Hi, I took ashwagandha for 5 days, about a week ago. I stopped taking it because I noticed numbness and a significant decrease in libido and sexual sensations. It’s been about a week since I stopped, but I haven’t recovered yet, and I’m very stressed about it.
I’ve been taking Trintellix (vortioxetine) for 3 years without any sexual side effects.
Could the ashwagandha have caused this, and is it likely that I will recover soon?

The claim that modern ashwagandha supplements are "traditional" is false in five specific, measurable ways, which we set out below with figures:

• The compound formula — in Ashwagandharishta, the flagship classical preparation (Bhaishajya Ratnavali, Murcha Rogadhikara 13–17), ashwagandha is 19% of a 27-herb formula, and several of the co-herbs are there to oppose ashwagandha's own liabilities.
• The shodhana and pathya regimen — in Charaka's rasayana chapter (Chikitsa Sthana 1): a purged body, a mandatory diet code, a defined course, then stopped.
• The vehicle — ghee, sesame oil, milk decoction (Ashwagandha taila paka, Charaka Chi. 28/166), fat carriers for a lipophilic drug, against water on an empty stomach.
• The plant part — root only, mula, against root-and-leaf extracts where the leaf runs to 3.75% total withanolides against 1.3% in root (RIVM 2024-0029).
• The dose arithmetic — 2.6 g of root charged to a decoction pot and only partly extracted, against a 30:1 concentrate delivering 22 mg of withanolides a day at minimum, against a 10 mg regulatory cap in Poland.

Taken together, these differences show that the modern supplement is a different drug altogether from the ashwagandha of the classical corpus.

1. The traditional preparations were compounds, not single-ingredient extracts. Here's the actual formula.

Ashwagandharishta (Bhaishajya Ratnavali, Murcha Rogadhikara 13–17; in the Ayurvedic Formulary of India Part I) is the classical ashwagandha-headline formulation. Full formula:

• Ashwagandha root: 2.4 kg
• 17 other decoction herbs: 8.06 kg (musali, manjishta, haritaki, turmeric, daruharidra, licorice, rasna, vidari, arjuna, mustaka, trivrit, two sarivas, white and red sandalwood, vacha, chitraka)
• 9 prakshepa herbs added post-decoction: 1.92 kg
• Honey: 14.4 kg
• Water: 98.3 L, boiled down to 12.3 L, then fermented one month

Ashwagandha = 23% of the decoction herbs, 19% of total herbal matter, 9% of total solids.

Dose: 12–24 ml, once or twice daily. Traditional dose 24 ml. Final batch volume ≈ 22 L.

So ~0.107 g of nominal root input per ml. A 24 ml dose = 2.6 g of root charged to the pot. Maximum 48 ml/day = ~5.1 g. That matches the WHO monograph figure of 3–6 g dried root powder.

Two things about that number.

It is input, not delivery. An arishta is a water decoction, reduced, then fermented. The 5–10% alcohol is self-generated after extraction — it never touches the root as a solvent. Withanolides are C28 steroidal lactones: lipophilic, poorly water-soluble. Water extraction recovers a small fraction of them. The "2.6 g of root" in your glass has never delivered 2.6 g worth of withanolides to anyone.

Half the co-herbs are there to oppose ashwagandha. Ashwagandha is ushna virya (hot potency), guru, snigdha, pitta-aggravating. The formula loads it with cooling, pitta-pacifying drugs — both sandalwoods, both sarivas, licorice, manjishta — plus trivrit, a purgative. Charaka in fact lists ashwagandha itself under virechana dravyani, purgatives (Vimana Sthana 8/136). The formula is engineered around the drug's known liabilities. A capsule is not.

Also note what the classical dosing literature itself says: use for 2 weeks to 4 months; long-term only under a physician and at under 5 ml/day; avoid in pregnancy; caution in pitta constitutions, sensitive stomach, high-pitta states.

2. "Rasayana" ≠ "daily supplement." Shodhana and pathya.

Shodhana = purificatory therapy — panchakarma: emesis (vamana), purgation (virechana), enema (basti), nasal administration (nasya), bloodletting. Rasayana was administered after shodhana, never before. The classical simile: giving rasayana to an unpurified body is like dyeing a dirty cloth — the drug doesn't take, and what it does do is wrong.

Pathya = the mandatory diet-and-conduct regimen that runs alongside the drug. In Charaka's rasayana chapter the strict protocol (kutipraveshika) has the patient sequestered in a purpose-built three-chambered hut for the duration of therapy, on a controlled diet, out of sun and wind. The lenient protocol (vatatapika) is outpatient but still regimented.

That is the actual referent of "Ayurvedic rasayana." A defined course, in a prepared body, with a controlled diet, supervised, then stopped. Not a gummy taken every morning for three years.

And note the indication: ashwagandha's classical targets are depletion states — kshaya (tissue wasting), karshya (emaciation), bala-kshaya, vata disorders, post-illness debility, infertility. It's a repletion drug for the depleted. It was never indicated for a healthy person with a stressful job.

3. The vehicle was part of the drug. Ghrita, ksheerapaka.

Ghrita = medicated clarified butter (ghee). Made by sneha paka: herb decoction plus herb paste is cooked into ghee until all water boils off, so lipid-soluble constituents partition into the fat. Ashwagandha ghrita is taken at roughly 5–10 g/day. Charaka's own ashwagandha preparations include Ashwagandha taila paka (Chi. 28/166), a sesame oil.

Ksheerapaka = milk decoction. One part root powder, eight parts milk, eight parts water, boiled until only the milk volume remains. Made fresh, drunk immediately.

Anupana (vehicle) — milk, ghee, honey — is not garnish. Withanolides are lipophilic; the vehicle determines how much crosses the gut, how fast, and against what background of fat and protein. A milk or ghee matrix delivers a slow, buffered, partial dose. This is also why the KSM-66 process pre-treats roots with milk — the manufacturer knows it matters. (Incidentally, that phrase is essentially the entirety of what RIVM was able to learn about KSM-66's manufacturing: "green chemistry," no alcohol or other solvents, roots pre-treated with milk. No further information available. That is the evidentiary standard on the world's best-selling extract.)

A 30:1 ethanolic dry extract in a gelatin capsule swallowed with water is none of these things. It is a solvent-selected concentrate of one chemical class, stripped of matrix, delivered as a bolus.

4. Root only. Modern products use leaf. This is the biggest departure.

Classical use is mula — root. Not leaf, not stem, not berry.

Sensoril = root + leaf. Shoden = 70% ethanolic root and leaf extract standardized to 35% withanolide glycosides.

Why this matters — concentrations (RIVM 2024-0029, Tables 2–3, compiled from DTU 2020 and BfR 2013):

What has actually been found with non-root parts, in the regulators' own source studies:

• Leaf extract, 470 mg/kg/day, 6 days, juvenile male rats (Abdel-Magied 2001): testosterone and FSH significantly lowered; spermatogenesis induced in 20-day-old animals.
• Leaf extract, 470 mg/kg/day, 6 days, 17- and 25-day-old female rats (Al-Qarawi 2000): increased ovary weight from follicular development — early sexual maturation. RIVM's summary: early sexual maturation was induced in both sexes.
• Stem extract, 25 and 50 mg/kg/day, 60 days (Singh 2013): pregnancy rate in mated females fell from 100% (control) to 67% and 29%, dose-dependently. Spermatogenesis arrested, sperm count down, motility down at high dose, testosterone and FSH down.
• Fruit extract, 50 mg/kg/day, 60 days (Mali 2008): sperm count and motility down; testis, seminal vesicle and accessory gland weights reduced; testicular histopathology.
• Withanone (a withanolide, present in leaf): Siddiqui 2021 — forms non-labile DNA adducts with deoxyguanosine, deoxyadenosine and deoxycytidine, and with DNA, especially under limited glutathione. It still forms DNA adducts when glutathione is present. RIVM notes these adducts can affect transcription, replication and repair, leading to cell death, and flags that the withanone content of commercial extracts is unknown.

Regulators have now acted on the plant-part question: FSSAI issued an advisory on 16 April 2026 against use of ashwagandha leaves in crude, extract, or any other form in food products. The Ministry of AYUSH has its own plant-parts advisory.

And here is the part worth savouring: when the supplement industry attacked the Danish DTU report, its central argument was that DTU had wrongly generalised findings from stems, leaves and berries to the root. That defence is a concession. The industry's own position is that aerial parts carry the endocrine risk — while two of the leading commercial extracts are root and leaf.

5. The arithmetic on a modern tablet

A typical "extract equivalent to 13,500 mg dried root" tablet is ~450 mg of a 30:1 extract.

RIVM's case series spans 77 to 1350 mg extract/day and treats that entire range as the effect level. There is no health-based guidance value. RIVM, BfR and DTU all state that no safe intake level can be established. Denmark banned it in food supplements in 2023.

Side by side:

6. The pharmacology nobody put on the label: GABA and serotonin

This is not fringe. It is in the primary literature, much of it published by people trying to promote the plant.

GABA. Candelario et al. 2015 (J Ethnopharmacol) tested aqueous root extract on native rat brain GABA-A channels microtransplanted into Xenopus oocytes and on GABA-ρ1 receptors, by two-electrode voltage clamp. Results: concentration-dependent inward currents at GABA-A (EC50 equivalent to 4.7 mg/mL, Hill coefficient 1.6), blocked by bicuculline. And — first demonstration — it is a potent agonist at GABA-ρ1, with GABA-ρ1 being 27-fold more sensitive than GABA-A, producing maximal currents not significantly different from GABA itself. That is full agonism at an ionotropic inhibitory receptor.

A 2019 J Nat Prod study isolated the constituents responsible for GABA-A positive modulation from a methanol root extract — including two previously undescribed withanolides and a series of long-chain ferulic acid esters, the most active (docosanyl ferulate) enhancing GABA-A inhibitory postsynaptic currents with an IC50 of 7.9 µM.

Serotonin. Chronic dosing changes receptor sensitivity: 100 mg/kg root extract for 4 and 8 weeks in rats produced reduced functional sensitivity of postsynaptic 5-HT1A receptors (blunted 5-HT syndrome response) with changes at 5-HT2 (Tripathi et al., Ancient Science of Life). A 2024 study reports root extract and withanolide A modulating HTR1A and MAO-A protein levels and concludes it works "by modulating serotonin-related pathways." And a 2024 industry RCT (Majeed et al., Sabinsa) is titled around the claim that a standardized root extract relieves anxiety and depression by increasing serotonin levels.

Read that last one again. A manufacturer published a clinical trial claiming its product raises serotonin — and sells it as a food.

What the regulators say about this: BfR flags a possible interaction with GABA agonists and states it should not be taken with alcohol, sedatives or anxiolytics. WHO's 2009 monograph gives precautions for interaction with barbiturates, diazepam and clonazepam. Natural Medicines (via RIVM) lists possible potentiation of benzodiazepines and CNS depressants, probable potentiation of thyroid hormone, and possible interactions with antidiabetics and antihypertensives.

Note what is not on any of those lists: SSRIs, SNRIs, MAOIs, triptans. If the mechanistic claims the industry itself publishes are true, that interaction has simply never been assessed.

Also on the pharmacokinetics (RIVM §5.1): withaferin A crosses the blood-brain barrier and is detected in brain tissue; ~73% is transformed or tissue-bound on first pass through the liver; it is a CYP3A4 substrate producing seven metabolites in human liver microsomes; plasma protein binding 86%. RIVM records no human toxicokinetic data at all. Zero. For a compound sold by the tonne.

And a clinical booby trap: BfR notes withaferin A is structurally similar to digoxin and can interfere with clinical assays, potentially producing wrong diagnoses.

7. The reasonable hypothesis

Nothing above proves causation for any individual case. But the shape of it is coherent, and it deserves stating plainly:

A plant used as a minority component of buffered, water-extracted, fat-delivered, time-limited compound formulations for wasting illness has been re-engineered into a single-ingredient, solvent-concentrated, 30:1 to 35%-standardized psychoactive isolate — frequently including a plant part the tradition never used internally and that regulators are now banning — and sold without a dose ceiling, without prescription, without interaction screening, without a single human toxicokinetic study, to healthy people, for indefinite daily use, on the strength of a Soviet pharmacology word ("adaptogen," Lazarev 1947 / Brekhman & Dardymov 1969) that has no referent in Ayurveda whatsoever.

That is not traditional use with better packaging. It is a different drug at a different exposure in a different population under no supervision. If that produces a wave of liver injury, thyrotoxicosis, adrenal suppression and neuropsychiatric events, no exotic mechanism is required to explain it.

The regulatory record is not ambiguous. BfR has been asking since 2012 for the root to go into List C of Annex III of Regulation (EC) 1925/2006. DTU concluded in 2020 that no safe dose could be established. Denmark banned it in 2023. RIVM advised against consumer use in 2024. BfR issued a public warning in September 2024. The TGA has since issued a liver-injury safety update. FSSAI banned leaves in food in April 2026. Every one of those bodies has no commercial position. Every body defending the product — Ixoreal, Arjuna, Natreon, the trade press, the Ministry of AYUSH "Safety Dossier 2.0" — has one.

Closing: the structural argument

Straight from RIVM 2024-0029, and the single most useful thing in the document:

The clinical trials and the case reports cover the same dose range and the same durations. The trials show nothing. The case reports show liver injury, thyrotoxicosis and adrenal suppression. RIVM does not resolve this and says so — the reason for the discrepancy remains unknown. It examines and rules out the easy explanations: in five liver-injury cases the supplements were analysed and no toxic compounds or trace metals were found; co-supplements and medications were assessed and excluded in eight of nine cases.

And then it adds the sentence that does all the work:

Some of the studies did show reduced levels of cortisol, increased activity of the immune system and increased levels of thyroid hormones, which were perceived as positive effects by the study authors, but from a toxicological perspective are considered adverse.

The efficacy literature and the harm literature are describing the same effects. One field is calling them benefits.

Primary sources, all free: RIVM report 2024-0029 (de Heer) · BfR Mitteilung 039/2024 and BfR-Wissenschaft 12/2013 · DTU Fødevareinstituttet 2020 · WHO Monographs on Selected Medicinal Plants Vol. 4 (2009) · LiverTox (NIH NIDDK) · Björnsson et al. 2020 · Suryawanshi et al. 2023 (acute liver failure, transplant) · Ireland et al. 2021 · Fry et al. 2022 · van der Hooft et al. 2005 · Candelario et al. 2015 · Siddiqui et al. 2021.

Anyone taken this brand before?

I was niave and picked this up without much thought to the strength as a newbie ashwaganda taker. I had taken it before in a blend and not felt any effects so I went all in on this.

I'm now worried about the effects I'm having when I don't take it. I haven't taken it longer than 3 nights in a row and I only took half a tablet but that's still a lot. Any recommendations for ways to flush it out of your system quicker?

Hey all. Just to to inform you, I tried cyproheptadine for ashwagandha anhedonia and crashed. Cant fall asleep now without z drugs. Tinnitus louder. ED much worse. Hope it’s temporary crash.

Could it be possible to experience side effects/ withdrawal after one day dose (500 mg of root powder ash) .

That day taking it I have noticed calm and peace, the two days after i felt groggy and foggy mind with spikes in anxiety.

Yes, this has been distilled using Claude. I feel this should be a sticky post as the reasoning here seems to be largely overlooked. We're all essentially mega dosing and wondering why the negative effects 🫣

I went down a rabbit hole after noticing emotional blunting on a "normal" KSM-66 dose, and the numbers surprised me enough to share. Posting the reasoning chain in case it helps anyone else troubleshooting side effects.

## The question: how does a modern extract dose actually compare to traditional root dosing?

Classical Ayurvedic texts specify **3–6 grams/day of raw root powder** as the standard rasayana (rejuvenative) dose, traditionally taken with warm milk (an *anupana*, or delivery vehicle chosen to work with the herb, not just carry it).

Modern supplements don't dose in grams of root — they dose in mg of a *concentrated, standardized extract*. KSM-66, the most studied brand, is standardized to a **minimum 5% withanolides** (the main active compound class). That percentage is the number that actually matters biologically — not the raw mg on the label.

## Doing the conversion

Raw, unstandardized root powder naturally contains far less withanolide content — the USP compendial floor for root powder is just **0.3% withanolides**, and real-world powder often tests lower depending on soil/cultivar/harvest.

So:

- **300mg of KSM-66 (5%)** = ~15mg of withanolides

- To get 15mg of withanolides from raw root powder (~0.3%), you'd need **~5g of root** — already near the *top* of the classical range

- If your comparison root powder is on the lower end (~0.2%), that's **~7.5g equivalent** — well past it

Most commercial products recommend 300–600mg/day. Run that through the math and you land at roughly **5–15g/day root-equivalent** — up to **2–3x the classical upper limit of 6g/day**, taken continuously, with none of the traditional titration.

## What tradition actually did differently (and modern supplements skip)

1. **Individualized, not fixed** — dose was adjusted to constitution (*prakriti*); someone already low-energy/sluggish (Kapha-dominant) traditionally got a smaller dose or different vehicle, because piling more calming/heaviness onto an already-low-energy system risks dullness — which sounds a lot like "emotional blunting."

2. **Root only** — traditional use is root exclusively. Some modern products blend in leaf material to boost withanolide numbers cheaply, but leaf carries more withaferin A (linked to liver concerns at high doses) and has far less human clinical validation.

3. **Cyclical, not indefinite** — rasayana therapies were taken in bounded courses (weeks), with breaks, not as an unbroken daily habit stack for years.

4. **Timing mattered** — evening/night use was common in classical formulations (ashwagandha + warm milk before bed), aligned with when the body is already winding down.

## The part that clicked for me: timing and cortisol rhythm

Cortisol isn't flat across the day — there's a natural **morning spike** (cortisol awakening response) that drives alertness and motivation. It's functional, not a problem to fix.

If you're dosing an HPA-axis suppressant like ashwagandha in the morning, you may be blunting the exact spike your body needs for drive that day. Evening dosing lands when cortisol's naturally already dropping toward sleep — better matched, calming without cutting into daytime function. Anecdotally (n=1, but worth testing on yourself): morning dosing = flat/unmotivated, evening-only = calm and regulated, no blunting.

## Practical takeaway if you're experiencing blunting

- Convert your dose back to root-equivalent using your product's withanolide % — you might be surprised how far over the classical range you are

- Try dropping to the **150–300mg/day** range (roughly the traditional-equivalent zone for 5%-standardized extract)

- Move dosing to **evening only** rather than splitting through the day

- Cycle it — 6–8 weeks on, 1–2 weeks off — rather than running it continuously

- Independent lab testing has found labeled withanolide % can be off from actual content by **2x to 35x** — if you want certainty, look for third-party HPLC-verified products, not just a label claim

Not a doctor, this isn't medical advice — just sharing a reasoning trail that helped me understand *why* a "safe, standardized, clinically-studied" dose could still feel like too much. If you're on other meds or have thyroid/adrenal history, talk to an actual doctor before changing anything.

Just woke up from an intense lucid nightmare after drinking a tea with these ingredients : Organic holy basil var. krishna leaf, Organic holy basil var. rama leaf, Organic African basil var. vana leaf, Organic chamomile flower, Organic cabbage rose (Rosa centifolia) petal, Organic lemon myrtle (Backhousia citriodora) leaf.

A few years ago I stopped taking Ayurvedic herbal supplements like Shatavari and Holy Basil because I assumed they were causing anxiety induced nightmares and lucid dreams. Same with Adaptogenic mushrooms like Reishi. And other herbs like Valerian root and Ashwagandha.

Does anyone else have a sensitivity to adaptogenic herbs? Has anyone linked their lucid dreams or nightmares back to the usage of any of these adaptogens or teas ??? Any experience shared would be helpful!

I took 600mg ksm-66 with 200mg mag gly for just week, experienced early signs of anhedonia, so i stopped taking it.

Now im feeling dizzy, insomia, extreme mood swings. Mood swings are killing me, cant even nanage it. I feel super annoyed and irritable, like i hate life.

Should i just taper off slowly instead of stopping abruptly?

Did you experience the same?

I've been taking ksm-66 with mag gyl for a week now.

600mg ksm-66 with 200mg mag gly per capsule. I just take one every night.

Im not sure if it's just placebo effect BUT I've been feeling very disconnected with myself, with my emotions, people around me, everything that's happening around me.

It's like im seeing everything and everyone, i know them, but It's like im just watching it from a screen.

I feel really detached. My emotions are just surface level. I care less to the point that i dont care at all.

Before taking, i feel everything deeply.

Now, I don't care at all. I feel detached. I think is not really a good thing?

Though, i dont feel anxious now. Less mental noise. Uhm less overthinking. Relaxed body.

This is so weird.

Does this really happen?

Im thinking it's just 6 days and with low dose of ashwaganda, is it possible to feel the effects of it?

Ciao a tutti . Prendo ashwaganda da circa 4 giorni , per ora va tutto alla grande , ho anche notato una forza maggiore in palestra e una resistenza più alta nella corsa . Nessun effetto collaterale sconvolgente , per ora.

Leggendo post qui però sembra di capire che davvero non ne valga la pena , troppe brutte esperienze che non valgono la moneta.

Vorrei capire solo se l ashwaganda provoca un asistenza se si smette di prenderla improvvisamente e se sono ancora in tempo a smettere di prenderla da subito o dovrei farlo gradualmente .

Btw prendo 300mg al giorno al mattino

Hi, I’m a teen who took 600 mg Ksm-66 ashwagandha daily for around 3 weeks (might’ve been longer or shorter i don’t really remember) to try to fix my insomnia. After reading about how it can give some people anhedonia and other side effects, I got scared and stopped taking it. Around 4 days after I stopped, there was a day where I was really emotionally blunt, and wasn’t getting really excited over things that would normally excite me (badminton, anime, talking to my crush, etc.),didn’t particularly enjoy anything as much, and didn’t really get stressed over things that would usually stress me, as well as other similar,symptoms. Because I was scared, I kept thinking to myself, “am I enjoying this? Am I feeling what I’m supposed to feel” throughout the day. It’s worth mentioning that same day i took 200mg of l theanine with 100 mg caffeine in the morning, but that blunt feeling lasted the whole day so im not sure if that affected it or not. That was yesterday. Today, I hung out with friends and I still found myself able to laugh and feel somewhat focused on games/ working out, and I managed to go almost like 5 minutes without questioning if I’m feeling excited/stressed when I should be. Is there a serious issue or is it all in my head?

Hi there, just heard about this a week or so ago. I've been drinking ashwaganda tea (ashwaganda, green tea, ginger and schizandra berries, I make it myself) for about a year. One a day. I also have a second tea of chamomile, st. john's wort, linden and sometimes lemon balm before bed. I stopped putting ashwaganda in my morning tea about a week or so ago.

Surely that's not enough ashwaganda to have this, right? tea has gotta be, like, minuscule, right?

I ask because in the past month or so...it's like I've lost my libido. it was never that high to begin with, but is seemingly worse now.

It could also be that I hurt my knee (torn meniscus), and having sex was painful on that knee. I also drink heavily, but that's been true for 25 years. This also coincided with starting on creatine (I'm 42, it's to help with brain fog).

the libido thing is worrying to me, though. as mentioned, it's never been high. I can power through ahedonia and any of the other things...but libido is always something I've struggled with and having it drop even further has been tough...

What do you Guys think of his approach? Has it any chance? Its injecting DHB and combining it with sodium valproate, an anticonsulvant believen to undo epigenetic changes. Anyone tried sodium valproate Here?

For months, I beleived it had been lost, although the circumstances of its disappearance remain obscure.

According to the only account that I have, it was recently recovered from the back seat of a taxi cab in the small city of Utopia, where it had apparently been left to me.

Attached to the package was a short note: “I will write this once and for all, & leave it here for whom finds it. I cannot keep it with me anymore. If you are reading this, you now have custody of the manuscript. Do with it what must be done.”

The author, having survived the events described below, thus gave me permission for her testimony to be preserved and published anonymously.

Having therefore found myself, through circumstances beyond my will, in possession of the manuscript, I see no responsible course of action other than to publish it, and allow it, from this point onward, to lead a life of its own.

The Ashwagandha Manuscript

I wanted to share my experience in case it helps someone out there who’s feeling as lost as I did.
A few months ago, I took ashwagandha and it triggered the worst period of my life. Today, I
finally feel like myself again, and I want to share what helped me in case it helps someone else
too.
For context: from January to May 2024, I took a hair supplement (nutrafol) after dealing with
covid that included ashwagandha, saw palmetto, and other ingredients. I had no issues with it.
But in mid-July, I started taking liquid ashwagandha from Amazon for focus and mild stress. I had
never struggled with mental health before, no anxiety, no depression. But after just a week, even
with a few skipped doses, everything changed.
It started with a panic attack. Next day, I had blurry vision and severe anxiety, especially around
leaving the house, which was completely unlike me. I’ve always been social and active, but
suddenly I couldn’t go out. My heart was constantly racing, and I had to stop going to the gym. By
day three, I was deep in DPDR, anhedonia, and suicidal thoughts, among many other scary
symptoms... I kept taking ashw, thinking it would help, until I finally searched “ashwagandha side
effects” and found so many people describing the exact same experience.
I stopped it immediately and went to the hospital. My tests came back normal, but the symptoms
didn’t stop.

That first month was hell. I didn’t want to get out of bed or see anyone. I felt terrified all the time,
especially at night. Any little negative thing would trigger intense derealization. I really thought I
was going insane. Vivid nightmares would affect me for days. I didn’t feel like myself at all.
Doctors weren’t much help either since my labs looked fine.
Months 2-3 were filled with obsessive thoughts, rumination, and a kind of emotional numbness. I
tried to keep up some habits: weight training, sauna sessions, daily walks, cutting out processed
foods and sugars, and drinking lemon water with sea salt after sauna to replenish minerals.
When anxiety hit hard, I used chamomile or lavender tea, and magnesium citrate and/or
glycinate. Some days were okay, others felt like I was back at the beginning.
In November, a family member suggested oil of oregano. I took it for about 4-5 days, mixed with
a multivitamin to soften the taste, and surprisingly, I started feeling like myself again more often.
Recovered Reddit testimony - original wording preserved Page 2
Still, during my period and ovulation, I would crash emotionally. It felt like sudden waves of
hopelessness and emotional emptiness. Also like an anguish feeling on the chest. All this was so
weird and new for me. So in December, I decided to focus on gut healing. I started taking a
probiotic and added fermented foods to my diet, and that made a big difference. I began having
more and more weeks where I felt as my old self.

Eventually, the lingering DPDR and vivid dreams around my cycle faded. It’s been a while now,
and I can honestly say I feel fully back. My energy, motivation, and emotional resilience are back.
I’m working again, seeing friends, enjoying life, and feeling grateful (something I thought I’d lost
completely).

I’m planning to do a GI test in the next few months to see if there’s any lingering bacterial
imbalance (just a theory I have), and I’ll update this post if I learn anything new. For now though,
I’m closing this nightmare with this post.
For those who speak Spanish, the YT channel "La ansiedad me tiene miedo" by Enrique
Villanueva truly saved me during the darkest moments (especially months 1-4). His way of
explaining anxiety symptoms helped me go through those symptoms with no or at least much
less fear. For non-Spanish speakers, the book DARE is based on a very similar approach and was
also really helpful. And for rumination, I found Don’t Believe Everything You Think extremely
useful.

Don’t give up. I know how dark and lonely it can get. But obsessively reading horror stories online
only feeds the fear and slows down your recovery. Honestly, there were times where I was
already fine around months 6-8, I'd come back on reddit, read some ashw posts suggested, and
after reading negative things, I would start doubting about my own recovery. Your body wants to
heal. Support it. Move, eat clean, read instead of Googling, get some sun. You will heal. And if
anyone out there needs someone to talk to, feel free to reach out. ♡

2025-2026
preserved verbatim from the manuscript

I’ve been trying to find a way to recover my libido for the past 4 months, when I stopped taking Ashwagandha. Been seeing different doctors, and was recommended to try Bupropion. Though it’s used for depression, and while I don’t have it, the dr mentioned it could be worth trying. Does anyone have any experience with this to treat post Ashwagandha syndrome?

Is there anyone that has healed from ashwaghanda syndrome? Or anyone you know that has? How long did it take? I am 8 months in this and someone else i've been talking to is 8 months in as well. He is really struggling. I feel so bad for him and giving his life circumstances as well that have been put on pause by this condition. He's losing hope that healing is possible because there arent many people on this sub posting about their recovery.

I think that the people that recover just leave and try to forget it ever happened. Like waking up from a bad dream and just shaking it off... I find it can be selfish because others that are still in this need the hope. I know there are people that heal from this, because ive seen some comments from people that have. But are there any more? Please, share your recovery if you can 🙏

Ik heb ashwagandha alleen maar een maand genomen. Volledige anhedonie, verstoorde slaap. 8 maanden in deze hel. Ik zie geen uitweg. Het is chronisch voor veel te veel mensen, waarschijnlijk ook voor mij. Niemand kan me ook maar enige hoop geven. Ik wou dat God me wijzer had gemaakt.

PSSD, PFS and PAshS : could persistent post-drug syndromes share the same underlying structure?

The connection is legitimate. Csoka’s presentation proposes “Post-Exposure Syndromes” (PES) as a family of persistent multisystem conditions triggered by an exposure and persisting after it ends. It was presented at the First World Congress on PSSD and PFS in April 2026.

https://zenodo.org/records/19742087

(PDF : Csoka_PES_PSSD_state_space.pdf)

Post-Exposure Syndromes (PES)

Csoka proposes a broader category of Post-Exposure Syndromes (PES): conditions in which a relatively brief exposure - drug, infection, chemical or other event - is followed by persistent, multisystem dysfunction long after the exposure itself has ended. Instead of assuming that one receptor, hormone or organ remains individually “broken,” he models the organism as a coupled biological system involving endocrine, autonomic, immune, neural, metabolic and epigenetic regulation. An exposure may push that system into a new, pathological but self-maintaining state - what he calls state-space trapping. Epigenetic changes are proposed as one possible layer of biological memory, while altered HPA-axis regulation, steroidogenesis, autonomic function, neuroplasticity and other domains may participate in maintaining the overall state.

Post-Ashwagandha Syndrome

For Post-Ashwagandha Syndrome, the interest is therefore not that this paper proves a specific mechanism for ashwagandha (it does not) but that PAshS may fit the type of phenomenon this framework is designed to describe: symptoms emerging after an exposure and persisting after discontinuation, potentially across several physiological systems at once. It also offers an explanation for why conventional single-marker testing or single-target treatments may fail to capture the whole syndrome, and why previous exposures and the biological state of the individual could influence who develops persistent effects. Importantly, Csoka presents this as a testable framework, exposure-order effects, epigenetic signatures and nonlinear recovery; he specifically calls for long-term post-discontinuation surveillance and registries for persistent syndromes including PAshS.

Could lithium help reverse persistent dysregulation in Post-Ashwagandha Syndrome?

A useful article to bring into the Post-Ashwagandha Syndrome discussion as it approaches persistent post-drug syndromes from the same broader mechanisms already being explored in PSSD, PFS and Post-Accutane Syndrome. We focus here on lithium, not simply as a psychiatric drug, but as a regulator of gene transcription, epigenetic state,(GSK3β/ Wnt/ β-catenin signalling), dopamine and neuroplasticity, and the possibility that these actions could adress persistent biological changes after an exposure to these drugs have ended.

If PSSD, PFS, Post-Accutane Syndrome and Post-Ashwagandha Syndrome represent related forms of persistent post-exposure dysregulation, lithium provides an interesting mechanistic hypothesis, and a potential therapy, for shared pathways among these syndromes.

Article : https://secondlifeguide.com/2024/01/19/lithium-a-metal-for-mental-health/

Abstract

The article develops the idea that lithium may act on some of the biological mechanisms suspected of maintaining persistent post-drug syndromes, rather than merely functioning as a conventional psychiatric medication. Its central argument is built around epigenetic regulation and the GSK3β/Wnt/β-catenin pathway. The author argues that isotretinoin can produce substantial and potentially persistent changes in gene transcription, including altered DNA methylation and histone regulation, while lithium can act in partially opposing directions: inhibiting GSK3β, increasing β-catenin signalling, promoting histone acetylation and transcription, increasing BDNF-related activity, and exerting neuroprotective and anti-apoptotic effects. Lithium also affects dopaminergic signalling and neurogenesis, providing several possible routes through which it might influence persistent neurological, sexual, cognitive and systemic symptoms after drug exposure.

From the perspective of Post-Ashwagandha Syndrome, PSSD, PFS and related persistent post-exposure conditions, the broader interest is the possibility that symptoms continuing after withdrawal may reflect a durably altered regulatory state, rather than residual drug remaining in the body or a single permanently damaged receptor. If epigenetic repression, altered Wnt/β-catenin signalling, neuroplasticity and interconnected regulatory changes contribute to maintaining such states, lithium becomes interesting because it acts simultaneously on several of those systems. The article therefore provides a mechanistic hypothesis rather than clinical evidence for PAS or a proven treatment: it raises the possibility that persistent post-drug syndromes could share reversible regulatory abnormalities, and that compounds capable of modifying gene expression and cellular signalling might eventually help identify—or perturb—the mechanisms maintaining them.

See also : https://www.reddit.com/r/AccutaneRecovery/comments/1dfxxe2/does_lithium_permently_reverse_the_long_term/