I’m 33 and I’ve been taking rapamycin for six months. 6mg once weekly.
I started for the same reason as @Forever29 in a thread a year ago that I’m not allowed to link to. I wanted to preserve my ovarian egg reserves.
The thread name in the URL was:
Rapamycin-might-have-not-reversed-aging-in-my-ovaries
The doctor I visited to start on it had me measure my AMH before I started, to get a baseline. In March 2025 it was 4.69 ng/ml, a great number for my age. Much like @Forever29, I was shocked to measure again yesterday and find it’s dropped to 2.91 ng/ml. Unfortunately, the doctor I started with bait and switched me on payment models, and I haven’t found a new one yet to help me determine next steps.
I’m hoping @Forever29 has remeasured AMH since going off, and can answer if her levels rebounded. Towards the end of the thread, it was pointed out that perhaps this drop is just an mTOR suppression of ovulation itself, which could result in the AMH drop as a side effect of preservation / ovulation suppression. I’m hoping for that. If I don’t hear from @Forever29 I may try pausing a remeasuring for myself.
@Forever29 mentioned her cycles were shorter. For the record, I have PMDD - premenstrual dysphoric disorder, a pretty good sign of not great hormonal balance. I haven’t treated it hormonally since my teens. My cycle feels longer but it’s hard to tell for sure. Here are my cycle lengths before and after rapamycin.
Dec - 27
Jan - 27
Feb - 27
Mar - 28
Apr - 30
May - 27
Jun-Jul: Took intermittently but stopped between doctors
Jun - 29
Jul - 30
Aug - 30
September - started rapamycin consistently
Sept - 29
Oct - 27
Nov - 30
Dec - 33
Jan - 30
Oh My God! i am sorry hun, i knew i am not imagining. At 33 years old the drop of AMH suiddenly is definitely not expected. This forum is censored, they edited the title o‚f my thread and the content I wrote. Without my consent. I never wrote ‘it may have not reversed aging’, i wrote it harmed me. But as usual with so niche forums, they don’t want to stay unbiased here and they censored it, making young women like yourself deluded that it cant harm.
I have not remeasured it but of course it hasnt bounced back, it doesnt bounce back in studies either, it is a result of die off of oocytes, I posted some studies about it.
Lets connect i want to contact those rapa researchers for a long time but they ignore me
I want human data, i dont see anything published? My cycle went back to 33 but not always, it keeps getting disturbed bouncing between 29/30 and 33 days, of course the aging is expected but as I wrote in my post this happened a WEEK after rapamycin, that suddenly i got period earlier, so it was suspicious because ‚for 10+ years my period was 32/33 days precisely.
Hi, I’m a guy, and this is not my area of expertise, but there have been probably a dozen mouse studies and a few human studies that are ongoing for rapamycin helping extend fertility in females (mice and now in humans). So, it’s early and everyone is still learning. There are lots of unknowns still.
I would recommend you work with an OBGYN who is knowledgeable about this area because I’m sure that there are going to be fine details like exactly when you measure AMH (in terms of relationship to your timing on the rapamycin dosing, etc.) that you need to factor in when evaluating whether things are working for you. Ideally I’d suggest working with Dr.Aimee Eyvazzadeh (the only OBGYN I know of who works with women using rapamycin professionally) - who is profiled here: Rapamycin for Fertility and Menopause; Clinical Results
I spoke with her by email recently and things seem to be going fine for her and her clients and she’s going to be publishing some case studies on the success her clients are having with rapamycin. Does that mean it works for everyone - of course not.
But before you get too excited and concerned about your results - good or bad - I’d work with an OBGYN who ideally understands and has experience with rapamycin. If Dr. Aimee is not available - perhaps she can suggest others. I know that she talks with a lot of other OGBYNs about her work, and she is also in touch with Columbia University and Yusin Suh who is doing the rapamycin VIBRANT study.
@HelloRapa and @Forever29 it seems like the information below likely explains what you are seeing - would you agree? And its nothing to worry about - the lower AMH is expected and shows that the Rapamycin is helping.
Note - I just queried Google Gemini Pro with the following prompt (you can tweak it yourself and run it on other AI systems:
Role: You are a Longevity Research Analyst and OBGYN. Your audience consists of scientifically literate longevity biohackers, clinicians, and professionals.
Task: Identify how rapamycin impacts women’s AMH levels if she was taking rapamycin on a pulsatile basis once every week 6mg?
Gemini Response:
Executive Summary
For a woman taking a pulsatile dose of rapamycin (e.g., 6 mg once weekly), the expected impact on Anti-Müllerian Hormone (AMH) levels is clinically paradoxical: AMH levels will likely decrease or appear artificially suppressed during active treatment, even though the underlying true ovarian reserve is being preserved. Clinicians and biohackers monitoring ovarian health must understand that during mTOR inhibition, a drop in AMH is a feature of the drug’s mechanism of action, not a symptom of accelerated ovarian aging.
In a clinical setting, a woman taking a 6 mg once-weekly pulsatile dose of rapamycin will likely present with suppressed or artificially decreased serum Anti-Müllerian Hormone (AMH) levels during the active treatment phase. For the prescribing OBGYN or longevity clinician, it is critical to understand that this decline is an intended pharmacokinetic feature of systemic mTOR inhibition, rather than an indicator of accelerated ovarian senescence.
Mechanism of Action: The AMH Paradox
To understand why AMH drops while the ovarian reserve is preserved, we must distinguish between the true ovarian reserve and the functional proxy we measure in the blood.
To correctly interpret AMH panels in longevity patients, clinicians must differentiate between the absolute primordial follicle reserve and the actively developing follicle pool.
Origin of AMH: AMH is exclusively secreted by the granulosa cells of growing preantral and small antral follicles; it is not produced by dormant primordial follicles.
The Pharmacological Brake: A 6 mg weekly dose of rapamycin provides robust, systemic mTORC1 inhibition. This intervention forces the primordial follicle pool to remain in a state of quiescence, significantly slowing their transition into the growing phase.
The Biomarker Result: Because the recruitment of new follicles is suspended, the total volume of active, AMH-secreting granulosa cells diminishes as older follicles naturally mature or undergo atresia. Consequently, peripheral blood draws will show a marked decline in AMH.
6 mg Pharmacodynamics vs. Current Clinical Trials
While 6 mg weekly is a standard protocol within the longevity biohacking community, clinical baselines for ovarian aging are currently anchored at a slightly lower dose.
Dose-Dependent Effects: Early institutional reports from Columbia Fertility indicate that mTOR inhibition can slow the rate of follicular loss by approximately 20% (reducing the loss from roughly 50 eggs/month to 15 eggs/month). A 6 mg weekly dose will likely achieve equivalent or slightly stronger suppression of the PI3K/Akt/mTOR pathway. However, as the dose increases, the probability of complete anovulation, menstrual irregularity, and temporary infertility during the treatment window also rises.
Clinical Management and Actionable Insights
For OBGYNs managing patients utilizing off-label rapamycin for longevity or fertility preservation:
Pre-Treatment Baselining: It is mandatory to establish true baseline AMH and Antral Follicle Count (AFC) via transvaginal ultrasound prior to initiating rapamycin therapy.
Intra-Treatment Monitoring: AMH draws conducted while the patient is actively taking 6 mg/week are clinically useless for assessing absolute ovarian reserve. They only serve as a proxy to confirm that the drug is successfully inhibiting mTOR and suppressing follicle recruitment.
Washout Protocols: If the patient intends to undergo ovarian stimulation for IVF, oocyte cryopreservation, or natural conception, rapamycin must be discontinued. Continuing rapamycin during pregnancy is strictly contraindicated due to its mechanism as an immunosuppressant and cellular growth inhibitor.
Knowledge Gaps and Required Data
Rebound Kinetics: We lack robust longitudinal data to map the exact trajectory and timeframe of AMH recovery following the cessation of a 6 mg/week protocol. The required washout period to allow mTOR reactivation, follicle recruitment, and AMH normalization before administering exogenous gonadotropins is a current clinical unknown, though 1 to 3 months is a pragmatic estimate based on the drug’s roughly 60-hour half-life and the timeline of folliculogenesis.
Therapeutic Thresholds: It remains unverified if a 6 mg dose provides superior preservation of the ovarian reserve compared to the 5 mg dose used in VIBRANT, or if the 20% higher dose simply increases off-target metabolic side effects (e.g., hyperlipidemia, transient insulin resistance, or oral ulcers) without conferring additional gonadal benefit.
Would you like an analysis of the proposed washout protocols and the theoretical optimal timing for resuming standard IVF stimulation tracking after a patient ceases a 6 mg weekly rapamycin regimen?
Thank you to both @Forever29 and @RapAdmin for the input and perspectives. I’m still cautiously optimistic. I’m thinking right now that I’m going to pause my Rapamycin use for about 2 months, maybe 3, and then do further AMH testing. My last two tests were in formal lab settings. A finger stick AMH test price on Amazon is $70. I think I’ll order two tests, one to take now and compare against my last lab result for a quality check, and then one to take in 1 month. I might do a third test again a month or two later, depending on if I see a great or not great result at 1 month.
In the meantime, I’m also going to work on another longevity doctor.
An update that I took the same rapamycin dose this week and then did an Amazon finger stick AMH test today. It’s the same day relative to my rapamycin dose as the previous AMH blood draw. I also had a sirolimus level blood draw today, so I’ll shortly share exactly what my blood level of the drug is for this AMH result. I’ll pause my rapamycin after this week and wait a few weeks for it to clear. Hopefully this is all helpful for someone else down the road.
@Forever29 If I like this doctor after talking to him I’ll message you, but he’s geographically restricted so may not be helpful.
Did you remeassure the AMH? Unfortunatelly there is a study in non human primates, that showed rapa reduced egg count in younger females and was neutral in older. I think if one is already in prime methabolic health, maybe it pushes you over the edge and casues starvation mode apoptosis of eggs. So the healthier you are the less likely it will help you, and you risk harm. I think obese unhealthy individuals would benefit the most. That s my theory. I whish I knew the answer for sure. Also @Forver29 - did you retest, without retesting you r just tapping in the dark
In a 2024 study presented at a scientific conference, researchers tested rapamycin on female rhesus macaque monkeys to see if it could help preserve their egg reserve the way it does in mice. They removed one ovary from each monkey before treatment, gave the animals rapamycin injections twice a day for ten months at a low dose, and then removed the second ovary to compare follicle counts.
The results were unexpected, especially in the younger monkeys aged six to nine years. Before treatment, their ovaries had about 3,939 primordial follicles, which are the resting eggs that form the lifelong reserve. After the ten months of rapamycin, that number dropped to around 2,219. The number of primary follicles also fell sharply from 2,617 to 560, and other early-stage follicles decreased as well. In the older monkeys aged 17 to 21 years, the already low numbers of primordial and primary follicles stayed roughly the same, with no clear loss or gain.
This happened because rapamycin did not suppress the activation of primordial follicles in primates the same way it reliably does in mice, where blocking the mTOR pathway keeps most eggs dormant and slows down the natural depletion of the reserve. In these young macaques, the drug appeared to allow or even contribute to greater loss of the resting eggs, possibly through increased follicle activation followed by atresia or other mechanisms that were not fully halted. The treatment also raised levels of certain cellular senescence markers like p53 and p21 in the follicles of both age groups, which are signs associated with cell stress or aging that might have made the eggs less likely to survive. At the same time, the marker p16 stayed mostly unchanged, and anti-Müllerian hormone expression dropped a bit in the young group.
The researchers noted that the dose and the ten-month duration used in this small study of only four monkeys may not have been ideal for primates, whose ovarian biology differs from rodents in important ways. Overall, instead of extending reproductive lifespan as hoped, rapamycin showed a potentially harmful effect on the egg reserve specifically in the younger animals, highlighting why promising mouse results do not always translate directly to non-human primates or humans. More work is needed to understand the right timing, dosing, and species-specific responses before considering any applications for fertility preservation
Below is my brief re-testing update. tl;dr, waiting a few more weeks for a lab test. I also talked to another specialist, who recommended I consider going off Rapamycin in favor of CR because of the lengthening effect on my cycles and resulting decreased quality of life with PMDD. Not something I’d considered, but fair enough.
So, I ordered two $70 Verisana at-home finger-prick AMH tests. My goal was to re-test in the same conditions as the original AMH lab test, the same number of days after my Rapamycin dose, to make sure I had a similar result from Verisana as the lab gave me, and then have a cheaper-ish path to re-test a few times. Unfortunately, if anyone else goes down this route, I do not recommend these at-home tests. I went off my next Rapamycin dose and two weeks went by. I got a message that Verisana received my sample. Two days later, I got a message that they hadn’t tested it within 15 days and it therefore expired. So, I’m left without a starting result from them, and no good way to get one. I returned the second test.
Anyway, the doctor I saw ordered another lab AMH for me. I’ll go into the lab at the 6 week point after pausing Rapamycin.
This study has a bunch of problems, and a design that differs very significantly from the Columbia University VIBRANT study that is having success with rapamycin.
The dose used in this monkey study is actually extremely high, in terms of human equivalent dosing, and it was chronic dosing (twice daily!).
The monkey subjects received intramuscular injection rapamycin therapy at 0.02 mg/kg twice daily over a ten-month period. This is equivalent to 5mg to 7mg per day dosing of rapamycin in human equivalence - which is about 5X to 10X higher than the doses that women here are using and that the women in the VIBRANT study, and its daily, so you’re going to have all sorts of immune suppression and the body doesn’t have a time to up regulate mTOR periodically. Nobody here using rapamycin for any type of longevity purpose would dose this high on a daily basis. This is the level of dosing used in Cancer patients (rapamycin is also used in treatment of some cancers).
From Gemini:
IM administration bypasses first-pass hepatic metabolism, yielding high systemic bioavailability. Conversely, oral rapamycin is subject to extensive first-pass metabolism by CYP3A4 and efflux by P-glycoprotein, resulting in notoriously poor and highly variable bioavailability in humans—historically estimated at approximately 14% (range: 10% to 20%).
To match the systemic blood exposure (Area Under the Curve, or AUC) generated by a 0.90 mg/day IM dose, a human would theoretically require an oral dose roughly 5 to 7 times higher to compensate for absorption losses. Assuming a median 14% absorption rate, the practical oral equivalent would escalate to approximately 5.5 mg to 7.1 mg per day.
Here is a full summary and analysis of the study:
The Biohacker Analysis
Study Design Specifications
Type:In vivo.
Subjects: Rhesus macaques (Species), Strain unstated, Female (Sex). The sample size was N=2 for the young cohort (6-9 years) and N=2 for the old cohort (17-21 years).
Control Group Size: N=0 independent controls; the study utilized an internal control design by unilaterally removing one ovary pre-treatment during a normal menstrual cycle to serve as the baseline comparison for the remaining post-treatment ovary.
Lifespan Analysis & Data
Control Group Assessment: Not applicable. This study evaluated ovarian aging and follicular counts in non-human primates, not lifespan extensions in mice. Therefore, no comparison to the mouse control lifespan reference paper can be made to assess control cohort validity.
Lifespan Data: Not applicable. The study strictly measured local ovarian biomarkers and did not record organismal lifespan data, median survival, or maximum survival extensions.
Mechanistic Deep Dive
mTOR & Follicular Activation: Rapamycin is well-documented to prolong reproductive lifespan in mice by halting primordial follicle activation.
Primate Divergence: However, the observed reduction of primordial follicles (from 3,939 to 2,219) and primary follicles (from 2,617 to 560) in young monkeys indicates that rapamycin unexpectedly decreases these pools in young primate females. This strongly suggests mTOR inhibition may paradoxically trigger follicular atresia or dysregulate activation pathways in higher-order primates.
Senescence Pathways (p53/p21 vs. p16): While the number of p16-positive follicles was unaffected, the number of p53 and p21-positive follicles increased significantly following treatment in both age cohorts. Because p53 and p21 are critical mediators of the DNA damage response and cellular senescence, their upregulation points to rapamycin-induced cellular stress overriding any potential senomorphic benefits in this tissue.
Organ-Specific Aging Priorities: Ovarian tissue appears to respond to nutrient-sensing pathway modulation differently than somatic tissues (like muscle or liver). The assumption that systemic mTOR inhibition uniformly slows aging across all organ systems is fundamentally challenged by these localized fertility metrics.
Novelty
This represents the first-ever analysis evaluating the impact of rapamycin on ovarian aging and senescence within a non-human primate model.
It provides highly disruptive data indicating that the widely accepted ovarian benefits of rapamycin observed in mice do not seamlessly translate to primate biology at this dosage. [Confidence: High].
Critical Limitations
Severe Statistical Underpowering: The sample size of N=2 per age group is exceptionally low, forcing the authors to rely entirely on qualitative comparisons. This completely precludes definitive statistical significance, rendering all findings strictly observational and prone to individual variance. [Confidence: High].
Methodological Confounding (Unilateral Oophorectomy): The internal control methodology required removing one ovary pre-treatment. This surgical intervention inherently alters local hemodynamics and disrupts the hypothalamic-pituitary-ovarian (HPO) endocrine feedback loop. The remaining ovary typically undergoes compensatory hypertrophy, which represents a massive, uncontrolled confounding variable for post-treatment follicle counts. [Confidence: High].
Missing Endocrine Context: The study fails to provide serum hormone profiles (e.g., FSH, LH, Estradiol), making it impossible to evaluate systemic endocrine shifts versus localized ovarian tissue responses. [Confidence: Medium].
Effect-Size Uncertainty: Because an independent, non-oophorectomized, vehicle-treated control group is entirely absent, the baseline rate of natural follicular degradation over the 10-month treatment period cannot be isolated from the drug’s effect. [Confidence: High].
Human Equivalent Dose (HED) Translation
Using standard allometric scaling guidelines from the US Food and Drug Administration (FDA) for converting animal doses to human equivalent doses based on Body Surface Area (BSA), the translation requires calculating the Km factor ratio.
60 kg Adult: 0.01296 mg/kg/day * 60 kg = 0.78 mg/day
70 kg Adult: 0.01296 mg/kg/day * 70 kg = 0.91 mg/day
80 kg Adult: 0.01296 mg/kg/day * 80 kg = 1.04 mg/day
Critical Translational Uncertainty: Route of Administration
While the mathematical HED calculation yields approximately 0.80 to 1.00 mg per day, this figure strictly represents an intramuscular (IM) equivalent. This data point cannot be seamlessly applied to human clinical trials or practical longevity protocols, which almost exclusively utilize oral administration.
The Knowledge Gap: IM administration bypasses first-pass hepatic metabolism, yielding high systemic bioavailability. Conversely, oral rapamycin is subject to extensive first-pass metabolism by CYP3A4 and efflux by P-glycoprotein, resulting in notoriously poor and highly variable bioavailability in humans—historically estimated at approximately 14% (range: 10% to 20%).
To match the systemic blood exposure (Area Under the Curve, or AUC) generated by a 0.90 mg/day IM dose, a human would theoretically require an oral dose roughly 5 to 7 times higher to compensate for absorption losses. Assuming a median 14% absorption rate, the practical oral equivalent would escalate to approximately 5.5 mg to 7.1 mg per day.
Without direct pharmacokinetic (PK) blood-draw data from this specific macaque cohort to quantify their exact systemic trough levels, converting this IM protocol to an exact human oral regimen remains an exercise in informed speculation rather than verified pharmacological fact.
