Ashwagandha And The Thyroid: A Different Organ From The One This Website Already Covers

Sourced from the product label and PubMed-indexed researchLast updated September 202611 min readSafety

This website has already published one safety article about ashwagandha, covering two case series of liver injury and the signs a reader should watch for. This is a second article about the same ingredient, and it is worth saying plainly why it exists rather than folding it into the first: the liver and the thyroid are different organs, the case reports behind each concern are entirely separate patients in separate countries, and a reader who only knows the liver signal would have no reason to recognise the thyroid one if it happened to them.

Why this is a second ashwagandha safety article, not a repeat

Ashwagandha (Withania somnifera) has a genuinely reasonable efficacy literature behind its general use, including a 2024 pooled analysis of nine randomised trials that found consistent effects on perceived stress, on a standard anxiety scale and on cortisol. It also has more than one published safety signal, and this website has taken the position, on the liver article, that two independent case series reporting the same pattern is the point at which a signal stops being anecdote. The same standard applies here. Two case reports, from different continents and nineteen years apart, describing thyrotoxicosis after ashwagandha use, and resolving after the person stopped, meet that same bar for a second, separate caution.

The two organs are not connected in a way that makes one warning stand in for the other. A person who knows to watch for the liver signs — the ones covered in the earlier article — is not thereby watching for a racing heart, unexplained weight loss or heat intolerance, which is what this article is about.

Ashwagandha on the Jelly Force panel

The Supplement Facts panel lists “Ashwagandha” as one of nine names inside the 82 mg proprietary blend, with no standalone amount, no percentage of any active fraction and no statement of which part of the plant was used. The best-evidenced trial behind this category’s ashwagandha claim used a standardized extract delivering 21 mg of withanolide glycosides a day for eight weeks (Lopresti 2019), a detail this website’s standardization article covers in full. Nothing about that trial, or the panel it is being set against here, changes because of what follows. What follows is a separate question: not how much ashwagandha is in this blend, but what has been reported when people took ashwagandha, at doses the published case reports do not always specify precisely, and developed a thyroid problem afterward.

The first case: a Japanese man, two months in

The more recent report, published in 2024, describes a previously healthy 47-year-old Japanese man who began taking ashwagandha and, two months later, presented to hospital with classic thyrotoxicosis symptoms: a sense of fatigue, fever at night, weight loss, followed by diarrhoea and headache (Hayashi 2024). Blood tests confirmed thyrotoxicosis. Thyroid ultrasound showed an uneven internal pattern with no increase in blood flow, and a thyroid scan showed reduced iodine uptake — a combination that pointed specifically to painless thyroiditis, a form of thyroid inflammation that releases stored hormone into the blood without the gland actually overproducing it, rather than to Graves’ disease or a hormone-producing nodule. After he stopped taking ashwagandha, both his symptoms and his thyroid blood markers improved.

The authors frame their own case plainly: it is a rare presentation, and it is reported specifically to raise the question of whether ashwagandha is safe for healthy people where thyroid toxicity is concerned. A single case does not establish causation on its own. What it does establish is a documented, published, temporally consistent pattern in one specific patient: no thyroid problem, then ashwagandha, then thyrotoxicosis, then improvement after stopping.

The second case: a Dutch woman, and a dose that was increased

The earlier report is a fuller case with an important extra detail. A 32-year-old healthy woman took ashwagandha-containing capsules for symptoms of chronic fatigue (van der Hooft 2005). For the first few weeks she took the capsules only occasionally and had no symptoms. After she increased the dose, she developed clinical symptoms consistent with thyrotoxicosis, confirmed on laboratory testing. She was not taking any other remedy or medication that could explain it. Her symptoms resolved on their own, and her lab values normalised, once she stopped the ashwagandha capsules.

The authors note something the more recent Japanese case does not: animal studies had already suggested, before this report, that ashwagandha can raise circulating thyroid hormone concentrations. Their case, published in 2005, was the first time that relationship had been reported in a human. The detail that her symptoms appeared specifically after she increased her dose, having taken smaller amounts without incident, is the closest thing either report offers to a dose signal, though neither report states the exact milligram amount she was taking at either point.

The trial behind this blend did not monitor for this

It is worth being precise about what the best-evidenced ashwagandha trial in this category actually measured, because it did not test for the thing these two case reports describe. The sixteen-week crossover study behind the Lopresti 2019 citation tracked the Profile of Mood States, an ageing-males symptom questionnaire, and salivary DHEA-S, testosterone, cortisol and estradiol. Thyroid hormones do not appear on that list. The trial reported that DHEA-S and testosterone rose significantly more on ashwagandha than on placebo, and that finding is itself a hormonal effect, not merely a mood or energy one; it does not tell a reader anything about what happened to thyroid hormone in the same participants, because nobody measured it.

That is not a criticism specific to this one trial; a great many supplement trials measure the hormones closest to their marketed claim and stop there. It does mean that a reader cannot look to this category’s own supporting research and find reassurance, one way or the other, about the thyroid. The absence of a signal in that trial is an absence of monitoring, not evidence the effect the two case reports describe does not occur at the amounts this category uses.

The signs to know, and how they differ from the liver signs

The liver article on this website lists jaundice, unusual fatigue, dark urine and abdominal discomfort as the signs worth knowing. The thyroid signs are a different list entirely, drawn from what both case reports actually recorded: a racing or pounding heartbeat, unexplained weight loss, a sense of fatigue that does not resolve with rest, feeling unusually warm or intolerant of heat, night fever, and in the Japanese case, gastrointestinal symptoms including diarrhoea alongside a headache. Because the underlying mechanism in at least the more recent case was thyroid inflammation rather than overproduction, these signs can appear even though the thyroid itself is not permanently overactive; painless thyroiditis, by definition, is often self-limiting once the inflamed gland stops releasing its stored hormone, which is broadly consistent with both patients improving after stopping ashwagandha rather than needing ongoing antithyroid treatment.

None of these signs is unique to ashwagandha, or even to supplements generally; they overlap with ordinary anxiety, with caffeine sensitivity, and with several unrelated thyroid conditions a person could have independent of anything they are taking. That overlap is exactly why a published, dated case report is useful: it gives a reader a documented reason to mention the supplement specifically if a doctor is working through the possible causes of these symptoms, rather than leaving ashwagandha out of the conversation because nobody thought to ask.

Who should be careful before starting

Three groups have the clearest reason to talk to a doctor before starting a daily ashwagandha-containing product, based on what these two reports and the underlying mechanism suggest. First, anyone with an existing thyroid condition, particularly hyperthyroidism, Graves’ disease, or a history of thyroiditis, since these two reports describe the effect occurring in people with no known thyroid disease beforehand, and the added stimulus in someone with a predisposed or already-inflamed gland is untested. Second, anyone taking thyroid medication, whether levothyroxine for an underactive thyroid or an antithyroid drug for an overactive one, since a supplement that can independently move thyroid hormone levels complicates the dose calculation either way. Third, anyone who notices any of the signs above after starting a new ashwagandha-containing product, particularly if the signs began after increasing the amount taken, echoing the pattern in the Dutch case specifically.

This is a distinct list from the population the liver article is written for, and a reader could reasonably fall into one list, both, or neither; there is no reason to assume the two risks travel together in the same person.

What this means for one name inside an 82 mg blend

Both case reports involve ashwagandha taken as a more concentrated, higher-dose preparation than one name sharing 77 mg with seven other botanicals in a gummy, and neither case report states an exact milligram amount that can be compared directly to this blend the way the tribulus or maca trial amounts can be in this website’s other articles. That difference in scale is real, and it is a reason for caution rather than alarm: idiosyncratic hormonal reactions, including thyroid ones, are not always cleanly dose-proportional in every individual, which is part of why case reports exist in the medical literature in the first place, to flag reactions that a large randomised trial, averaging across many participants, might not catch or might not have been designed to look for.

The honest summary is the same shape as the liver article’s: two independent, published, resolving cases, a plausible mechanism supported by earlier animal data, and a supporting trial for this category that never tested for the specific thing being described. That is enough to know the sign and mention the supplement to a doctor if it appears. It is not, on two case reports against a much larger literature of trials that did not report this outcome, enough to call the effect common or to say it should be expected.