoms after suddenly discontinuing 600 mg per day of ashwagandha extract. No other medical or psychosocial causes were identified, and the timing closely followed cessation. The authors proposed that the withdrawal syndrome was mediated by the same GABAergic activity that makes the supplement calming during use.⁹

This parallels what happens with other GABA-enhancing substances. When you regularly boost GABA signaling, the brain can adjust by becoming slightly less sensitive to GABA on its own. Remove the external source suddenly, and you get a rebound of neural excitability: anxiety, racing heart, poor sleep. The effect is much milder than benzodiazepine withdrawal, but it is real enough that tapering off gradually makes more sense than quitting cold turkey if you have been using ashwagandha daily for weeks or months.

Extract Type and Dose Make a Bigger Difference Than Most People Realize

Not all ashwagandha products are created equal, and this matters for the “high” question. The supplement market includes raw root powder, water extracts, hydroalcoholic extracts, and concentrated patented formulations like KSM-66 and Sensoril. These vary enormously in their withanolide content and in which specific compounds they concentrate.

Traditionally, ashwagandha root was consumed as a powder mixed into warm milk or ghee.¹⁰ That delivers a broad but relatively dilute mix of active compounds. Modern concentrated extracts can pack far more withanolides per capsule than a traditional preparation, which means the neurological effects are correspondingly stronger. Someone who switches from a basic root powder to a standardized high-potency extract without adjusting the dose is effectively doubling or tripling their exposure to the active constituents.

The method of extraction also matters because different solvents pull out different compounds. Water extracts tend to be richer in the alkaloids and glycowithanolides thought to drive the GABAergic effect. Alcohol-based extracts concentrate different withanolide profiles. This is why two different ashwagandha products at the same milligram dose can produce noticeably different subjective effects, one might feel sedating while the other feels more stimulating.

If the “high” feeling is bothering you, the simplest fix before quitting entirely is to cut your dose in half. Many people find that the anxiety-relief and sleep benefits persist at lower doses while the intoxicated feeling fades. Timing also matters. Taking ashwagandha at night rather than in the morning channels the sedation toward better sleep rather than daytime impairment.

Individual Variation Is Enormous

The range of responses to ashwagandha is unusually wide compared to most supplements, and the reasons go beyond dose and extract type. Liver enzyme speed plays a major role: people with slower CYP enzyme activity will maintain higher blood levels of ashwagandha’s active compounds for longer, intensifying the brain effects. The neurotoxicity case mentioned earlier specifically pointed to interindividual variability in drug metabolism as a likely explanation for why that patient reacted so strongly.⁷

Your baseline neurochemistry also matters. Someone with naturally low GABA tone, which often correlates with being anxiety-prone, may feel a more dramatic shift when GABA activity is enhanced externally. The same person is also more likely to experience rebound symptoms upon stopping. Conversely, someone with naturally high GABA activity may feel almost nothing from the same dose.

Hormonal status adds another layer. Since ashwagandha affects thyroid function and cortisol levels, people with existing thyroid conditions or adrenal issues may experience amplified or unexpected effects. Women at different points in the menstrual cycle can also respond differently, since estrogen and progesterone both influence GABA receptor sensitivity.

All of this means that asking “is this normal?” when you feel high from ashwagandha is hard to answer in a general way. The effect is pharmacologically explainable and not uncommon, but it is also not universal. If the feeling is mild and pleasant, adjusting the dose or timing usually handles it. If the feeling includes confusion, memory gaps, or a racing heart, that warrants stopping the supplement and talking to a doctor, because those symptoms suggest either an unusually strong GABAergic response, thyroid overstimulation, or an interaction with something else you are taking.

Why the Research Lags Behind the Popularity

Ashwagandha has become one of the best-selling herbal supplements in the Western market, but the research on its neurological effects remains surprisingly thin. Most of the mechanistic evidence, including the GABA and monoamine studies cited in this article, comes from cell cultures and animal models rather than controlled human trials. The clinical studies that do exist in humans tend to focus on stress and anxiety questionnaire scores, not on the subjective feeling of being “high” or the specific brain receptor changes that cause it.

This gap matters because the people reporting these experiences online are essentially running an uncontrolled experiment. The doses they use often exceed what was studied in clinical trials, the extract formulations vary wildly, and there is almost no formal tracking of adverse neurological events beyond the occasional case report that makes it into a medical journal. The withdrawal case and the neurotoxicity case described above are notable precisely because so few clinicians think to connect neurological symptoms with an herbal supplement their patient may not even have mentioned.

Researchers have called for better pharmacokinetic data on ashwagandha’s active compounds in humans, particularly around how quickly different withanolides cross the blood-brain barrier and how genetic polymorphisms in liver enzymes affect their clearance. Until that work is done, the honest answer to “why does this make me feel high?” is that the basic mechanism is clear (GABA, serotonin, dopamine) but the details of who will feel it, how strongly, and at what dose remain poorly mapped.