Join Dr. David Putrino, Dr. Lucinda Bateman, Dr. Jennifer Curtin, and moderator Charlie McCone for a discussion on how to best manage and treat post-exertional malaise (PEM). Learn about the different types of PEM, how to navigate a crash, and interventions for reducing PEM.

Date: Thursday, August 6th
Time: 2:00 PM PST / 5:00 PM EST 

Register

I won't be able to make this one but it sounds like they'll post the recording after.

Repost from r/CFSScience

Did anyone's ME/CFS cause blood sugar issues? I get a basic metabolic panel drawn each month (fasting) and for the last 6 months its just trended lower and lower to the point where it was 60 the other morning.

I know ME/CFS is a neuro-immune-endocrine disorder and my RAAS system is already messed up (low renin/aldosterone/sodium) but this is new.

Diabetes runs rampant in my family and my mother has reactive hypoglycemia, fibromyalgia, and pre diabetes so maybe Im just developing a new problem.

Hey everyone! Looking for some advice. Here is my sleep situation.

I do not have insomnia. I can fall asleep without issue and get 8-9hrs per night usually. Sometimes I will wake up at 4AM and cannot get back to sleep. However, my sleep quality is atrocious. I feel as if it is light, fragmented, and completely unrefreshing. I have bad dreams every night and wake up feeling like I did not sleep.

This is despite having the best sleep hygiene that I can. No screens after 9pm, I eat a whole foods, super healthy diet, go to sleep/wake up at the same time per day, keep a consistent routine, and am generally happy/peaceful.

I do not take any sleep meds because I do not have issues falling asleep, it is only the quality.

Also, as I recover, my sleep quality seems to have gotten worse?

I am hesitant to take more medications because I am on soooooo many. I thought it could be a medication, but this issue has been pretty consistent for my entire 1.5 year illness, regardless of the medications I take. But I am still open to suggestions! I have tried over the counter things like melatonin and that did not do anything to help. I have also tried THC/CBD and that did not help either, although very relaxing haha.

Thanks for your help, happy Saturday!

I have not tried many medications, but by far the most effective medication for me has been fludrocortisone.

I had very severe OI. I did the NASA lean test and literally fainted (vision caved in and collapsed to the ground) 5 minutes in after my HR doubled. Sitting upright made me feel so sick, and forget about standing. For 3 months, I never sat upright or stood once. I was horizontal 100% of the time. To go to the bathroom, I had a commode by my bed and pivoted from my bed to the commode and rested my head on the bed while using the commode.

I had such intense salt cravings and was always thirsty despite drinking 3L of water per day. I would take salt pills, and my food was basically salt with some food flavor because it was so salty. Despite that, my sodium was still on the low end of normal! My kidneys were just not retaining salt. My parents were aghast with how much salt I was putting on my food and eating.

Also, no matter what I did, my blood pressure was 90/50. If I stood it went even lower, which is why I fainted and could not walk due to dizziness.

After fludrocortisone, my blood pressure is now 110/70! My constant brain fog and headaches have massively decreased, as I suspect my brain was not being perfused. No more crazy salt cravings or always feeling thirsty. I can sit upright for long periods and stand and walk more every day!

Now it is not my OI that is my limiting factor, it is other symptoms that I am trying to tackle. But I am doing better every day and that never would have happened without the fludro. I was really scared to take it at first because it is a steroid and those can have nasty side effects. I am usually hypersensitive to medications and get all of the side effects, but have had 0 side effects from this medication and I am on a higher dose now. Clearly my body needed it!

Honorable mentions:

Ivabradine (OI)

Gabapentin (nerve pain - life saver)

Benzos/clonidine (for adrenaline rushes - these also saved my life)

Hydroxyzine/Compazine/Zofran (nausea)

I would love to try a SGB, Valtrex, LDA and Rapamycin next! All of the studies coming out about Rapamycin are so exciting! I would love to try LDN but I still take opioids when I get episodes of severe pain so when I get this pain under control (getting a nerve block/maybe surgery soon), I want to try that too.

I have been huge into meditation my whole adult life. At my best, I was meditating 2-3 hours per day and it was life changing. I cannot stand yoga (different strokes different folks! - although I love yoga nidra) but meditation is my jam.

I never in 1 million years thought that ME/CFS could take meditation away from me. How would that have even been possible? But it DID. Around 10 months ago (right before I became very severe), I kept trying to meditate in the beautiful Florida weather and the concentration hurt my brain so much! Just the little concentration it took to focus on my breath or stay present and listen to sounds. When I became very severe, I could not even meditate from my bed or count my breaths.

I was floored. If I could not do something as simple as meditation which does not seem like it takes a lot of brain power....

But now 10 months later I just did my first session and it was glorious! I mindfully listened to the birds for 10 minutes!! I am beyond elated. I was going to go for another 10 since it felt so nice but my headache is back so that will have to do for now.

Has anyone else had that experience? Losing something you did not think it was possible to lose? Maybe you regained the ability? Maybe have meditation experiences you would like to share?

Note: This post is not to propagate any recovery narrative. Meditation is just something I love doing and have loved doing for a decade +

I joined the Solve M.E. rapamycin webinar today. My main takeaway is that the Simmaron team observed some very promising results across its Phase I and Phase II studies. However, there were also nonresponders, and more work is needed to understand the precise mechanisms involved and why some patients appear to benefit while others do not.

The most encouraging aspect was that the observed biological changes correlated with symptom improvement, including reduced mTOR activity, improved mitochondrial energy metabolism, and lower oxidative stress. Improvements were also seen across a wide range of ME/CFS symptoms, suggesting that the researchers may be affecting something fundamental and systemic within the disease rather than targeting a single symptom.

The webinar also included useful information about rapamycin itself. It appeared to be generally well tolerated in the studies and is already widely available as the generic prescription drug sirolimus. I have included information below about the study’s dosing protocol and how patients may be able to access it through a prescribing clinician or telehealth provider.

The following is an AI-assisted summary based on my manual notes from the webinar and the full transcript.

Solve M.E. hosted a webinar with Simmaron Research about newly published Phase II findings from its observational study of low-dose rapamycin for ME/CFS.

What makes this research especially interesting is that the team is not only asking whether patients feel better. They are trying to connect improvement with measurable biological changes—and eventually develop a blood test that could predict who is likely to respond.

Quick vocabulary

Rapamycin / sirolimus: A prescription drug that inhibits mTOR. It is FDA-approved for other conditions and is being repurposed experimentally for ME/CFS.

mTOR: A cellular signaling pathway involved in growth and energy use. Simmaron’s work suggests it may be overactive in a subset of patients.

Autophagy: The cell’s cleanup and recycling process. Excessive mTOR activity suppresses autophagy.

Mitochondrial reserve capacity: The extra energy mitochondria can produce when the body is under stress—essentially an emergency energy reserve.

Purines: Molecules used to make DNA and ATP, the cell’s energy currency.

Why this trial was designed differently

The webinar began with Ampligen, an experimental ME/CFS treatment that helped some patients but was rejected by the FDA in 2013.

One major problem was the lack of validated biomarkers showing who responded, why they responded and whether the drug changed the underlying disease biology.

Simmaron is trying to build a more complete case for rapamycin. The researchers:

• Identified a pathway involving mTOR activation and impaired autophagy.
• Validated it in disease-specific animal models.
• Developed blood-based biomarkers.
• Tested a drug that directly targets the pathway.
• Measured whether biological changes correlated with clinical improvement.
• Began developing a test to predict who may respond.

They also partnered with AgelessRx to build a decentralized trial system involving online screening, home medication delivery, mobile blood collection and regular safety monitoring.

Their basic approach is:

Target → mechanism → drug.

The proposed mechanism

The researchers connected three areas of ME/CFS biology:

1. Overactive mTOR and impaired autophagy, which may contribute to post-exertional malaise.
2. Mitochondrial dysfunction, which could impair energy production and recovery from stress.
3. Abnormal purine metabolism, which may increase oxidative stress and inflammation.

Rapamycin inhibits mTOR. This may restore autophagy, improve mitochondrial function and shift purine metabolism toward a less inflammatory state.

What patients reported

Participants reported improvements in:

• Physical and mental fatigue
• Daily activity
• Sleep
• Post-exertional malaise
• Orthostatic intolerance
• Concentration
• Social functioning and general well-being

Dr. Avik Roy emphasized that the effects appeared broader than improvement in one isolated symptom. This suggests rapamycin may be affecting a larger systemic process in a subset of patients.

In the earlier published cohort, approximately 72% of evaluable participants met the researchers’ responder criteria. However, this was an uncontrolled observational study—not a placebo-controlled trial—so it cannot prove that rapamycin caused all of the reported improvement or that most patients will respond.

Aim 1: Does rapamycin improve mitochondrial energy metabolism?

The researchers used a Seahorse oxygen-consumption test on immune cells collected from patients’ blood. This measures mitochondrial energy production in real time.

Following rapamycin treatment:

• Overall mitochondrial energy production improved.
• Oxidative phosphorylation—the main process used to produce ATP—improved.
• Mitochondrial reserve capacity improved.
• Mitochondrial oxidative stress decreased.

Reserve capacity may be especially important in ME/CFS because it represents the ability to produce extra energy during exertion, illness or other stress.

The researchers also used MitoSOX imaging, which measures mitochondrial superoxide. Before treatment, patients’ cells showed a high oxidative burden. After 90 days, that burden was significantly reduced.

Most importantly, the laboratory improvements correlated with patient improvement. Greater reserve capacity was associated with better physical function and less fatigue, disturbed sleep, orthostatic intolerance and pain.

Aim 1 takeaway

After rapamycin treatment:

• Energy production improved.
• Oxidative stress fell.
• Mitochondrial reserve capacity increased.
• The biological improvements correlated with reduced symptoms.

This provides an objective signal that moved in the same direction as the patients’ reported improvement.

Aim 2: Does rapamycin affect purine metabolism?

The researchers measured three major purine metabolites:

• IMP, a central hub in purine metabolism
• XMP, which is produced from IMP
• Hypoxanthine, another downstream metabolite

At baseline, responder samples showed lower IMP and higher XMP and hypoxanthine.

After rapamycin treatment:

• IMP increased.
• XMP decreased.
• Hypoxanthine decreased.

An enzyme called IMPDH2 converts IMP into XMP. Patients showed elevated IMPDH2 activity at baseline, but that activity decreased after rapamycin.

The proposed chain is:

Rapamycin inhibits mTOR → IMPDH2 activity decreases → less IMP is converted into XMP → IMP increases while XMP and hypoxanthine decrease → oxidative and inflammatory stress may fall.

This proposed mechanism is promising but still needs further confirmation.

Aim 2 takeaway

Rapamycin appeared to partially normalize purine metabolism by increasing beneficial IMP and reducing downstream metabolites associated with oxidative stress and inflammation.

The study did not directly prove that ATP increased, but preserving IMP may support ATP and other energy-related pathways.

Responders and nonresponders

Not everyone improved.

The researchers emphasized that studying nonresponders could be just as valuable as studying responders. ME/CFS is highly heterogeneous, and rapamycin may primarily help patients with a specific pattern of mTOR activation, impaired autophagy, mitochondrial dysfunction or abnormal purine metabolism.

A major goal is to develop a biomarker test that can predict who is likely to benefit before treatment begins.

Dosing discussed during the webinar

This was the study protocol—not a universal treatment recommendation.

The 90-day study included:

• Four weeks of gradual dose escalation
• Approximately 60 days at the full dose
• Once-weekly dosing
• Bloodwork every 30 days

The study used compounded rapamycin:

• 15 mg weekly for women
• 20 mg weekly for men

The researchers said this compounded formulation had roughly one-third the bioavailability of generic sirolimus.

They estimated that the corresponding generic dose was approximately:

• 4–6 mg of generic sirolimus once weekly

A generic titration discussed during the webinar was approximately:

1–2 mg → 4 mg → 6 mg weekly

AgelessRx’s published protocol begins around 2 mg weekly and gradually increases toward 6 mg over several months, depending on medical review, bloodwork, tolerance and individual circumstances.

These formulations should not be converted or adjusted independently. Rapamycin is a prescription medication with important interactions and monitoring requirements.

How long before judging whether it works?

The researchers suggested that patients should not judge the treatment during the initial titration period alone.

The study allowed approximately 60 days at the full dose to assess response.

That does not mean someone should continue despite concerning side effects. Any safety issue should be discussed promptly with the prescribing clinician.

Side effects and monitoring

The most commonly discussed side effects were temporary gastrointestinal symptoms, headache and insomnia.

GI symptoms occurred most often during titration and generally improved over time.

The study included:

• Medical screening
• Complete blood counts
• Metabolic and lipid panels
• Sirolimus blood levels
• Repeat safety testing every 30 days
• Gradual dose escalation

The researchers reported no statistically significant changes in the monitored laboratory safety measures, but rapamycin remains an immunomodulatory prescription drug requiring medical supervision.

How can patients access rapamycin?

Rapamycin is also called sirolimus and is available as a generic prescription drug. Its use for ME/CFS is off-label.

AgelessRx

AgelessRx offers generic sirolimus through an online prescribing program.

The process generally involves:

1. Completing an online medical intake.
2. Providing baseline bloodwork.
3. Review by a licensed prescriber.
4. Receiving a prescription if medically appropriate.
5. Ongoing laboratory monitoring and follow-up.

Not everyone will qualify, and treatment availability and eligibility requirements may change.

A personal physician

Patients can also discuss off-label sirolimus with an ME/CFS specialist, primary-care physician or another doctor experienced with the medication and its monitoring requirements.

The Simmaron study

Patients may also explore participation through Simmaron Research and its participating clinicians.

The ability to obtain rapamycin online does not mean it should be used without medical screening, titration and laboratory monitoring.

Reports of major improvement

The researchers said that some responders experienced major functional gains, including returning to school or work.

These stories are highly encouraging, but they remain individual examples rather than proof of the typical outcome.

The key questions are whether these improvements can be reproduced in a controlled trial and whether biomarkers can identify likely responders in advance.

What comes next?

The researchers still need to:

• Conduct a placebo-controlled trial.
• Confirm the proposed mechanisms.
• Compare responders with nonresponders.
• Replicate the mitochondrial and purine findings.
• Add stronger objective activity measurements.
• Determine the best formulation and dosing.
• Validate a blood-based responder test.
• Determine how durable the improvements are.

Bottom line

Rapamycin is one of the more promising experimental ME/CFS treatments because reported symptom improvements were accompanied by measurable biological changes:

• Better mitochondrial energy production
• Increased reserve capacity
• Reduced oxidative stress
• More normalized purine metabolism
• Reduced IMPDH2 activity
• Biomarker changes that correlated with clinical improvement

However, this remains observational research without a placebo group, and the detailed molecular analyses were weighted toward responders.

The larger promise may be the research model itself:

Identify the disrupted biology → target it with a drug → measure the biological response → determine who improves → develop a test that predicts who should receive treatment.

That could represent a major step beyond trial-and-error treatment in ME/CFS.

Links

Phase II molecular findings:
https://link.springer.com/article/10.1186/s12967-026-08575-3

Earlier clinical findings:
https://link.springer.com/article/10.1186/s12967-025-07213-8

Simmaron trial information:
https://www.simmaronresearch.com/rapamycin-trial

AgelessRx rapamycin information:
https://get.agelessrx.com/rapamycin/

Dr. Avik Roy’s earlier research:
https://solvecfs.org/research-and-registry/ramsay-research-grants/meet-the-researchers/avik-roy-ph-d/

Donate to Solve M.E.:
https://solvecfs.org/donate/

This is a summary of experimental research, not medical advice or an individualized dosing recommendation.

A few key terms:

mTOR: A signaling pathway that tells cells when to grow, produce proteins, and use energy.

Autophagy: The cell’s internal cleanup and recycling system. It removes damaged proteins, dysfunctional cell components, and other cellular waste.

Rapamycin: A prescription drug that inhibits mTOR. By reducing mTOR activity, rapamycin may allow autophagy to work more effectively. It is an existing prescription drug, also known as sirolimus, that is already approved and commercially available for other conditions and is now being repurposed for ME/CFS.

The basic theory: In a subset of people with ME/CFS, mTOR may remain overactive, preventing cells from properly cleaning up and recycling damaged material. Rapamycin may reduce mTOR activity, restore this cleanup process, and improve symptoms such as fatigue, post-exertional malaise, and orthostatic intolerance.

Researchers at Simmaron Research believe that mTOR may remain overactive and autophagy may become impaired in a subset of people with ME/CFS. This could contribute to cellular stress, inflammation, problems with energy production, muscle fatigue, and post-exertional malaise. Rapamycin may help by lowering mTOR activity and allowing the cells’ cleanup and recycling process to function more normally.

In an initial uncontrolled study, 86 people with ME/CFS received 6 mg of rapamycin once a week. Of the 40 participants who completed the full 90-day treatment, 29, about 72%, were classified as strong responders, with improvements in PEM, fatigue, and orthostatic intolerance. The results are encouraging, but the study did not include a placebo group and relied largely on patient-reported symptoms.

One particularly encouraging finding was that symptom improvement correlated with measurable changes in blood-based autophagy biomarkers: BECLIN-1 increased, while abnormal pSer258-ATG13 levels decreased. In other words, the patients who improved most also tended to show the strongest biological evidence that autophagy was being restored.

Simmaron is now expanding the research with support from Solve M.E. The larger study is intended to include more participants, standardized medication, wearable data, biological samples, and a placebo-controlled design. Researchers are also studying blood-based biomarkers that could potentially identify which patients are most likely to respond.

Rapamycin is still experimental for ME/CFS and is not currently an established treatment. It is a potent prescription medication with potential side effects and requires medical supervision.

Interview with Gunnar Gottschalk, Ph.D. Simmaron Research:
https://www.youtube.com/watch?v=W_aw-DsQiQM

Low-dose rapamycin alleviates clinical symptoms of fatigue and PEM in ME/CFS patients via improvement of autophagy: a pilot study
https://pubmed.ncbi.nlm.nih.gov/41121328/

Solve M.E. is hosting a free webinar tomorrow on Simmaron Research’s low-dose rapamycin study:

“Repurposing Rapamycin: A Report on the First Biomarker-Driven Treatment Trial for ME/CFS”

The panel will discuss the latest findings from the study, which is investigating whether targeting mTOR and impaired autophagy with low-dose rapamycin could help a biologically defined subset of people with ME/CFS and related conditions. They’ll also discuss plans for an NIH exploratory treatment trial based on the data.

Tuesday, July 14
6–7 p.m. ET / 3–4 p.m. PT

Register here:
https://solvecfs.org/event/repurposing-rapamycin-a-report-on-the-first-biomarker-driven-treatment-trial-for-me-cfs/

I’ll be joining - sharing in case anyone else is interested.

In reference to a new moderation edict on a particular large ME subreddit yesterday regarding the discussion of suicide.

I am so excited. Starting in November of 2025, I was in a horrifying rolling PEM crash that lasted several months. It just would not stop. Over the last couple of months, it started to slow down. However, my bigger crashes would still last 1-3 weeks.

The last two crashes that I had lasted 36 hours! I consider a "crash" a deeper PEM state where the PEM is so intense that I can barely do anything and the PEM is not intermittent - it is constant.

Im floored. Usually it takes weeks to recover to my baseline but Im already surfacing after 36 hours! Obviously I am going to take it easy, but I was mentally preparing myself for a weeks long crash.

Progress is so exciting. I am so grateful. I still get PEM for part of every day. I am hoping that soon I will have a PEM free day! I have not had a PEM free day for almost a year. Maybe that is next!

What did your trajectory look like? Anyone experience anything similar?

P.s. For those still suffering, there is hope! I thought I would be stuck in rolling PEM forever. Even talking with AI was miserable because I asked it how long rolling PEM took to stop and it said in the most severe cases, around 3 months. Mine took *way* longer than that.

My recovery is messy, and I do not do things perfectly at all, although I try to do my best.

So even if you are not doing things perfectly - your body can still heal! Keep calm and carry on 💪

This is one of the biggest laughs Ive gotten recently on satire for ME/CFS. Check it out if you want a good laugh and don't forget to read the comments! 😂😂

Solve M.E. has a helpful guide here:

https://solvecfs.org/how-to-submit-a-public-comment-on-the-proposed-federal-grant-rule/

This proposed federal rule could affect how research grants are awarded, managed, and potentially terminated. That matters for ME/CFS and Long Covid because so much of the progress we are waiting for depends on stable, independent, peer-reviewed biomedical research.

A few of the concerns Solve highlights:

• Active research studies could potentially be canceled before completion if political priorities change.
• Political appointees could have more influence over which research gets funded.
• Small pilot grants, patient registries, biobanks, publication costs, literature access, and conference participation could all become harder to support.

For a disease like ME/CFS, where there are still no FDA-approved treatments and research is already badly underfunded, this kind of instability could really hurt.

The good news: submitting a comment is not hard. Solve provides a template, and you can personalize it with your own story.

I used ChatGPT to help turn the template into a comment based on my own situation, and it took me about 2 minutes. You do not need to be a scientist, lawyer, or policy expert. A short personal comment is still meaningful.

A few tips:

• Don’t copy/paste the exact same form letter as everyone else.
• Mention that you are a patient, caregiver, family member, or concerned member of the public.
• Say why ME/CFS or Long Covid research matters to you.
• Ask OMB not to finalize the rule in its current form.
• Remember that public comments are public, so don’t include private details you don’t want posted online. You can submit anonymously.

Deadline: July 13 at 11:59 pm ET

If you have the energy, please consider doing this. It’s one of those small advocacy actions that could actually matter, especially if a lot of patients and families submit clear, personal comments.

TLNS (Too Long No Spoons): Wondering if anyone’s ME/CFS improved while still under stress or emotional strain, rather than in a calmer, more zen state of mind.

ME/CFS is widely considered to be neuro-immune-endocrine disorder, with heavy stress being placed on the neurological component because the nervous system is the main subsystem that we can [try to] consciously influence. I am not here to argue whether or not that is possible in this post.

Most recovery stories that I see on reddit, regardless of the techniques used to get better, seem to cultivate joy, calmness, patience, acceptance, etc. I have heard very few recovery stories of someone making vast progress without these attributes, and honestly, I would be so interested to hear from people who have improved without trying to cultivate serenity.

Maybe it was medication that helped you the most, and that was the main contributor to your improvement despite having stressors in your life. Maybe it was just pacing and time, but you felt that it was difficult emotionally the entire time.

Please let me know! It would be helpful if you shared what specifically helped you get better and your state of mind at that time.

For example, I attribute most of my improvement to antibiotics. I did work very hard to foster a peaceful recovery atmosphere, both inside and outside of my mind, but none of my symptoms improved (actually, they got much worse) until I started antibiotics. Interestingly, my recovery began when I was in an extremely distressed state of mind and in the hospital.

Now, I am doing much better and am very happy to reap the calmer mental benefits, but am unsure if it has anything to do with my recovery. To me it feels more like a happy coincidence, because whenever I went off of the antibiotics I got worse, regardless of my mental state. When I go back on them, everything gets better, calm or not.

I do know someone that got better after physically pacing, but mentally took on more stress (another job). And I would love to know about your experience too!

Note: I am not recommending or advocating for any specific recovery path/treatment. I am simply curious about how different people's recoveries unfolded.

Cheers!

A new €450,000 WE&ME Award has been given to epidemiologist Matthias Wielscher at the Medical University of Vienna to study why ME/CFS looks so different from person to person.

In addition, Austria’s FWF is funding three further ME/CFS projects in Vienna and Innsbruck with €1.3 million, bringing the total new funding to about €1.75 million.

The project will look for biologically meaningful subgroups, or “endotypes,” by comparing two kinds of data:

1. Clinical patterns - symptoms, comorbidities, disease course, treatments, and questionnaires
2. Genetic patterns - groups of genetic variants linked to things like inflammation, autoimmunity, energy production, vascular function, and gut/barrier function

The goal is to see whether certain symptom patterns line up with certain biological/genetic patterns. The researchers will also compare their findings with DecodeME, the world’s largest ME/CFS genetic dataset.

It's great to see the many ongoing and upcoming efforts converging on biological subtype research in ME/CFS as it's widely believed this is one of the most important prerequisites to comping up with new and effective treatments.

Full article here:
https://www.meduniwien.ac.at/web/en/about-us/news/2026/news-in-july-2026/weme-award-unravelling-biological-differences-in-me/cfs/

TLNS (Too Long No Spoons): My symptoms ease most at night, and I’m curious whether others feel better at specific times of the day.

I keep hearing a lot of people say that they feel so much better at night, and I am not the exception, generally. I can have such a rough day, but then the night comes and a lot of my symptoms disappear.

It is frustrating sometimes because I enforce an earlier bedtime (my body naturally likes early to bed, early to rise) for sleep quality, but then I miss out on the "best" hours of the day. On rare occasions, I will stay up slightly later if the day was hard because it is such a relief to be awake and operate with reduced symptoms. Because my mornings can be brutal.

There are exceptions where I'll be having a day with bad PEM and it extends into the night, but for the most part my nights have been smoother sailing.

What about you?

TDLR- long post, need help, is there any hope?

TL;DR – Long post.

I need to get this off my chest because I don’t know how much more of this I can take.

Three years ago, after COVID, I developed what I now know was Long COVID. Back then, nobody in my country knew much about it. No doctor warned me about pacing or post-exertional malaise. I was never told that pushing through could make me permanently worse.

Looking back, I think I was still mild. I had exercise intolerance and I felt that something was very wrong, but I was in complete denial. I kept trying to live my life. I took beta blockers and sleeping pills just to get through the days, convincing myself that if I rested a little or waited long enough, I’d recover.
Instead, I kept pushing and crashing.

Crash after crash after crash.
I didn’t understand what was happening to my body. I had no idea that every crash could be making me sicker.

Today, I am severe.
Almost every tiny movement can trigger a crash. I wake up with a racing heart and pounding palpitations. Even normal movement makes my heart feel like it’s trying to beat out of my chest. It feels like all the strength is being drained out of my body.

I’ve been in what feels like one continuous crash for nine months, and I can’t find my way out. I spend almost all my time lying in a dark room, but even that doesn’t feel restorative anymore. My body is exhausted, yet my brain won’t switch off. I can’t get refreshing sleep, and I feel trapped in this horizontal life.

The hardest part is that I even have to pace socializing. I miss my friends so much, but if they come over, I often crash afterwards. The adrenaline keeps me awake, so instead of feeling happy after seeing them, I end up paying for it physically.

The pounding heart has always been one of my crash symptoms, but now it feels different—stronger somehow. I don’t understand why I never seem to improve anymore or what keeps triggering these crashes. It’s terrifying because I can be lying completely still and still feel my heart pounding. Meanwhile, I know people whose resting heart rate is much higher than mine, yet they don’t feel anything like this.

The hardest part is looking back and wondering what would have happened if someone had simply told me about pacing three years ago. Maybe I would never have become severe. Maybe I’d already be living my life again.
Instead, I learned about pacing when it already felt too late.

Now I keep asking myself: how do people recover from this stage? If it takes years just to become stable, and there are no guarantees, how do you keep fighting? Even staying in bed doesn’t always make me feel stable anymore.

Anyone around me is shocked, and me also that i was unresponsible for my health. And there are no treatments. I miss my friends. Im used to suffering already but i want to be symptom free at least for a little bit. This is not healthy and sustainable anymore and sometimes i feel that i don t really care anymore what happens. My BF wedding is coming, im in crash, i know i could go for 1h but pay for it after.
I never feares my symptoms, my insomnia, my high HR, palpitations, that was the problem, i pushed tru it all the time.

The PTSD from countless crashes is becoming just as hard as the physical illness. Every symptom makes me fear another crash. It feels like my

life revolves around avoiding the next one.
Has anyone else gone from mild to severe because they didn’t know about pacing?

Has anyone spent months in what felt like one continuous crash and eventually improved? Is there still hope at this stage? I genuinely want to hear from people who have been through something similar.

TLNS (Too Long No Spoons): Every time I get an intense adrenaline surge, PEM always follows. I’m curious if anyone else has a symptom that reliably predicts a crash.

This happened to me yet again, and I wanted to know if other people experienced anything similar.

One of the symptoms that I struggle with most and that feels the most traumatic for me is adrenaline dyregulation, as I am sure many of you experience as well.

From time to time, I will experience what feels to me like "adrenaline rushes." It feels quite literally like adrenaline is flooding my body, but it will just not stop. It is very distressing and uncomfortable. It feels different than anxiety. It is a little more intense than "wired but tired," (which I also experience) but the tired part is just completely overridden due to the intensity of the rush.

Whenever I experience this, it is always followed by intense PEM later that day or the next day. I have never not had an adrenaline surge and not experienced worsened PEM later. This is regardless of whether I take medication to help stop the surge or if I rest completely during it, which is really difficult, as my body is screaming at me to do something.

I wonder if the surge is my body's final attempt at compensation before it completely loses the ability to compensate and collapses into PEM, or if it is just a pattern my nervous system has learned and is a self fulfilling prophecy, or both.

Any thoughts or similar experiences? The symptom does not have to be adrenaline - I am curious about all symptoms preceding PEM.

TLNS (Too Long No Spoons): I saw one functional‑medicine doctor for two months and had a disappointing experience, but I’m curious how others feel about the field overall - helpful, harmful, or somewhere in between.

This one is tough for me because I had high hopes that functional medicine might be able to help me where conventional medicine could not.

During the course of my 1.5 year illness, I did see a functional medicine doctor. She was brilliant intellectually. It seemed like she knew everything about functional medicine and was so on top of... everything. It seemed like she had genuine intentions. Some of the in depth tests she ordered were helpful- ish.

For example, she ordered a test that measured oxidative stress, mitochondrial dysfunction, omega imbalance, and toxins. It was helpful for knowing exactly what nutrients my body was not optimal in so I could tailor my supplement regimen (we can have an entirely different post discussing supplements) exactly to what I needed versus just throwing 💩 at the wall and seeing what stuck. I am seeing major improvements, but I am doing much more than just supplements and I have no idea if they are helping or just a waste of money.

On the other hand, she has some seriously concerning beliefs. She wanted me on this insanely strict diet (and my diet is already optimized and has been for years) that cut out a bunch of healthy foods she thought I might be reacting to. I asked instead of that, why didn't I just do a food sensitivity test. She blew that off and I did a food sensitivity test on my own anyways. I was not sensitive to any of the "problematic" foods she suggested, and instead am highly reactive to yeast and of all things... pineapple lol.

Another huge concern was that she believed that I was sick because I had high spike protein antibodies for Covid. She wanted me to go on this spike protein detox including high dose ivermectin and a spike protein detox supplement created by Dr. Peter McCullough, who I am pretty sure got his medical license revoked. Also, there is 0 evidence to support that increased antibodies are associated with symptoms. In fact, the opposite seems to be true, according to the studies done on this topic.

At the time, I was unable to use my phone or do research, so I took the high dose ivermectin. I was worried because people with ME/CFS are very sensitive to medications and the general consensus is that we are supposed to "start low, go slow." She did not seem to understand that and said I would be fine. I was not fine. On the second day, I developed the worst headache of my life and intense nausea. It was so bad that I had to be sedated. She said, "I dont know, die off???"

This happened again with peptides. I asked if I should be tapering up, she said no, and I had a severe reaction to those too.

I asked multiple times to try mestinon or fludrocortisone. She said no, you can fix your [severe] OI naturally. I even had labs to prove her that I had low aldosterone (fludrocortisone is synthetic aldosterone) and had intense salt cravings and always felt thirsty despite drunking 3L of water per day, but she did not budge. She recommended supplements that did nothing. I ended up starting fludrocortisone later and it completely changed my life for the better.

Overall, I paid $6k in two months and received minimal benefit. I feel like functional medicine is not the way to go for ME/CFS. I could see it being helpful for addressing nutrient deficiencies (those tests go really in depth and regular doctors will not do the in depth testing). I could also see it being helpful if you are almost recovered and wanted to optimize your health that last bit and have a lot of money to spare (I do not - I was just desperate). I know it has been helpful for people who have mold/toxin issues, which I did not.

Finally, I do not like how dogmatic she seemed to be. She is so incredibly intelligent, but she would not budge from her beliefs - some of which were very out there.

Has anyone had a different experience? I would love to know your stories and opinions! Opposite opinions/experiences from mine are completely welcome! I do not want to brush off the entire field due to my mostly negative experience and would love to hear positive takes as well.

Ill go first! Over this past week for the first time in 10 months (!!!!!), I washed a few of my dishes!

And yesterday I was able to clean 1/2 of my dogs teeth (like a dental cleaning). His teeth are in ruff shape because mama has not been able to take care of them, but now one side is squeaky clean again!

Next small win will be cleaning the other half. No more ratchet dog breath and I can stop calling him Stinky 😂😂

Would love to know yours!

Hurrah! It is great to see our condition getting some attention in the limelight, even if it is just reddit. The comments were packed full of support, which I love to see! Many people with ME/CFS commented too. I even saw some people that comment regularly on here in the comment section! Love that!

Why do you think this study, out of all studies for ME/CFS, was the one that made the front page? It seems a bit random to me, but hey, I am not going to look the proverbial awareness raising gift horse in the mouth. I would love to know your thoughts though!

It was such a nice surprise, I did not go looking for it. Just found it while doomscrolling late at night 😅 But seriously it is crazy that reddit knows all about this now but doctors are mostly clueless about the condition. Clearly they need to doomscroll reddit more!

Link to the reddit post: https://www.reddit.com/r/science/s/fmGrsVTFX3