Ashwagandha raises T3 and T4 in some studies, and that is the whole problem: if you take levothyroxine or liothyronine, your dose was set against a measured baseline, and an agent that moves thyroid hormone levels makes that dose wrong in a direction nobody is monitoring. It can precipitate thyrotoxicosis, so anyone with hyperthyroidism should avoid it and anyone on thyroid replacement should not start it without their prescriber. Separately, NIH LiverTox assigns ashwagandha a likelihood score of B — a likely cause of clinically apparent liver injury — with roughly 23 published cases as of the 2024 update, latency typically 2 to 12 weeks. Denmark and Iceland have restricted or advised against ashwagandha products.

The mechanism

Levothyroxine is replacement, not stimulation. Your prescriber measures TSH, sets a dose that brings it into range, and re-measures. The system only works because the input is stable and known.

Ashwagandha (Withania somnifera) is documented as raising T3 and T4 in some studies.13 Whatever the underlying pathway, the practical consequence is straightforward: an unmeasured second source of thyroid hormone activity sits on top of a carefully titrated first one. Two things can follow. The replacement dose becomes effectively too high, which looks like over-replacement. Or you stop the ashwagandha — because the bottle ran out, because you forgot — and the effect disappears without anyone knowing to look for it.

This is not a case where the mechanism is speculative and the effect unobserved. The thyroid effect in the cross-cutting interaction literature is listed as documented, which is a stronger label than most supplement interactions earn.

⚠️ Talk to your prescriber first

If you take levothyroxine or liothyronine, or have Graves’ disease or any form of hyperthyroidism, do not start ashwagandha on your own. If you have already started it, do not stop abruptly without telling them either — an unannounced stop moves your thyroid levels just as an unannounced start does. Tell them the dose, the brand and the date you started, and let them decide whether to re-check your TSH.

What has actually been documented

EvidencePopulationDoseDurationFinding
2026 systematic review and meta-analysis, Frontiers in Pharmacology20 RCTs, 1,249 participants, published 2011–2025; 14 of 20 trials conducted in India225–675 mg/day root extract, most commonly 600 mg/dayMostly 8 weeks (range 7 days–16 weeks)Memory SMD 0.52; attention/processing speed SMD 0.29; executive function SMD −0.42; visuospatial SMD 0.39 after sensitivity analysis
Thyroid hormone effectHuman studies referenced in interaction sourcesNot consistently reported—Raises T3/T4 in some studies; documented ability to precipitate thyrotoxicosis; may make levothyroxine dosing unstable
NIH LiverTox, 2024 update~23 published cases of clinically apparent liver injury154–2,100 mg/day across casesLatency typically 2–12 weeksLikelihood score B (likely cause). Predominantly cholestatic or mixed pattern, with jaundice and pruritus. Most self-limited, resolving in 1–4 months after stopping; rare fatal injury or emergency transplant, particularly with pre-existing cirrhosis
Ashwagandha with levothyroxine, prospectively———No trial exists. The interaction is inferred from the hormone data plus clinical pharmacology, not from a study of the pair

The efficacy numbers in the top row need reading with their caveats attached, because they are the reason people take it in the first place. Fourteen of twenty trials were conducted in India, many with manufacturer involvement; publication bias in this literature is a genuine concern; only one study assessed global cognition; and most durations were eight weeks.1 Ashwagandha’s most robust and consistent effect is on subjective stress, anxiety and cortisol — and part of the cognitive signal is plausibly downstream of reduced stress and better sleep rather than a direct effect on memory.

The second signal: liver injury

Evidence that ashwagandha can cause clinically apparent liver injury: Moderate — LiverTox likelihood score B, meaning a likely cause.2 This is separate from the thyroid question and applies to everyone, not only to people on thyroid medication.

The case series has a consistent shape. Latency of two to twelve weeks after starting. A predominantly cholestatic or mixed pattern — jaundice and itching more than a pure transaminase rise. Doses across the reported cases spanned 154 to 2,100 mg/day, which means the low end overlaps the ordinary consumer dose and there is no “safe” number to point at. Most cases resolved within one to four months of stopping, but there are rare instances of fatal liver injury or emergency transplant, concentrated in people with pre-existing cirrhosis.23

Two national regulators have acted on this: Denmark and Iceland have restricted or advised against ashwagandha products.24 That is a stronger regulatory position than almost anything else in this category has attracted.

How serious this is

Two different levels of seriousness are being stacked here and they deserve separating.

  • Thyroid. Not an emergency, and not a reason for panic if you have taken a few doses. It is a reason for the combination to be supervised rather than improvised, because the failure mode is silent — a drifting TSH that nobody re-checks because nobody knew anything had changed.
  • Liver. Rare in absolute terms, but the consequences at the severe end are not reversible, and the people at highest risk — those with existing liver disease — are exactly the people least likely to connect a supplement to how they feel.

Other listed cautions worth knowing before this becomes a longer list than you expected: additive CNS depression with sedatives, benzodiazepines and alcohol; immunostimulant activity, so it is avoided in autoimmune disease and in transplant patients on immunosuppressants; additive lowering with blood-pressure and diabetes medication; contraindicated in pregnancy; and nightshade-family allergy is possible.14

Other supplements that interfere with thyroid medication

Thyroid medication is the most under-flagged interaction category in this whole field, and ashwagandha is not the only offender in a typical brain-supplement cabinet.

  • Acetyl-L-carnitine is a peripheral antagonist of thyroid hormone action — it can reduce levothyroxine’s effectiveness and may worsen hypothyroidism. Its own cognitive evidence rests on trials that are 20 to 35 years old, small, and heavily sponsored by a single manufacturer, and Cochrane’s older review found no evidence to recommend routine use in dementia.56
  • L-tyrosine is a thyroid hormone precursor. Contraindicated in Graves’ disease and hyperthyroidism, and a caution on replacement therapy.7
  • Bacopa monnieri has shown T4 elevation in rodents — preclinical, not human, and flagged here as a reason for thyroid patients to check rather than as an observed human effect. Its human evidence is a small effect on speed of attention after at least 12 weeks.89
  • Minerals and multivitamins. Calcium, magnesium (including magnesium L-threonate), iron and iron-containing multivitamins impair levothyroxine absorption — separate them by at least four hours. Coffee does the same to a lesser degree; separate by at least 60 minutes.

Signs that would mean stopping

⚠️ Stop and see a doctor

Jaundice (yellowing of skin or eyes), dark urine, pale stool, pain in the upper right abdomen, unexplained fatigue, or itching. Latency for supplement-associated liver injury is typically 2 to 12 weeks after starting, so a symptom that appears a month in is not too late to be related. Stop the supplement and get liver enzymes checked — do not wait to see whether it settles.

On the thyroid side, the things to report rather than to self-diagnose are palpitations, new heat intolerance, tremor, unexplained weight loss, or anxiety that arrived with the supplement. Those are questions for the clinician who manages your replacement dose, and the answer is a blood test, not a forum thread.

What would change our mind

A prospective study in adults stably treated with levothyroxine, randomized to a standardized ashwagandha extract or placebo, with serial TSH, free T4 and free T3 over at least twelve weeks. If TSH held steady, the practical advice on this page would soften from “not without supervision” to “monitor once.” Nothing in the existing literature does that job: the 20 trials in the 2026 meta-analysis were cognitive and stress trials, not endocrine ones, and people on thyroid medication were not the population being studied.

Frequently asked questions

Can I take ashwagandha if I have Hashimoto’s?

This is a question for your clinician, and there are two reasons rather than one. The thyroid hormone effect is the obvious one. The second is that ashwagandha has immunostimulant activity and is listed as one to avoid in autoimmune disease — Hashimoto’s is autoimmune.1

Does separating the doses by a few hours solve it?

No. Separation solves absorption interactions — that is why calcium, iron and magnesium are separated from levothyroxine by four hours. Ashwagandha’s issue is that it appears to change hormone levels, which is not fixed by timing.

Is KSM-66 or Sensoril safer than generic ashwagandha?

There is no evidence that any branded extract avoids either signal. KSM-66 trials typically use 300–600 mg/day and Sensoril 125–250 mg/day at a higher withanolide concentration, but the LiverTox case series spans 154 to 2,100 mg/day, which covers both.12

I took it for two weeks and felt fine. Do I need a liver test?

Feeling fine is not evidence of nothing happening, but it is also not a reason for routine testing in someone with no symptoms and no liver disease. If you are on thyroid medication, the more useful test is the TSH your prescriber would order anyway.

Related reading

These statements have not been evaluated by the Food and Drug Administration. Nothing here is intended to diagnose, treat, cure or prevent any disease.

This article is information, not medical advice. Talk to a doctor or pharmacist about your own situation, especially if you take prescription medication.