I recently read about biohacker Bryan Johnson being diagnosed with autoimmune gastritis, and it got me thinking about ME/CFS. Both conditions highlight how complex and interconnected the immune and digestive systems can be, and how difficult it can be to find clear answers when symptoms are persistent and multifaceted.

This is a man who has undergone thousands of tests and tracks almost everything happening in his body, yet this condition was apparently missed for years. His standard anemia markers were normal. One of the few clues was persistently low ferritin.

Autoimmune gastritis is a condition where the immune system slowly attacks the cells of the stomach lining. Because it often develops over many years, it can be surprisingly difficult to detect. Many people don’t have obvious stomach symptoms at all.

Instead, they may experience symptoms such as fatigue, brain fog, weakness, dizziness, headaches, numbness or tingling, poor concentration, memory problems, shortness of breath, exercise intolerance, low iron, low B12, and in some cases autonomic symptoms that can resemble conditions often seen alongside ME.

And this is where I became curious.

Before receiving an ME/CFS diagnosis, many of us are tested for things like anemia, ferritin, thyroid disease, inflammation and coeliac disease. But autoimmune gastritis itself doesn’t appear to be routinely ruled out. Tests such as parietal-cell antibodies, intrinsic-factor antibodies, gastrin and markers of stomach function are not usually part of a standard ME work-up.

Even a normal blood count doesn’t necessarily exclude the condition. In some people, iron deficiency can show up years before classic B12 deficiency or anemia develops.

I am not suggesting autoimmune gastritis is ME. ME has hallmark features, such as post-exertional malaise, that autoimmune gastritis alone would not explain. But considering the overlap in fatigue, cognitive symptoms, neurological symptoms and exercise intolerance, it does make me wonder:

How many people diagnosed with ME have actually been specifically tested for autoimmune gastritis?

Another thing that made me curious is the growing research around the gut in ME/CFS. Studies have reported changes in the gut microbiome, intestinal barrier function and immune activity connected to the gut.

Autoimmune gastritis is different — it involves an autoimmune attack against cells in the stomach lining — so we cannot say that the gut problems seen in ME cause this condition.

But it does make me wonder about the relationship in the other direction. Could chronic immune dysregulation and changes in the gastrointestinal environment in some people with ME make conditions like autoimmune gastritis more likely to develop alongside it? Could there be a subgroup of people carrying both conditions without realizing it?

I genuinely don’t know. I’m just thinking out loud. But considering how many gastrointestinal, immune and nutrient-absorption problems seem to appear alongside ME, I think it’s a question worth exploring.

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I wanted to share an update after writing my first four essays about the breakthroughs I’ve had with my ME and POTS.

A lot of my progress came through working with my nervous system, using exercises and stretches targeting my hip asymmetry and CCI, which you can read about here:

https://open.substack.com/pub/kristinmartensgaard/p/my-health-journey-how-it-all-led-f7e?r=31g90r&utm_medium=ios

Since then, it has been a bit of a wild ride. I started working again and taking on new interior architecture projects, which has been exciting and honestly so much fun. And then I got Covid. Not once, but twice within six months.

Between Covid and all kinds of milder viruses, I was sick for probably three out of those six months. My son was also in his first year of kindergarten and bringing absolutely everything home, and I seemed to catch all of it.

Strangely enough, the fact that I was getting properly sick actually felt like a sign that something in my body had changed. I don’t think I had a real fever in 13 years. For years, when I caught something, I wouldn’t get a normal flu response. I would just feel more ME-sick — extremely dizzy, weak and generally much worse.

Over the years, I slowly started getting more normal flu symptoms again. But after I began working on my hip asymmetry and nervous system, that response became even more noticeable. I could get headaches and flu-like symptoms that seemed to hang around for weeks after an infection.

Then one night something happened that changed the direction of everything for me.

I woke up feeling awful and couldn’t breathe properly. I tried to go back to sleep, but my throat felt like it was narrowing and I had shortness of breath and tightness in my chest. Eventually I gave up on sleep and went into the living room.

For some reason, I checked the weather. The humidity had risen dramatically during exactly the hours my breathing had become worse. Then I looked down at my arm. I had a large rash, my skin felt tight and my blood vessels looked incredibly dilated.

And suddenly it clicked:

This looks like a mast-cell reaction.

I had also developed urticaria — hives — something I hadn’t experienced since before I became sick in 2012.

Part of me was almost relieved because, for once, the reaction was so visible. But it also made me wonder: how much of the inflammation and other symptoms I have been dealing with could actually involve mast cells?

I had always thought of MCAS as another annoying piece of the ME puzzle — reacting to certain foods, getting bloated, maybe some flushing or strange allergic-type symptoms. One more condition to add to the long list.

But what if it wasn’t just another symptom? What if addressing it could actually make a bigger difference?

I wasn’t particularly hopeful that I would find a simple answer. A few weeks later, , completely by chance, a YouTube video started playing while I was preparing the exercise videos for my last POTS article.

I stopped what I was doing and watched.

The woman in the video told her story about POTS and EDS, and how she had become so sick that she was dying. She was reacting to almost every food and could no longer eat on her own. She had a Palliative team and had started to say goodbye to friends and family.

The way she described her symptoms felt so familiar, like I was looking in a mirror. I was crying for her as she told her story, but I was also crying for myself.

It added a whole new dimension to my understanding of what MCAS could actually do to the body. What really caught my attention was the instability she described — that feeling of instability throughout the body and joints. I had been experiencing something very similar and was scared that it was EDS and something I couldn’t change.

But that had never completely made sense to me. I hadn’t felt particularly unstable in my joints before I became sick. So a part of me started wondering — and hoping — whether some of the instability I was feeling could actually be driven by inflammation rather than something permanently wrong with the structure of my body.

Here is the video. It’s quite long, so I recommend watching it after reading this.

It also made me realise that I had never really understood MCAS properly and that the Information out there is very confusing.

Was it the same thing as histamine intolerance? Was histamine intolerance something completely different? Could you have both?

I had never thought of myself as particularly histamine intolerant because I wasn’t eating something and immediately having an obvious reaction. I knew what reacting to milk or gluten felt like, and this didn’t seem like that.

But the more I started reading, the more I realised that histamine intolerance and mast-cell activation are different things, but they can overlap. What surprised me most was how much mast-cell mediators can affect inflammation, blood vessels and the nervous system.

The difference between MCAS and histamine intolerance

Histamine intolerance happens when the amount of histamine in the body becomes greater than its ability to break it down. One possible reason is low activity of DAO (diamine oxidase), one of the main enzymes responsible for breaking down histamine in the gut. DAO activity can be influenced by genetics, but it can also be reduced by problems in the gut, certain medications and other factors.

MCAS is different. With MCAS, mast cells become overly reactive and release histamine along with many other chemical messengers. These messengers can cause blood vessels to widen and become more permeable, allowing fluid to leak into the surrounding tissues. They can also irritate and sensitise nearby nerves.

And this is where things became really interesting to me.

Mast cells and nerves communicate closely with each other. When mast cells release histamine and other inflammatory messengers, they can activate and sensitise nearby nerves. But those irritated nerves can then release their own chemical messengers, which can trigger mast cells again.

So you can end up with a cycle: mast cells irritate nerves, the nerves create more inflammation, and that inflammation can activate mast cells again.

This is called neurogenic inflammation — inflammation that is partly driven and maintained through communication between the nervous system and immune system.

Over time, this sensitisation of the nerves can contribute to symptoms like burning, tingling, pain and pins and needles. And that last one really caught my attention. Pins and needles have been one of the symptoms I have desperately been trying to find an explanation for.

The first step I took

It was clear that I needed to cut histamine right away to see if I was actually histamine intolerant and if it was triggering some of my symptoms. Since my headaches had become so bad after Covid and I was also getting visible rashes, I finally had something I could actually track.

So I cut out high-histamine foods and started drinking three cups of chamomile tea a day. Chamomile contains apigenin, a plant compound that has shown mast-cell-stabilising and anti-inflammatory effects in laboratory research, including reducing mast-cell degranulation and the release of histamine and other inflammatory chemicals.

It took four days.

My headaches started getting better, and I honestly couldn’t believe it.

After another week, I tried coffee and chocolate again, both of which I had cut out, and the headache came straight back. My muscle pain increased too. I continued doing this for about six weeks, adding different high-histamine foods back in to see what happened. And every time I reacted, I almost couldn’t believe how happy I was to have a headache and muscle pain. For once, a symptom was actually giving me an answer.

It felt like I was slowly emptying a histamine bucket that had been overflowing for years. And the longer I stayed away from high-histamine foods, the less reactive I seemed to become. To me, that was also encouraging. My goal isn’t to avoid these foods forever, but hopefully to get to a place where my body can tolerate more of them again.

The dreaded doctor’s appointment

I went to my doctor armed with printed-out papers about MCAS, its connection to POTS and ME, and my own little experiment showing how closely my symptoms seemed to follow histamine.

Of course, he knew very little about it, didn’t want to prescribe ketotifen or anything specifically for MCAS, and I had a bit of a meltdown. Blah blah blah. Haha. You know the drill with chronic illness.

He was, however, concerned about my breathing. I have mild asthma, so he referred me to a lung specialist.

And this is where I was actually surprised.

The lung specialist understood that histamine and other inflammatory mediators can play a role in asthma and allergic symptoms. He prescribed Montelukast Teva, an asthma medication, which I started taking together with Pepcid (famotidine), an H2 histamine blocker that is also sometimes used as part of MCAS treatment.

Montelukast works on a different pathway than antihistamines. When mast cells are activated, they don’t just release histamine — they also release inflammatory chemicals called leukotrienes. These can contribute to inflammation, swelling and tightening of the airways.

Montelukast blocks the receptors that these leukotrienes act on, which can reduce their effects, particularly in the lungs and airways.

It isn’t considered a mast-cell stabiliser, so it doesn’t simply stop mast cells from releasing their contents. Instead, it blocks the effects of one group of inflammatory chemicals that mast cells and other immune cells can produce.

Where I am now

I was about eight weeks into a low-histamine diet when I started the medication. I was already feeling much less inflamed, but within two weeks of starting the medication, my headaches disappeared completely.

I generally felt much calmer in my body. The SCM muscle on the side of my neck, which always feels inflamed and switched on, suddenly relaxed. The stiffness in my ribcage and shoulders, especially bad in the mornings, became noticeably better too.

Then I went on holiday for a week and ate everything. Coffee, ice cream, even a beer — all the things I had been avoiding — and I didn’t have any major reactions.

How much of this comes from lowering histamine and how much comes from the medication is difficult to say. But I do know that both have made a difference for me.

Right now, mast-cell and histamine-related inflammation feels like one of the main remaining drivers of inflammation in my body. And I feel almost euphoric about finally finding something that helps — but also a little heartbroken.

Could I have done something about this years ago? Did half of my twenties and my entire thirties really need to disappear like that?

I can’t help thinking about how much better I might have become, and how much earlier, if I had combined all the work I’ve done with my nervous system with addressing histamine and mast-cell activation.

I had already fixed so many things in my nervous system and muscular system. What felt like neuroinflammation in my brain had reduced dramatically. I could think again without all that brain fog. My body had become stronger, more stable and more functional through all the exercises and stretching I had done.

But somehow, it felt like I had been working incredibly hard to calm and retrain my nervous system and rebuild my muscular system, while my immune system was still throwing inflammatory chemicals into the mix.

Seeing such a quick change from lowering histamine made another piece of the puzzle fall into place for me. And since then, I’ve read many stories from people who have been extremely ill and also noticed changes surprisingly quickly when they started addressing histamine and mast-cell activation.

So I feel like I’m entering a new chapter now, with more energy than I’ve had in 13 years, diving deeper into MCAS and seeing what happens when my body is exposed to less histamine and fewer inflammatory mediators every day — and when my nerves, muscles and tissues finally get a little more peace.

And if you’re reading this and you’ve been thinking about exploring histamine, you don’t necessarily have to start with a cupboard full of expensive supplements. For me, the first step was simply trying a low-histamine diet and chamomile tea and seeing what happened.

Medication is different, and I think that part is worth discussing with a doctor or pharmacist — especially if you have breathing symptoms or take other medications. Pepcid (famotidine) is available without prescription in some countries, but that doesn’t mean it’s right for everyone.

Take one step at a time and pay attention to what your own body is telling you.

Maybe the stars were in my favour the day that YouTube video appeared on my screen.

Maybe this is your sign today.

If you like my work and want to support me in continuing to research and write about this, feel free to subscribe or buy me a coffee here : https://buymeacoffee.com/krismartens

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After years of living with POTS, I slowly discovered that rebuilding the connection between my brain, muscles, and nervous system was one of the missing pieces in my recovery. Looking back, it’s the approach I wish I had known from the beginning.

This article shares my personal experience of recovering from POTS. It isn’t medical advice, and everyone’s situation is different. Always speak with your healthcare provider before starting a new exercise programme.

If you’ve never lived with POTS, it’s difficult to explain how something as simple as standing up or even just being upright can be such a challenge.

For years, making a cup of coffee felt like running a marathon.

Most mornings I woke up already exhausted. I often lay in bed for hours, trying to gather enough strength to sit up, because I knew what would happen the moment I stood. My heart would begin racing, the dizziness would set in, and my body would feel as though it was fighting gravity itself. Eventually, I would make my way to the kitchen, put the kettle on, and stand there watching the water boil while my heart rate climbed above 120 beats per minute. I wasn’t exercising or carrying anything heavy—I was simply standing still.

By the time the coffee was ready, I was usually back on the sofa wrapped in a blanket, trying to calm the dizziness before I could even think about starting my day. Those first few hours often disappeared like that. While the rest of the world was getting ready for work, taking children to school, or making plans for the day, I was simply waiting for my body to reach some sort of stabilization.

Looking back, I realise how much of my life revolved around trying to avoid symptoms by resting or being Horizontal.

Showering often left me feeling as though I was about to faint. Standing on the bus was so difficult that I dreaded every journey. More than once I offered my seat to an elderly person because I didn’t want people to think I was rude, even though I was desperately hoping to sit down.

POTS affects far more than your heart rate. It changes the way you move through the world. Simple conversations become difficult when your brain is struggling to get enough blood flow. If my partner spoke to me while I was standing in the kitchen waiting for the kettle to boil, I often found myself nodding without really taking in what he was saying. My body was already under so much stress from simply being upright that there wasn’t much energy left for anything else.

The physical symptoms could also be frightening. In the beginning, I regularly had what felt like near-fainting episodes in the shower and was often left feeling intensely nauseous afterwards. My chest frequently hurt, my heart skipped beats, and some nights I woke up convinced it had stopped for a split second before suddenly thudding back into rhythm. Even though I later learned that these sensations can be part of POTS, they were terrifying to experience.

When I was finally diagnosed, I felt relieved to have an explanation. Like many people, I hoped a diagnosis would be followed by a clear treatment plan and the beginning of my recovery.

Instead, I was advised to increase my salt intake, drink more water, and, if possible, use a rowing machine. Years later I was prescribed beta blockers, which helped quiet some of the constant overactivity in my nervous system. They reduced the feeling of being permanently on edge and eased the pins and needles I often experienced, but they never really changed the symptom that affected my life the most.

Standing was still difficult.

My mornings still disappeared.

And my world remained painfully small.

Like so many people living with chronic illness, I spent years searching for answers. I read research papers late into the night, listened to podcasts, followed other patients’ recovery stories, and tried more treatments than I can remember. Some helped a little. Many didn’t seem to help at all. Looking back now, I don’t think my recovery was ever about finding one miracle treatment. It was about collecting small pieces of a puzzle that only made sense once I could finally step back and see the whole picture.

One of those pieces appeared when I was offered a place at a rehabilitation centre I applied for through the Norwegian public healthcare system.

By that point, I had been living with ME and POTS for years and had received no treatment that made a meaningful difference. I remember feeling incredibly grateful when I was accepted into the programme, convinced that this might finally be the place where things started to change at least a little bit.

Instead, the first thing it gave me was perspective.

Until then, my illness had quietly become my normal. I had adjusted to a much smaller life without really noticing it. The rehabilitation centre pulled me out of that bubble. Suddenly I found myself surrounded by people recovering from strokes, neurological injuries, and serious accidents. Many of them were decades older than me, yet they walked the corridors with more energy than I had.

I remember lying in bed one afternoon watching people in their eighties heading off to activities while I was trying to gather enough strength to make it downstairs for lunch. It wasn’t inspiring. It was devastating. I really saw just how much my illness had taken from me.

But that rehabilitation stay also became the first time I experienced genuine improvement.

One of the physiotherapists brought me into the therapy pool and asked me to hold onto the edge while floating on my back. My only job was to kick my legs underneath the water as hard as I could for about a minute, rest, and then repeat it several times. It sounded almost too simple to make any real difference, but I trusted the process and did the sessions every other day for the three weeks I was there.

The exercises pushed me hard. They made me dizzy, my heart raced, and there were days when simply getting into the pool felt overwhelming. Sometimes I became emotional halfway through because every kick reminded me how different my body had become. Questions I had tried to ignore for years suddenly came rushing back.

Why me?

How did my body end up like this?

Will I ever have a normal life again?

Eventually, I realised those thoughts weren’t helping me through the exercise. They only pulled my attention back to everything I had lost. So I started doing something different. Instead of thinking about my illness, I focused entirely on the movement itself. I paid attention to how the water felt around my legs, how my muscles contracted, and how my breathing changed as I became tired. For those few minutes, I stopped trying to solve my entire illness and simply concentrated on the exercise in front of me.

By the end of the three weeks, something unexpected had happened.

My POTS symptoms had improved by around ten percent.

Ten percent might not sound like much, but when standing long enough to make a cup of coffee feels impossible, it feels enormous. More importantly, it gave me something I hadn’t felt in years.

Hope.

Not because I thought I had found a cure, but because it was the first time my body had shown me that it was still capable of adapting.

I left the rehabilitation centre determined to continue.

I planned to join a gym, keep training, and build on the progress I had made. But when I got home, reality caught up with me. The walk to the gym was exhausting, the noise inside overwhelmed my nervous system, and before long, the routine fell apart.

At the time, I thought I had failed.

Looking back,? I don’t think I failed at all.

I simply didn’t understand why those exercises had helped me, but I believe those sessions were the beginning of something much bigger.

The Question I Couldn’t Stop Asking

After leaving the rehabilitation centre, I couldn’t stop thinking about those sessions in the pool.

They hadn’t cured my POTS, but they had done something that years of supplements, medications, and searching hadn’t managed to do. For the first time since becoming ill, my symptoms had measurably improved.

That left me with one question.

Why?

At the time, I didn’t have an answer. It would take me several more years of reading research, trying different rehabilitation programmes, and paying close attention to my own body before the pieces finally began to fit together.

Like many people with chronic illness, I went through periods where I believed I had finally found the missing piece. First it was Lyme disease. Later, because of my unstable spine, I became convinced that craniocervical instability (CCI) explained everything. Treating my neck absolutely helped. I became stronger, my body felt more stable, and I could lift weights again.

But even after all that progress, I still had POTS.

Every morning I was still sitting on the sofa with a cup of coffee, waiting for my heart rate to settle before I could begin my day.

That was when I realised something important.

It wasn’t enough to become stronger.

My body also needed to become better at communicating.

To understand why I think that matters, it helps to understand what POTS actually is.

POTS, or Postural Orthostatic Tachycardia Syndrome, is a disorder of the autonomic nervous system. This is the part of the nervous system that controls automatic functions such as heart rate, blood pressure, breathing, digestion, and temperature regulation.

When a healthy person stands up, several things happen at once without them ever noticing. Blood vessels tighten, muscles in the legs and core contract, and blood is efficiently pumped back towards the heart and brain. The whole system works together automatically.

With POTS, that response becomes less efficient. Blood can pool in the legs, less blood returns to the heart, and the body compensates by increasing the heart rate. That’s why simply standing in a queue or waiting for the kettle to boil can feel exhausting.

POTS can develop for many different reasons. Some people develop it after a viral infection, while others develop it after Lyme disease, surgery, pregnancy, concussion, autoimmune illness, or prolonged bed rest. It’s also common in people with hypermobility, including hEDS, and many people living with ME/CFS also experience POTS or significant orthostatic intolerance.

Although the causes may differ, many of us end up with the same daily struggle: our bodies don’t respond efficiently to being upright.

As I continued reading and experimenting, I discovered something that completely changed how I thought about recovery.

I learned that there were already well-established rehabilitation methods designed to improve communication between the brain and the body. Some were used after traumatic brain injuries and neurological conditions. Others focused on rebuilding stability, improving body awareness, and teaching the nervous system to respond more efficiently to movement.

At first, they seemed completely different.

But the more I learned, the more I realised they were all asking my body to do the same thing.

They challenged my brain, muscles, blood vessels, and nervous system to work together more efficiently.

Looking back, I realised these approaches had become one of the missing pieces in my recovery.

I also realised I had been approaching recovery the wrong way.

For years, I tried to solve every aspect of my illness at the same time. I worried about infections, inflammation, gut health, hormones, supplements, medications, and every new theory I came across.

Eventually, I changed my focus.

Instead of asking, How do I fix everything? I started asking, Which symptom is limiting my life the most right now?

For me, the answer was POTS.

Reducing my POTS didn’t cure my ME/CFS, and it didn’t solve every health problem I was dealing with. But it gave me enough function back to begin living again instead of spending every morning trying to survive.

Looking back, I realised almost everything that helped my POTS followed the same progression. I didn’t discover it in this order, but if I were starting again today, this is exactly how I would do it.

The first stage teaches your brain and body to communicate more efficiently again.

The second stage rebuilds stability and strength without placing unnecessary stress on your joints or nervous system.

The third stage gradually teaches your body to tolerate movement and exertion again while improving circulation and cardiovascular fitness.

Those three stages became the foundation of my recovery from POTS.

In the rest of this article, I’ll walk you through each stage in detail, including the exact exercises I used, how I progressed from one stage to the next, a weekly training plan, the videos I recommend, and the nutrition and supplements that supported my recovery.

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I have been asked to share the B1 protocol that I have been mentioning in my writing, and thankfully Ola Kjempengren-Vold has kindly given me permission to publish it here.

The protocol is based on several studies and observations around thiamine (Vitamin B1), mitochondrial dysfunction, ME/CFS, fibromyalgia, and energy metabolism. One good introduction to the science behind it can be found here:

https://www.healthrising.org/blog/2021/04/15/thiamine-b-1-chronic-fatigue-syndrome-fibromyalgia/?utm_source=chatgpt.com

Ola is the creator of the Norwegian Facebook group “10-trinnsprotokollen” (“The 10-Step Protocol”), where he has spent years helping people understand and experiment with this approach. He is incredibly generous with his time, deeply passionate about the topic, and has continued developing and refining the protocol over the years based on both research and community feedback.

I also know he hopes to create an English-speaking community around the protocol in the future if time allows.

This was one of the first I tired that really made a difference. It reduced pressure to my head gave me more energy and allowed me to be a little more social and was a big help when I started slowly to start exercising. But it was the movement itself that helped me to get rid of POTS not the supplements. People have mixed experiences with B1 some feel almost symptom free, some feel it is a good support.

Ola also really recommend this test (Metabolomix) to get as good result as possible. I have not taken it, I might do it in the future.

https://www.lab1.no/analyser/metabolomix?gad_source=1&gad_campaignid=22489277511&gbraid=0AAAAADRpgkjHN9mN51TLDzaEyhacMglSJ&gclid=CjwKCAjw5ZXQBhBdEiwAI5XVWRo7LFBVvaBrQ8kYgXMO1-g41PFkS9kJHZW9ZX9l-L0L_skSjKPeAhoCDEEQAvD_BwE

What’s really important here is the magnesium and potassium balance if you start to get cramps its most likely due to low Magnesium and potassium witch you need a lot of taking high doses of b1. My personal dose if B1 is 600mg based on my weight witch have been between 62-66 kilo last couple of years.

Medical Disclaimer:
This protocol is intended for educational purposes only and is not medical advice. Some supplements in this protocol, especially potassium and high-dose thiamine derivatives — may affect medications, heart rhythm, blood pressure, and electrolyte balance. Work with a qualified healthcare practitioner before attempting high-dose supplementation.

Step 1 — Multivitamin with Molybdenum, Selenium & Manganese

Start with a strong multivitamin that includes:

• Molybdenum

• Selenium

• Manganese

• Active B vitamins

The protocol specifically recommends the Dr. Best formula because it appears to work well for many people.

Suggested product

• Doctor’s Best Fully Active B Complex

Suggested starting dose

• 1 capsule daily

Some people who struggle with sulfur sensitivity may eventually need:

• 2–3 capsules daily

Step 2 — Molybdenum

Molybdenum is considered one of the foundational supplements in this protocol because it helps the body process sulfur compounds — especially later when introducing NAC.

Suggested dose

• Start with 1 mg morning + 1 mg evening

• Total: 2 mg daily

Some individuals may eventually require:

• 3–9 mg daily

Important notes

Before increasing NAC later in the protocol:

• Test tolerance with 500 mg NAC once weekly

• Reactions may appear after several days, so increase slowly

The purpose of molybdenum is to help the body tolerate sulfur-containing supplements.

Suggested product

• Carlson Chelated Molybdenum

NAC test product

• Natural Factors NAC 500 mg

Additional gut support suggestions

The original protocol also mentions:

• Probiotics

• Lactobacillus reuteri

• Bifidobacteria

• Kiwi fruit for gut support

Step 3 — Magnesium

Magnesium becomes increasingly important as thiamine doses increase.

Suggested dose

Either:

• 500 mg regular magnesium

or:

• 100–200 mg sucrosomial magnesium

Suggested products

• Legion Athletics Sucrosomial Magnesium

• MicroMag Sucrosomial Magnesium

Important notes

• Low magnesium may reduce the effectiveness of B1

• Some people develop loose stools from regular magnesium

• Sucrosomial magnesium is often easier to tolerate

If magnesium causes stomach issues:

• Some people add calcium alongside magnesium

Step 4 — Potassium

Potassium becomes increasingly important once high-dose B1 is introduced.

Suggested starting dose

• 300 mg potassium daily

The theory behind the protocol is that increasing mitochondrial activity may increase intracellular potassium demand.

Suggested products

Potassium Chloride

• Nutrics Potassium Chloride Capsules

Potassium Citrate

• Potassium Citrate Capsules

Important warning

High potassium intake can be dangerous.

Symptoms of excessive potassium may include:

• Numbness

• Tingling

• Heart palpitations

• Weakness

• Abnormal heartbeat

The original protocol suggests using:

• A pulse monitor or smartwatch

• Resting heart rate as feedback

Step 5 — B Complex with Choline

A strong B-complex is considered essential for mitochondrial function.

The protocol emphasizes that:

• Riboflavin (Vitamin B2) is especially important

• B2 helps activate B3, B6, and B9

Some individuals may require additional B2 beyond what is included in a standard B complex.

Suggested products

B50

• NOW Foods B-50

B100

• NOW Foods B-100

Active B Complex

• Doctor’s Best Fully Active B Complex

Suggested B2 support

Some people use:

• ~200 mg active riboflavin daily

Step 6 — Manganese

Manganese is included as a mitochondrial cofactor.

Suggested dose

• 5–10 mg in the morning

Suggested product

• Source Naturals Manganese 10 mg

Important note

10 mg is considered near the upper recommended intake in many countries.

Step 7 — Glutamine

Glutamine is described as one of the building blocks of glutathione.

Suggested dose

• 500 mg in the morning

Suggested product

• NOW Foods L-Glutamine 500 mg

Notes

The protocol suggests skipping glutamine if:

• Fibromyalgia symptoms worsen

• Restless legs increase

Step 8 — Glycine

Glycine is another glutathione precursor and may help support sleep and relaxation.

Suggested dose

• 2,000 mg in the evening

Suggested product

• NOW Foods Glycine 1000 mg

Notes

The protocol claims:

• Glycine may improve sleep quality

• Some people react negatively if molybdenum is too low

• Individuals with ADHD may respond differently

If glycine causes overstimulation:

• Consider increasing molybdenum

Step 9 — NAC (N-Acetyl Cysteine)

NAC is introduced carefully because it strongly affects sulfur metabolism and glutathione production.

Suggested dose

• 2,000 mg in the evening

Suggested product

• Source Naturals NAC 1000 mg

Important notes

As NAC increases:

• Molybdenum requirements may also increase

• B9 and B12 demand may rise

The protocol suggests splitting NAC doses throughout the day.

Possible signs of poor NAC tolerance

• Nausea

• Acid reflux

• Bloating

• Diarrhea

• Pain

• Worse sleep

• “False energy”

• Increased fatigue afterward

And to follow this markers trough with doctor.

Step 10 — High-Dose Vitamin B1 (Thiamine)

This is the core of the protocol.

The theory is that impaired pyruvate dehydrogenase (PDH) activity may reduce mitochondrial ATP production.

High-dose thiamine is intended to help restore carbohydrate metabolism and ATP production.

Forms of B1 Used

Thiamine HCl

Standard thiamine form.

Benfotiamine

Fat-soluble and better absorbed.

TTFD (Thiamine Tetrahydrofurfuryl Disulfide)

A highly bioavailable sulfur-containing thiamine derivative.

Example B1/ Magnesium Potassium Ratios

Suggested Starting Strategy

Take B1:

• First thing in the morning

• Away from coffee or tea if possible

Important

Tea and coffee may reduce thiamine absorption.

Certain medications may also interfere with B1 metabolism.

Increasing B1 Safely

As B1 increases:

• Magnesium and potassium often need to increase first

The protocol repeatedly emphasizes:

Do not increase B1 aggressively without electrolyte support.

Thiamine HCl

Possible Improvements Reported

According to the protocol, people sometimes report:

• Better temperature regulation

• Improved sleep quality

• Reduced PEM

• Less severe POTS symptoms

• More stable mood

• Increased physical energy

Recommended Lab Testing Before Starting

Before beginning this protocol, consider discussing the following laboratory tests with your healthcare provider:

Basic Blood Work

• Complete Blood Count (CBC)

• Comprehensive Metabolic Panel (CMP)

• Kidney function (Creatinine, eGFR)

• Liver enzymes (ALT, AST, GGT)

Electrolytes

• Potassium

• Sodium

• Calcium

• Magnesium (serum magnesium at minimum)

Vitamins and Nutrients

• Vitamin B12

• Folate (B9)

• Vitamin D

• Ferritin

• Iron studies (Iron, Transferrin Saturation, TIBC)

Thyroid Function

• TSH

• Free T4

• Free T3 (if available)

Optional Tests

• Homocysteine

• Methylmalonic Acid (MMA)

• RBC Magnesium

• Organic Acids Test (OAT)

• Metabolomix or similar nutritional testing

Important

Because this protocol involves significant changes in thiamine intake and may require adjustments in potassium and magnesium intake, periodic monitoring of electrolytes and kidney function is advisable, particularly when using higher doses.

I had taken all these tests already so I just started, but I have fallowed up later with bloodwork.

Final Thoughts

This protocol is highly experimental and involves unusually high doses of several nutrients.

Key principles:

• Go slowly

• Increase one thing at a time

• Monitor symptoms carefully

• Prioritize magnesium and potassium balance

• Reduce dosage if symptoms worsen

Many individuals spend months gradually adjusting doses to find their personal tolerance level.

I hope this reaches someone who truly needs it and proves helpful to those who are trying. I’d love to hear your thoughts and feedback.

At first, it seemed coincidental. But the overlap kept appearing.

Eventually I started wondering if this was more than just chance. Emerging research suggests that ADHD is significantly overrepresented in people with hypermobility spectrum disorders and hEDS. Some studies report rates as high as 40–50%, compared to roughly 5–8% in the general population. That is a striking difference.

If these numbers hold true, it suggests that connective tissue differences and neurodevelopmental traits may sometimes intersect in ways we do not yet fully understand.

For me, this observation became the starting point for looking more closely at the possible links between connective tissue, the nervous system, and conditions like ME/CFS.

Connective Tissue and the Body’s Internal Systems

Ehlers-Danlos syndrome is a group of connective tissue disorders affecting collagen—the protein that gives structure and elasticity to ligaments, blood vessels, skin, and internal tissues. In hypermobile EDS, joints are more flexible and tissues may be more fragile.

But connective tissue is more than structural scaffolding. It is woven throughout blood vessels, nerves, and organs, helping regulate how signals and fluids move through the body. The connective tissue surrounding blood vessels also plays a role in microcirculation—the tiny networks that deliver oxygen and nutrients to tissues.

Tissue Physiology in ME/CFS

A growing body of research suggests that ME/CFS involves abnormalities in tissue physiology. Invasive exercise studies by David M. Systrom have shown that many patients have impaired oxygen extraction in skeletal muscle during exertion.

In simple terms, oxygen may reach the tissues, but the muscles appear to struggle to use it efficiently.

Other research points to disturbances in microcirculation, mitochondrial signaling, and cellular metabolism. Together, these findings suggest that ME/CFS may involve problems in how tissues receive and use oxygen and energy, rather than structural damage to the tissues themselves.

A recent large proteomics study conducted by researchers in Bergen and London adds another layer to this picture. By analyzing thousands of proteins in blood samples, the researchers identified patterns suggesting changes in muscle metabolism, vascular signaling, and metabolic stress. While the study did not measure oxygen directly, the molecular signals are consistent with disturbances in tissue metabolism and circulation.

When those signals are reduced, it may suggest that cells are not functioning or communicating normally.

In practical terms, this could reflect what many patients experience: muscles that fatigue unusually quickly, a body that struggles to sustain activity, and tissues that seem to run out of energy faster than expected. Instead of the strong metabolic “conversation” between tissues and the bloodstream that supports movement and recovery, the signals appear quieter.

A Similar Signal in Hypermobile EDS

Interestingly, recent research in hypermobile Ehlers-Danlos syndrome is pointing in a somewhat similar direction.

A 2025 proteomics study analyzing blood proteins in people with hEDS found that the majority of altered proteins were not primarily related to collagen structure. Instead, most were linked to immune signaling, inflammation, and blood-clotting pathways.

This raises an intriguing possibility: that in some cases, the connective tissue differences seen in hEDS may be downstream effects of immune dysregulation, rather than purely a structural genetic collagen problem.

What is particularly striking is how similar this systems-level signal is to what researchers are now seeing in ME/CFS. Both the ME proteomics study and the hEDS study point toward disturbances in immune activity, vascular regulation, and metabolic stress, rather than obvious tissue damage.

In both cases, the emerging picture is not one of broken tissues, but of dysregulated systems that influence how blood vessels, immune signaling, and cellular metabolism interact.

Shared Systems

This does not mean that ME/CFS and Ehlers-Danlos syndrome are the same condition.

But the research emerging in both fields increasingly points toward disturbances in overlapping biological systems—particularly those involved in immune signaling, circulation, connective tissue regulation, and how tissues use oxygen and energy.

These shared pathways may help explain why conditions like hypermobility, POTS, mast cell activation symptoms, and ME/CFS so often appear together in the same individuals.

And for many patients, these patterns are not just theoretical. They are something we began noticing long before the research started catching up.

The Intensification of ADHD Symptoms After Illness

Last summer, I was diagnosed with ADD. I felt conflicted. I didn’t fully recognize myself in the stereotype. What confused me most was that my concentration problems became dramatically worse after I became ill in 2012. It felt as though my “ADD” appeared overnight.

That never fully made sense to me. I didn’t want to be medicated for something I didn’t have, but at the same time I was desperate for something that could help with my concentration and sleep. I remember reading about ADHD in my teens and being able to relate to some of it. But over twenty years ago there wasn’t much real understanding of how it unfolds in girls.

If I had been diagnosed back then, I probably wouldn’t have gone on medication. The best thing for me might have been support with sleep, such as melatonin, and help understanding some of the bowel movement issues I was dealing with, which are actually common in people with ADHD. Many people also have delayed sleep phase syndrome, which was definitely an issue for me. It led me to having to retake several courses in my final year of high school because I couldn’t document my absences due to lack of sleep.

Many girls who are missed end up blaming themselves, or the symptoms get labeled as anxiety. That is often the easiest way for society or doctors to place us.

But as I started reading more, I learned that ADHD symptoms can intensify when circulation is impaired, when sleep deteriorates, when inflammation increases, and when the autonomic nervous system becomes unstable.

I had struggled with insomnia since childhood, but after developing ME, my ability to fall asleep without medication became almost zero. That even included taking naps during the day — my body simply would not go to sleep. Sleep has probably been my most persistent symptom.

Instead of asking, “Why did I suddenly develop ADHD?” the question shifts to: “What changed in the signaling environment of my nervous system?”

Rather than seeing this as a new defect appearing, it may be more accurate to think that inflammatory and autonomic changes amplified pre-existing vulnerabilities in attentional regulation. In this framework, infection and neuroimmune activation do not create neurodivergence, but they may intensify its functional impact.

There are still parts of me that wonder whether my ADD is genetic from birth, or whether some of these symptoms developed after neck trauma or instability. It is a fascinating question whether tissue itself may be responsible for some of these symptoms in certain cases.

When it comes to the connection to EDS, I do not know. I do have very visible blood vessels and bruise very easily. As I mentioned in an earlier essay, my mother has hip dysplasia, which involves some of the same genes seen in people with EDS. That is still an open question for me. It has not been easy to get evaluated within the healthcare system, so I have instead focused on building my body while keeping that possibility in mind.

I don’t see neurodivergence as a defect. It is part of the natural spectrum of human cognitive variation. Nobody is broken. But variation still has biology. And biology responds to stress.

Tissue as Barrier and Messenger

We tend to think of connective tissue as passive scaffolding. But it is more than structure. It is barrier, support, and communication system all at once.

Collagen and connective tissues help maintain the integrity of the gut lining, the blood–brain barrier, the blood–nerve barrier, and vascular walls. When these barriers are strong and well-regulated, the immune and nervous systems communicate in controlled ways. But when barrier integrity weakens, immune activation may increase. Mast cells may become more reactive. Signals that should quiet down may persist.

Some clinicians like Dr Erin Nance describe chronic illness through a “cellular barrier permeability” lens. In this view, illness is not necessarily about one broken organ, but about protective barriers becoming dysregulated. Symptoms like POTS, brain fog, gut dysfunction, and mast cell activation may reflect ongoing miscommunication between immune and nervous systems rather than permanent structural damage.

A related idea is the Epithelial Barrier Hypothesis, proposed by researchers including Cezmi Akdis. This hypothesis argues that modern environmental exposures—industrial chemicals, detergents, pollution, processed foods—have damaged epithelial linings in the gut, lungs, and skin over the past century. As these barriers weaken, allergies, autoimmune conditions, and chronic inflammatory diseases rise.

One model emphasizes internal vulnerability. The other emphasizes environmental pressure. But perhaps they describe the same equation from different sides: a barrier system under strain.

Can Connective Tissue Change After Infection?

Some clinicians have suggested that connective tissue changes observed in patients with ME/CFS, fibromyalgia, or Long COVID may not always be purely genetic. Discussions by David Kaufman and Ilene Ruhoy have raised the possibility that inflammatory insults may alter specific connective tissues later in life.

This pattern resembles aspects of autoimmune diseases such as Sjögren’s syndrome, where connective tissue throughout the body may be affected unevenly.

In some patients, upper cervical ligaments appear weakened, contributing to features consistent with Craniocervical instability (CCI). Even localized ligamentous instability in the neck could theoretically alter proprioceptive signaling, cerebrospinal fluid dynamics, or brainstem regulation of autonomic function. Neck injury alone can sometimes lead to spinal instability, and infection-related inflammation may further exacerbate tissue vulnerability.

In my own experience, my entire spine felt inflamed, and standing was difficult due to orthostatic intolerance. Even sitting sometimes worsened symptoms because of spinal pressure and insufficient muscular support. The resulting weakness felt neurological rather than purely muscular. Like there where weak nerve signals not speaking the the mucle corectly.I belive in my case nerves where compressed and that the signaling problems stems som a structral problem.

This suggests a possible interaction: ligament injury activating the autonomic nervous system, infection destabilizing cardiovascular regulation, and immune activation sustaining inflammation. The sequence likely differs between individuals, but the outcome may converge on chronic signaling dysregulation.

When the Body’s Signals Don’t Reset

For some people with ME, the illness may involve both structural strain in the body and signaling that does not fully reset.

Different systems in the body communicate constantly. When something disrupts that communication, problems can build over time.

Signals may come from several places:

• Mechanical signals from unstable or strained tissue

• Immune signals that stay activated after infection

• Autonomic signals that keep the nervous system in a stress state

• Neural signals that amplify stress instead of calming it

If someone already has vulnerable connective tissue or a sensitive nervous system, it may take less to push the body out of balance. Infection, injury, or environmental stress may push the system past a tipping point.

When these stresses interact, the body may struggle to return to its normal baseline

Conclusion: Different Roots, Similar Signals

When we step back and look at the broader picture, a pattern emerges.

Connective tissue fragility, chronic inflammation, environmental barrier injury, infection-triggered immune dysregulation, or cellular permeability changes may begin from very different starting points. One person may have inherited hypermobility. Another may develop inflammatory changes after infection. Another may experience environmental barrier breakdown. Someone else may have localized ligament injury.

The causes differ.

But the downstream effects can converge.

When tissue is weakened—whether genetically, immunologically, or environmentally—the same physiological systems may become destabilized. Loose ligaments and fragile connective structures can contribute to structural instability, including conditions like Craniocervical instability (CCI), where the skull–spine junction becomes unstable. Weak tissues can trap or irritate nerves, leading to neuropathy. Connective vulnerability can increase the risk of structural changes such as Chiari malformation or cerebrospinal fluid flow disturbances.

At the same time, persistent immune activation may alter vascular tone and autonomic regulation. Environmental barrier injury may amplify inflammatory signaling. Cellular permeability changes may increase cross-talk between immune and nervous systems.

Different roots.

Similar signaling consequences.

When instability or inflammation affects the upper cervical region, the brainstem becomes a critical point of convergence. Brainstem compression—often associated with CCI or atlantoaxial instability—occurs when weakened ligaments fail to securely stabilize the skull and upper vertebrae. Even subtle mechanical stress in this region can have widespread effects, because the brainstem regulates some of the body’s most fundamental functions.

The brainstem plays a central role in:

• Circulation and blood pressure regulation

• Autonomic balance and vagal tone

• Heart rate control

• Temperature regulation

• Sleep–wake cycles

• Swallowing and respiratory rhythm

When compressed or chronically irritated, symptoms can resemble many core features of ME:

• Dysautonomia, including POTS, dizziness, and fainting

• A feeling that the head is too heavy for the neck to support, often with occipital headaches

• Blurred or double vision, light sensitivity, tinnitus

• Brain fog, slowed thinking, memory difficulty

• Limb weakness, tingling, swallowing problems

• Sleep disturbances, including central sleep apnea

This does not mean that brainstem compression explains all cases of ME. Nor does it suggest a single structural cause.

But it illustrates an important principle:

When connective tissue is weakened—whether by genetics, inflammation, environmental stress, or barrier dysfunction—the resulting instability can generate neurological symptoms that look remarkably similar across individuals.

The underlying cause may differ.

The signaling disruption may converge.

In this sense, ME/CFS may not be one uniform disease, but a final common pathway of dysregulated communication between tissue, immune system, autonomic networks, and the brainstem.

Understanding those pathways—rather than arguing for a single origin—may bring us closer to meaningful subgroup identification, more precise interventions, and a deeper recognition that the body is not failing randomly.

It is responding to instability.

And sometimes, different beginnings can lead to the same neurological language.

Supporting Tissue Healing and Nervous System Function

One of the most important parts of my recovery has been focusing on rehabilitating my neck and spine addressing CCI and AAI instability and improving blood flow to inflamed areas. Doing exercisises and micro- steching for Hip asymmatry has aslo been a huge part of me getting my spine less inflamed and nerves less compressed.

You can read about how I did this here in these thee essays:

https://open.substack.com/pub/kristinmartensgaard/p/my-health-journey-how-it-all-led-f7e?r=31g90r&utm_campaign=post&utm_medium=web

https://open.substack.com/pub/kristinmartensgaard/p/from-one-treatment-facility-to-another?r=31g90r&utm_campaign=post&utm_medium=web

https://open.substack.com/pub/kristinmartensgaard/p/how-restoring-nervous-system-stability-0b1?r=31g90r&utm_campaign=post&utm_medium=web

One treatment that has been particularly helpful for me is shockwave therapy. Shockwaves create small mechanical pulses that stress damaged cells in a controlled way, stimulating blood flow and activating cellular repair processes. In simple terms, the therapy sends a signal to the body that the tissue needs to rebuild and reorganize.

Combined with careful rehabilitation, this approach appears to support structural remodeling of connective tissue and improved circulation in chronically inflamed areas.

Recovery can be slow, but over time I’ve noticed meaningful improvements in mobility, pain levels, and stability. And that it is safe to be in my body again.

Peptides and Tissue Repair

Alongside rehabilitation, I’ve been experimenting with peptide therapy, something that I believe could eventually change how we think about treating chronic illness and tissue damage.

Peptides are small chains of amino acids that act as signaling molecules in the body. Some of them appear to play roles in tissue regeneration, inflammation control, and cellular repair.

For the past six weeks, I’ve been using a combination of BPC-157 and TB-500, sometimes called the “Wolverine stack.”

• BPC-157 is thought to support tissue healing, nerve regeneration, and protection of the gut lining.

• TB-500 works more systemically, helping cells migrate to injured tissue and supporting structural remodeling.

I plan to take a short break, and then continue the protocol, as I see this more as a long-term strategy rather than a quick fix.

So far, I’ve noticed several encouraging changes:

• a clear reduction in inflammation

• less bloating, which makes me wonder about the connection between the gut barrier and the immune system

• a general sense that my body is recovering from stress more easily

The gut barrier is especially interesting to me. If the intestinal lining becomes more resilient, it could potentially reduce the constant immune activation that many people with chronic illness experience. The gut–immune interface is one of the most important signaling hubs in the body, and improving barrier integrity there could have ripple effects across multiple systems.

It’s still early, and I’m cautious about drawing conclusions. But I’m genuinely excited to see what the long-term results might look like.

Nutritional Support for Collagen and Tissue Repair

In addition to peptides, I try to support connective tissue repair through nutrients that are important for collagen formation and structural stability:

• Vitamin C (1000–2000 mg/day) – essential for collagen synthesis

• Glycine (1000–2000 mg at night) – supports collagen formation and sleep

• Collagen peptides (10–20 g/day) – provides building blocks for tissue repair

• Creatine (10–25 g/day) – supports cellular energy and muscle function

• Zinc, copper, and manganese – included in my multivitamin and important for stabilizing collagen fibers and tissue repair

Together with rehabilitation, these approaches are part of an ongoing attempt to strengthen connective tissue, calm inflammation, and stabilize nervous system signaling.

I’m still learning every day, and I’ll share more updates about my peptide protocol once I’ve completed the full regimen and observed the longer-term effects.

These nutrients help support collagen stability, connective tissue repair, and overall cellular energy metabolism.

A Personal Perspective

My goal in writing this is not to present a final answer, but to explore patterns that may help us understand chronic illness in a more integrated way.

If ME/CFS truly involves dysregulated signaling between connective tissue, barriers, immune responses, and the nervous system, it may explain why the condition appears so complex and varied between individuals. At the moment there is a lot of focus on nervous system regulation in the health community, this is not a bad thing, but if you have been affected by infection that have caused inflammatory respons that have affected the tissue or if you have cervical instability you need to take action in form of building muscle to support the spine and target where your nerves are compressed so your body becomes less tense. A person with EDS may have spent a lifetime with male positions in neck and spine and this can cause huge consequences for the nervous system.

I will continue sharing updates as I learn more and observe the long-term effects of these approaches.

If you found this work helpful or interesting, you can support my writing by subscribing to my Substack or buying me a coffee here: https://buymeacoffee.com/krismartens Every contribution helps me continue researching and sharing what I learn.

Reference list :

https://pubmed.ncbi.nlm.nih.gov/41785863/

https://pubmed.ncbi.nlm.nih.gov/39014464/

https://www.sciencedirect.com/science/article/pii/S1535947625005663

https://academic.oup.com/immunohorizons/article/9/10/vlaf044/8256436

https://www.healthrising.org/blog/2024/04/22/connective-tissue-chronic-fatigue-long-covid-fibromyalgia/

https://www.eds.clinic/articles/eds-and-adhd

While some people romanticize it, I was just trying to survive in a body that had completely stopped cooperating.

These photos from 2016 remind me of things I couldn’t explain back then.
The newer ones tell a different story.

In 2016, my world was very small. I was extremely thin, exhausted from constant pain, brain fog, and severe sleep deprivation. My nervous system was in overdrive. I had pins and needles all over my body, my heart would race just from standing, and adrenaline seemed to surge through me all day. I was on IV antibiotics for Lyme disease, traveling to another country for treatment, and spending most of my time alone, not knowing if I would ever get better.

didn’t know if my body would ever feel safe again.

Life looks very different now.

I go to the gym three times a week. I stretch every day. I can be social without needing days to recover afterward. I can carry my son, play with him, and actually be present. I take on small interior architecture projects. I write. I make plans. I live.

My health still isn’t perfect, and I still have ups and downs. But compared to 2016, the difference is huge. What once felt like surviving has slowly become living again.

If 2016 was a great year for you, I’m happy it was.

For me, surviving it was the victory.

And if 2016 wasn’t kind to you either, you’re not alone. I’d love to hear your story too.

As I’ve worked on these essays, I’ve revisited old blood tests, scientific studies, and personal notes — and had several “aha” moments. This time, I approach it differently: calmly, methodically, and with curiosity rather than desperation. I’m treating this as real work: first to understand and support my own healing, and then to share insights that might help others.

Writing it all down has given me a new perspective. What used to feel like a cluster of fragmented information is becoming something clearer, more connected, and shareable. In this post, I want to focus on infections — because they are often the starting point in ME/CFS. While my own improvements over the last years happened without consciously targeting infections, understanding their impact on the immune system helps make sense of this complex condition.

In this post, I want to focus on infections, because you can’t really talk about ME/CFS without addressing them. I’ve chosen to write about this separately, because there’s only so much information one can take in at once — and because my own health improvements over the past years happened without consciously focusing on infections. I want to be clear about where my attention was, and why.

I also want to highlight research showing that infections can cause lasting changes in the immune system, and that it may have a direct impact on the spine and nervous system — contributing to the complex and often misunderstood picture of ME/CFS.

It’s easy to forget that before the advent of vaccines and antibiotics, viruses and bacteria were among the greatest threats to human health. Infectious diseases were a leading cause of death worldwide, and outbreaks could wipe out entire communities. Antibiotics, beginning with penicillin in the 1940s, dramatically reduced deaths from bacterial infections. Vaccines — from smallpox in the late 18th century to broader immunization programs in the 20th century — lowered the burden of many viral diseases.

Today, many infections that were once fatal are preventable or treatable, especially in young and otherwise healthy people. Still, we shouldn’t take infections lightly. Post-viral conditions like ME/CFS are increasing, and more people are experiencing lingering, life-altering symptoms after infections. Yet within the medical system, many patients are still told their symptoms are psychosomatic if they don’t fully recover — as if the infection itself couldn’t have left a lasting imprint.

How infections shaped my journey

So many of us first became ill after an infection — including me. I had Epstein–Barr virus (EBV) in the months leading up to my collapse, and three years later I was diagnosed with Lyme disease.

What I didn’t understand back then, and what science has helped clarify — is that some infections can leave a long-lasting imprint on the immune system. For certain people, viruses don’t just pass through; they can push the immune system into a state where it struggles to switch off. EBV, for example, has been linked to autoimmune diseases like multiple sclerosis and lupus, where the immune system attacks the body instead of protecting it.

This doesn’t mean every virus leads to autoimmunity. But for people already vulnerable, an infection can become a turning point — a moment when the system tips out of balance.

In ME/CFS, infections can trigger immune dysregulation, secondary infections, and changes to tissue and joints that affect the spine. My experience reflects this:

For over five years, I didn’t get a “real” flu. When others were sick, I felt flu-ish and inflamed—but without fever, cough, or the usual progression. This mirrors what many ME/CFS patients describe: an immune system that is over-activated yet ineffective.

My Lyme and other infection treatments

But after all the Lyme treatments I tried between 2015 and 2018 — antibiotics, hyperbaric oxygen (HBO) therapy, hyperthermia — that didn’t help as much as I’d hoped, I had almost pushed this part of my story aside, just to survive and keep searching for something that actually worked.

That search only truly took shape once I was finally diagnosed with ME and POTS, and began following approaches that made sense for these conditions. With that said, I’m glad I did those Lyme treatments — I honestly don’t know where I would be today if I hadn’t.

I definitely had lots of infections. The question is: were they secondary infections, a consequence of an exhausted immune system that didn’t work? Or was Lyme the primary infection, allowing another pathogen to invade?

The immune system paradox in ME/CFS

The hardest part to explain — and something you almost have to live in an ME body to understand — is that the immune system can feel like it is both not working at all and going completely crazy at the same time.

Many people with ME/CFS don’t get normal infections early in the illness. This isn’t because the immune system is strong, but because it is stuck in an over-activated, defensive mode. Over time, this state can shift into immune exhaustion and immune dysregulation.

In the first months or years of ME/CFS, people often say things like:

• “I never catch colds anymore”

• “Everyone around me is sick, but I don’t get it”

• “I feel awful, but I’m not actually getting infections”

That was exactly my experience. For over five years, I didn’t get a real flu. When people around me were sick, I would feel angina-like, flu-ish, inflamed — but without the classic flu symptoms.

No fever. No cough. No normal course of infection.

Phase 1: Immune system stuck on high alert

ME/CFS appears to involve a time-dependent change in immune function. Rather than a single static problem, research suggests a progression from early immune overactivation to later immune exhaustion. The following phases describe this pattern and how it may shape symptoms over time.

After a trigger — such as a virus, physical stress, or injury — the immune system never fully switches off. It stays in a constant “danger mode.”

In early ME/CFS, this often includes:

• High levels of inflammatory signals (cytokines)

• Constant immune surveillance

• NK cells that are activated but inefficient

• An immune response that is loud, chaotic, and extremely energy-consuming

This state can suppress typical infections while still making the body feel deeply sick.

Phase 2: Immune exhaustion (later years)

If this state continues for too long:

• Immune cells become exhausted

• Energy production drops further

• Control over viruses weakens

• Old viruses may reactivate

• Secondary infections can appear more easily

This is when recurrent infections, gut issues, candida, and other problems often become more visible — but they are likely consequences of immune dysregulation, not the original cause of ME/CFS.

Secondary infections: a grey area

A secondary infection happens when the immune system is weakened or compromised by a primary infection, letting another pathogen take hold. It can be bacterial, viral, or fungal.

Many of us have spent years trying to treat these secondary infections — antibiotics, herbs, parasite cleanses — and for some, it helps. But for most, it doesn’t resolve the core ME/CFS symptoms. This suggest that secondary infections are effects of immune imbalance, not the root cause. In a study published in 2018 found people with ME/CFS have impaired TRPM3 ion channel function in immune cells, especially NK cells. TRPM3 channels allow calcium into cells, which is essential for:

• Activating immune cells

• Clearing pathogens

• Normal cell-to-cell and nervous system signaling

When TRPM3 doesn’t work properly, immune cells can be:

• Poor at clearing pathogens

• Dysregulated in signaling

• Chronically “activated,” yet ineffective

This provides a clear biological explanation for the immune paradox in ME/CFS: a system that is overactive but underperforming, closely matching my lived experience.

A second study that shows that ME affects the immune system is this study by Du Preez et al. (2023). The study showed that calcium entering NK cells through the TRPM7 channel was altered in people with ME/CFS. Calcium is important for immune cells because it helps them activate, communicate, and carry out their protective functions. When calcium signaling is disrupted, immune cells may not work as effectively. This finding suggests that calcium signaling problems may contribute to immune dysfunction in ME/CFS.

Read the study here:

https://pmc.ncbi.nlm.nih.gov/articles/PMC8848670/

https://pmc.ncbi.nlm.nih.gov/articles/PMC10377690/

Research in Bergen: A new approach to ME/CFS

Living in Bergen, the research happening at Haukeland University Hospital feels especially close to home. Researchers there are studying daratumumab, a medication that targets a specific group of immune cells that produce antibodies. The goal of the study is to target and modulate a specific part of the immune response — especially the plasma cells and the antibodies they produce — in hopes this will correct a pathologically stuck immune behavior in ME/CFS.

What makes this even more real for me is hearing from people who’ve participated. I spoke with a woman who received this treatment and regained much of her life. Her story made the research feel less abstract — a reminder that behind every study are real bodies, real lives, and real hope.

Pilot study results

On July 9, 2025, the research group published results from a pilot study of daratumumab in 10 women with moderate to severe ME/CFS. The study primarily aimed to see if the treatment was safe and feasible, while also tracking any signs of symptom improvement.

• Participants had been ill for 3 to 35 years, averaging 38 years old.

• Before treatment, their average daily step count was 3,359 steps, and self-reported physical function was very low.

Treatment:

• Four injections were given under the skin on the abdomen, with two-week intervals.

• Later participants also received maintenance treatments.

Results:

• All planned treatments were completed with no serious adverse events.

• Some mild side effects were reported, including temporary rapid heartbeat, minor infections, and blurred vision in a few participants.

• Six out of ten patients showed significant improvement:

  • Average daily steps more than doubled, from 3,363 to 7,392

  • Self-reported physical function scores rose from 32.2 to 78.3

  • Symptom burden decreased dramatically

Of these six, five maintained their improvement throughout the follow-up period.

What this means

Although this is a small pilot study and we cannot yet draw definitive conclusions, the results are encouraging. The study has been extended to include additional participants, and a larger randomized, double-blind trial of 66 patients is now underway, including patients who developed ME/CFS after COVID-19.

This research gives me hope — not just scientifically, but personally. It shows that targeted immune treatments may one day help reset the system in ME/CFS, and that recovery is possible for real people, living real lives.

You can read the full article in Frontiers of Medicine

The researchers are continuing this study, but it’s important to note that it relies entirely on donations from people affected by ME/CFS and the Norwegian ME Association. Despite these promising results and other studies showing clear biological abnormalities, the study has not received consistent government funding.

This is a stark example of the ongoing neglect and gaslighting faced by this patient group — the majority of whom are women. ME/CFS and POTS diagnoses are rising, especially after COVID-19, yet research remains underfunded and undervalued. This is particularly concerning given the severe impact on quality of life and the fact that most patients are unable to work, creating a substantial economic and societal burden.

ME/CFS is among the most disabling chronic illnesses. In large international surveys using the EuroQol EQ‑5D health scale, people with ME/CFS report the lowest health-related quality of life scores of all conditions studied, including cancer, diabetes, stroke, heart disease, lupus, and chronic kidney disease.

It’s clear that this research is not just scientifically important — it’s urgently needed for patients, families, and society.

How infections can affect the spine, joints, and stability

Research shows that infections may contribute to changes in connective tissue, neuromuscular function, or spinal stress. Inflammatory processes triggered by infection can alter tissue function, reduce blood flow and oxygen delivery, and impair circulation to the brain, muscles, and connective tissues. This can lead to feelings of instability, weakness, pain, dizziness, and autonomic symptoms—sometimes mimicking a connective tissue disorder even when none is present.

There is growing evidence that infections may contribute to craniocervical instability or other cervical spine changes. Inflammation can weaken ligaments and supporting structures or affect bone integrity, even without trauma. Jennifer Brea’s work on post-infectious ME/CFS highlights this connection, including rare but documented conditions such as Grisel’s syndrome, where infection alone causes ligament laxity in the neck. Certain infections, including tuberculosis, have also been associated with craniocervical instability.

When I became ill, my neck and joints suddenly felt unstable, with deep internal pain—especially around the kidneys. My tissues felt “gummy,” as if they could no longer properly support my bones. My shoulders seemed to pull downward, and holding my head upright required constant effort. This instability triggered autonomic symptoms such as a racing pulse, dizziness, brain fog, and blurred vision. Over time, gradually rebuilding muscle strength and stability reduced many of these symptoms.

People with Ehlers-Danlos syndrome often describe similar instability, but in my case the changes happened almost overnight and without a known connective tissue disorder. I believe this reflects a combination seen in ME/CFS: infection-driven tissue changes, impaired circulation, reduced oxygen delivery, and autonomic dysfunction. Poor blood vessel regulation can cause blood pooling in the limbs and reduced flow to the brain and postural muscles, increasing strain on ligaments and worsening instability—creating a feedback loop that contributes to symptoms like POTS.

This raises important questions about whether severe or prolonged physiological stress from infection could trigger epigenetic or functional tissue changes without a genetic connective tissue disorder.

Why this matters

Post-infectious illnesses like ME/CFS are still frequently dismissed as psychosomatic. Women are affected nearly twice as often as men and experience greater disease burden, yet research and recognition lag behind. This pattern reflects a long history of medical gaslighting, where symptoms that are difficult to measure are minimized rather than investigated. If this disease primarily affected men, it’s hard not to believe progress would be faster.

A brief historical reminder

International ME/CFS Awareness Day is held on May 12, the birthday of Florence Nightingale. She likely developed a chronic post-infectious illness after contracting brucellosis during the Crimean War, leaving her debilitated for decades. Despite this, she transformed nursing and public health—demonstrating that post-infectious illness is neither new nor imaginary.

Bringing It All Together: Recovery, the Immune System, and the Spine

Looking back on my journey, one thing has become very clear: ME/CFS isn’t just one problem — it’s a complex web of infections, immune dysregulation, nervous system stress, structural instability, and circulation issues. For me, addressing craniocervical instability (CCI) and hip asymmetry made a profound difference. I’ve also seen others recover just from correcting one of these issues, while some, like me, need to address both to see meaningful improvement.

The most fascinating part is that many people report their immune system symptoms improve once the spine is realigned, nerve tension is relieved, and circulation is restored. This raises questions I think about every day: if you correct the nervous system and structural issues, can the immune system naturally rebalance? Or can rehabilitation and movement help repair nerves that have been affected by infections over time?

Science is beginning to catch up with these observations. Studies on TRPM3 and TRPM7 ion channel dysfunction explain why immune cells in ME/CFS are chronically activated yet ineffective. Pilot research, like the daratumumab study in Bergen, shows that targeted interventions on the immune system can improve function and reduce symptoms. Yet, recovery seems to be most effective when multiple systems are addressed at once — immune regulation, nerve repair, and structural support.

For anyone living with ME/CFS, this is both a challenge and a hope. The disease is complex, debilitating, and often misunderstood, but real-world experience and emerging research suggest that coordinated approaches — addressing the spine, the nervous system, and the immune system together — may unlock meaningful improvements.

ME/CFS is real, measurable, and biologically grounded. The work being done in Bergen and elsewhere reminds us that patients’ experiences are valid, research matters, and recovery, even partial, is possible. It’s a reminder that our bodies are interconnected systems — when one part is healed, the others often follow.

In my opinion, studies from Bergen and from Karolinska institut in Sweden can suggest that patients may be classified into different subgroups, yet still share similar immune system changes, regardless of the presence or absence of cervical spine trauma.

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I describe the moment when years of invisible rehabilitation finally reached a tipping point, how targeted movement released deep neuromuscular tension, and why this shifted not only pain and fatigue but also emotional regulation, identity, and mental clarity. The final part of the text distills these insights into practical principles for rebuilding stability, circulation, and nervous-system resilience over time.

A Brief Note: This essay reflects my personal experience and interpretation of emerging research. It is not intended as medical advice, diagnosis, or treatment guidance. Everybody is different, and anyone considering changes to their healthcare should consult qualified medical professionals.My goal in sharing this story is not to provide full answers, but to expand the conversation around complex neurological illness — especially where current medical frameworks fall short.

The Breakthrough I Never Saw Coming

The summer of 2025 was far harsher than I ever expected. I thought all the work I had poured into healing would finally begin to show. Instead, I felt defeated.

My days revolved entirely around caring for my baby, and the constant lifting and carrying made my neck stiff and inflamed. It felt like there was no space or time for me to heal. At the same time, I was grieving the loss of my father, left to handle everything alone as his only child. The stress became unbearable.

The migraines returned daily. I found myself relying on pain medication again, just to function. I was exhausted, inflamed, grieving, and stretched far beyond what any nervous system is designed to bear.

Yet something small had shifted. The inflammation in my lower back slowly eased, though my neck muscles felt like solid iron.

When months of invisible work finally reached a tipping point

Despite everything, something subtle had changed. The inflammation in my lower back slowly eased, even though my neck still felt like solid iron.

In August, my treatment facilitator from ACRIUS came to my city for a routine check-in. He worked exactly as he had many times before. But this time, something extraordinary happened.

The crushing pressure in my head—pressure I had lived with for thirteen years—suddenly vanished. Neuromuscular tension that had wrapped itself around my skull began to melt.

He hadn’t done anything differently. The treatment was the same routine he had performed countless times. The change came from something else: all the quiet, repetitive work I had been doing for months. Stretching, exercising, showing up for my body even when it felt pointless. That consistency was quietly reshaping my nervous system

It felt like the breakthrough I had been waiting for—not just for three years, but perhaps my entire life. It was proof that I was finally on the right path. If a small intervention could unlock healing in one stubborn area, then I knew I had to continue targeting the places where tension held on the tightest. I became a detective again, but this time with clarity, confidence, and certainty.

Then one morning, an old YouTube video I had saved years ago suddenly popped into my head. I went back and watched it. It was a TOS (thoracic outlet syndrome) exercise video that focused on three areas: the trapezius, the levator scapulae, and the suboccipital muscles. I did the exercises without thinking much of it. A few hours later, I felt a sharp, shooting pain on the left side of my jaw. Strangely, it didn’t concern me. It felt like the pain of a nerve waking up.

Later that night, a miracle happened

My jaw relaxed first. Then the release spread outward in circles around my neck, like electricity moving through my body. My head felt clear and open—completely free of brain fog. Energy began pumping into my brain and body. It felt as if my nervous system was finally releasing the fascia that had been holding everything tight. Once again, a small movement had tricked my nervous system back into balance.

The following week, I didn’t recognize myself. Energy poured through me. I felt capable of things that had previously been unimaginable: noise, light, stimulation—life itself. I walked around and lived as if I wasn’t sick for about a week and a half. Then I could feel some tension slowly beginning to build again in my nervous system, but not nearly to the same extent as before. This release also removed other symptoms, like my lower back pain, which had made sitting extremely difficult for years. I was so grateful. Muscles that had been frozen for over a decade were finally waking up.

I created an extra recovery plan for myself, focusing on exercises and small stretches in all the areas that were stiff. I knew I had to wake everything up and restore circulation. I started with the hips, moved up to the shoulders with TOS exercises, and added small chin-tuck movements for CCI. I understood that progress would go up and down, and that this was part of the process. I believed that the day would come when every muscle fired properly and the deep compensatory tension would finally let go. Even now, I felt human again—like I had been given a second chance at life.

The big breakthrough for me is realizing that my remaining symptoms are caused by my nervous system. Once my nervous system tension went down, the pain, inflammation, and cognitive issues went away.

I also need to mention that my mental health shifted the very same night everything changed. I became less sensitive to overwhelming emotions. I felt clear and calm instead of anxious. There was no longer the sensation of my brain being dragged downward, no more pressure suffocating my thoughts. For the first time in years, my mind felt free.

This shows how damage and disruption to the nervous system can trap the emotional mind and change you into a completely different person. I was not this person before I got sick. I wasn’t this sensitive, riding a constant rollercoaster of emotions, crying for no reason. I lost myself completely. I didn’t even know how to dress anymore. I had to stop and think, What would Kristin have liked to wear?—because the neural connection to who I was felt gone.

My sense of identity, logic, and memory were no longer something I could rely on. They felt distant, weak, like something I only had a fragile connection to rather than something that belonged to me.

It felt like the breakthrough I had been waiting for. Proof that I was finally on the right path. If one small intervention could unlock a stubborn part of my body, maybe the rest could follow.

Two Decades of Biohacking — And What It’s Taught Me

I’ve now reached a place where I can take full control of my continuing journey—almost twenty years of biohacking, of being my own human guinea pig, always searching for root causes instead of symptom management. Before, my main tools were blood tests,diets and detox, Now, my main tool is movement.Today we call it biohacking, but back then it was simply sick people pushed out of the healthcare system, desperately searching for answers in a more holistic, integrative way—using new science long before it was accepted in mainstream medicine.

And I truly believe this grassroots curiosity has shifted how we think about health.When something changes your life, you want to share it. And that’s what we’re seeing everywhere now. A radical shift, especially around food. The way people view ultra-processed foods has transformed so quickly. Ten years ago, I never thought this change would happen in my lifetime.More and more people no longer assume that a diagnosis means a lifetime of pain. They’re researching. Questioning. Making their own decisions. Reclaiming their health.

And I genuinely believe this collective shift will move all of us toward a healthier future.

Why MRI Often Misses Ligament Damage

Many people wonder why ligament injuries in the neck don’t show up on routine MRI scans. The truth is that standard imaging often lacks the detail needed. Specialized positions and a radiologist familiar with these conditions are crucial.

It’s important to undergo a comprehensive evaluation by a manual therapist or musculoskeletal specialist. Such an assessment can document:

• Reduced cervical musculature

• Excessive cervical motion during rotational movements

Excessive cervical motion during rotational,This hypermobility is not necessarily due to a generalized hypermobility condition, but may result from ligamentous injury, leading to inadequate stabilization of the head and allowing the cervical joints to rotate beyond their normal range.

Women Are More at Risk

The neck is one of the most vulnerable parts of the body, and injuries affect women more frequently due to physiological and biomechanical differences, including generally lower neck muscle mass than men.

In medical evaluations, both the patient’s description of their symptoms and objective findings such as MRI results are important. Yet many women experience that their symptoms are not always taken seriously, often dismissed as stress, hormones, or emotions. Being heard and validated is essential.

How Instability in the Neck Can Affect the Brain — and Your Life

The emotional part of not having a brain that works

For a long time, the cognitive symptoms were the most terrifying part. Confusion, disorientation, memory loss, and losing words were only the beginning. Some days I couldn’t even write a simple sentence. Living with those changes without answers felt like a form experiencing of daily trauma over and over again.

The type of trauma a chronically sick person experiences is very different from something that happens once, like getting hit by a car. It stretches over years—living it every single day, reliving it in different aspects. First and foremost, there is the physical pain, then the social aspects, and not to mention the medical trauma: having nowhere to seek relief if things get worse, being gaslighted and mocked at the lowest point in your life.

The lack of validation of my symptoms in the medical world ruined my mental health at some point, and I had to see a psychiatrist, do EMDR sessions, and go on medication.

Social life became complicated in ways no one could see. Most of the day, I had to lie down just to stabilize myself. Only later in the evening—when symptoms eased a little—could I meet others, and even then, they saw only a fraction of the reality. I would sneak away to rest my head, hiding the tremors and dizziness that came from the smallest movements.

When you are mostly housebound and only have a few rare moments of connection, you learn to hide your symptoms because you want to feel human again. It helps you survive, yet not being understood by friends and family is one of the hardest parts. Isolation and cognitive decline slowly wear away your sense of self, and nobody is strong enough to face that without support.
Daily grounding—meditation, gratitude, slow breathing—became essential for me.

It’s hard to see doubt in people’s eyes when you are holding on by a thread. It’s easy to tell who has mentally left you, who no longer takes you seriously or who takes you for granted because you are sick. Some people seem to come in and out of your life when it suits them, depending on their own situation and what they need. That lack of consistency creates deep trust issues. Dealing with this while your mind is already compromised—emotionally sensitive and fragile—makes everything more intense and would break anybody.

Being sick with an illness the medical system cannot identify is completely different from having a known diagnosis. The lack of sympathy, understanding, and validation is enormous.

For anyone going through this, I am so deeply sorry. It is brutal. You are not alone, and you are not imagining this. Conditions like these are still underdiagnosed, and the gaslighting—especially of women—has gone on for far too long. With new research emerging and more patients sharing their stories, the narrative is finally beginning to change.

What My Scans Showed

I already shared that I have cranio-cervical instability (CCI), but imaging also revealed Chiari malformation type I. In many people, Chiari is present from birth, but it can also be acquired when the structures that support the skull become unstable—like in cranial-cervical instability. When the stabilizing ligaments at the top of the spine are injured, the relationship between the skull and cervical spine can shift in ways the body was never designed to handle.

In my situation, doctors believe the descent of my cerebellar tonsils is related to ligament damage and loss of muscular support, not genetics.

This lines up with the head and neck trauma I had at 12 years old, when I fell on my head from a play structure in the school yard. I remember inflammation, concentration problems, and emotional dysregulation afterward. Later in my teens, I developed allergies and asthma.

Once a ligament is damaged, you can compare it to ripped jeans—once the tear begins, it can continue to fray over time, especially with overuse or new injuries. For me, more strain came later when I fell off my bike in Copenhagen and then went through a viral infection. That’s the kind of combination that can turn a simple injury into something much bigger, overwhelming the nervous system until it starts to collapse.

What Exactly Is CCI and Chiari?

Chiari Malformation Type I

Chiari type I is a slow, structural change where the cerebellar tonsils extend downward below the opening at the base of the skull.

This can disturb normal cerebrospinal fluid (CSF) flow and contribute to pressure-related symptoms.

Cranio-Cervical Instability (CCI)

Cranio-cervical instability (CCI) is a condition where the ligaments that stabilize the skull and upper cervical spine become weakened or injured.

When this happens, the head and neck can move too much, which may irritate or compress the brainstem and upper spinal cord, and can sometimes disrupt normal blood or CSF flow.

Additional Symptoms

These are only short descriptions.

Patients often report many other symptoms, including:

• migraines

• nerve pain

• stomach or digestive issues

• vision changes

• sensory problems (light/sound sensitivity, numbness, tingling)

When My Brain Scans Finally Made Sense

The first time anyone told me I had abnormal brain scans was in 2020, when I was diagnosed with TOS (thoracic outlet syndrome). My MRI images were sent to a professor of neurosurgery specializing in skull-base surgery, who confirmed meningeal herniation / brain herniation.

The symptoms of this condition include headaches, nausea, vomiting, weakness, and changes in mental status. The MRI he reviewed was from 2012—during the period when all of these symptoms were at their worst. My pupils changed size, vomiting in the mornings was normal for me, and although that eventually stopped, my mental symptoms escalated. I had severe mood swings; my emotional state could shift multiple times within an hour. I would suddenly start crying on the bus without even realizing it—then I’d notice, feel embarrassed, and try to stop.

It felt as if I had become bipolar overnight. I was terrified I would end up in a psychiatric hospital. I told my doctor, but it didn’t seem to land as something important, so eventually I stopped mentioning it.

This is one of the hardest parts of ME: when you have nearly forty symptoms and are constantly asked, “What’s wrong with you now?”, you stop sharing everything. You become afraid doctors or friends will think you’re imagining it.

I was advised to speak with a neurosurgeon about the brain herniation, but at that time I simply didn’t have the energy to navigate the public healthcare system. I decided to focus on my neck instead.

Later, when I was diagnosed with Chiari and CCI, everything finally clicked. The constant head pressure I had been experiencing was in fact intracranial hypertension—something I had suspected many times before. And increased pressure can cause both brain herniation and Chiari malformation. This matched the findings of the 2020 ME study in Sweden, which showed a large portion of patients had optic nerve sheath enlargement on MRI, a classic sign of raised intracranial pressure,which also can cause brain herniation. This is still a onkwon piece to the puzzle, but since nothing more has happened,and I dont have most of the symptoms mentioned above I hope it’s a stable situation.

The reality of intracranial pressure

To feel your brain being pushed against your skull is something only people who go through it can truly understand. It feels like something out of a horror movie.

But I’m grateful I have those images — for my own sanity.

True brain herniation can lead to coma, respiratory arrest, or brain death. If what the neurosurgeon saw really was herniation, I’m lucky things didn’t end differently.

I sometimes wonder whether the stretching of those tissues contributed to some of my cognitive problems. A lot of this comes down to radiology measurements, who is reading the scan, and what they’re looking for. I still believe SPECT scans should be used in cases like mine. I requested one in 2016 but it was declined.

MRI shows structure.

SPECT shows function — blood flow.

Both matter.

I’ve been told that once you reach this stage, many strange neurological symptoms can appear. But by focusing on rehabilitation — rebuilding muscle, stabilizing the spine, and calming the nervous system — Chiari-like symptoms and intracranial hypertension can improve. That is the hopeful part.

What the Karolinska / Bragée ME/CFS Study Revealed — and Why It Matters

What helped me trust my own experience again were the studies coming out of Karolinska Institute and the Bragée Clinic in Sweden. They offered something I had been missing for years: objective evidence that what patients with ME/CFS feel in their bodies is real, measurable, and shared.

The findings were striking.

1. Signs of Raised Intracranial Pressure

A large proportion of patients showed optic nerve sheath enlargement on MRI — a classic marker of increased intracranial pressure.

• Around 83% of patients had optic nerve changes compatible with elevated cerebrospinal fluid (CSF) pressure.

• These findings were far more common than in the general population.

This matters because raised intracranial pressure can affect cognition, vision, mood, and autonomic function — symptoms many ME patients live with daily.

2. Structural and Mechanical Issues in the Neck

More than 80% of patients had abnormalities in the cervical spine, including:

• Narrowing at the craniocervical junction

• Disc protrusions

• Cervical stenosis

• Misalignments that may interfere with CSF or blood flow

Some patients also showed mild Chiari-like tonsillar descent.

These findings support the idea that ME/CFS is not purely metabolic or psychological, but often involves mechanical and neurological factors — especially at the junction between the brain and spine.

3. Hypermobility as a Risk Factor

About half of the patients met criteria for generalized hypermobility.

Hypermobility can contribute to:

• Ligament laxity

• Cervical instability

• Altered biomechanics

• Disrupted CSF and venous flow

The study suggests that hypermobility may create structural vulnerability, making some patients more susceptible to neurological overload under stress, infection, or injury.

On hypermobility:

This is one of the most important aspects when it comes to ME, CCI, and hip asymmetry in my own research. This is because I never in my life felt unstable joints or tissues before I got sick. However, I did easily bruise and burst blood vessels, which can be an indication of faulty collagen, similar to what is seen in people with EDS.

So I think this goes further than genetics alone. I believe the inflammatory state that ME creates somehow interferes with the tissues and the building blocks needed to form healthy collagen and even to build muscle.

Hypermobility can therefore affect anyone, but for those who have EDS or genes that affect collagen on a larger scale, it will be much worse, and they may become even more hypermobile than they were before they got sick. At that point, it becomes essential to make a plan to increase stability, and in my experience, strength training is the only thing that really works.

Ten key tips on how you can start your own healing journey and begin rebuilding your body and mind, based on the core strategies from my last four texts.

1. Find the right professionals

Take time to research clinicians who have experience with craniocervical instability (CCI) and related symptoms. Speak with other patients who have been treated there, ask what the treatment plan involves, and clarify costs before committing. It’s not always necessary to begin with expensive imaging—an experienced clinician can often recognize CCI and related dysfunctions through a careful clinical assessment.

That said, MRI can be helpful if you are considering treatments such as ESWT, PRP, or prolotherapy, as imaging allows for more precise and targeted therapy.

2. Look beyond the neck

Other contributing factors may need attention, particularly thoracic outlet syndrome (TOS) and hip asymmetry. TOS is usually relatively straightforward to diagnose. Hip asymmetry, however, was one of the most challenging issues for me to identify and address, but it turned out to be important.

3. Consider high-dose vitamin B1 (thiamine)

Some people find that high-dose B1 supports energy production and makes gentle movement more tolerable. For me, it provided the capacity I needed to begin exercising. This is an emerging area of research and should be approached thoughtfully.

Relevant research can be found here:

https://pubmed.ncbi.nlm.nih.gov/33210299/

4. Get assessed for POTS

POTS was the only objectively measurable diagnosis I received within the public healthcare system, and it helped me be taken more seriously. Beta blockers can be helpful for some people. In my case, my POTS symptoms have almost disappeared as my conditioning improved through exercise.

5. Start small if you don’t have access to a specialist

If seeing a specialist isn’t possible, begin with daily micro-stretching, focusing on areas of tightness. Use reputable online resources for guidance. If possible, work with a physiotherapist who can help you create a structured, gradual plan and ensure you’re moving safely.

6. Be cautious with how much attention you give brain symptoms

Try not to react emotionally to every symptom. Some people benefit from nervous-system retraining or “brain rewiring” approaches, especially visual or gentle methods. The goal isn’t to deny symptoms, but to avoid reinforcing fear responses in the nervous system.

7. Support your body nutritionally

Adequate protein intake is essential for tissue repair and recovery. Using a higher dose of creatine, along with protein powder added to smoothies, can support muscle function and provide the energy needed to gradually increase physical activity. This reflects my personal experience and is not intended as a universal recommendation—individual needs and tolerances vary.

8. Gradually introduce cardiovascular stress

This is often the most challenging step for people with ME. Once a basic level of strength has been established and muscles begin to activate properly, short interval-based cardiovascular training can be introduced. Performed a couple of times per week, this can support circulation, lymphatic flow, and lung function when done carefully and progressively.

Example: 2 minutes at higher intensity (approaching your maximum safe pulse), followed by 1 minute of recovery, repeated 4 times.

9. Care for your mental and emotional health

Having a mental or spiritual practice can help you stay grounded during long periods of recovery. While your external life may feel paused, inner growth is still possible. Practices like meditation can help regulate the nervous system and create moments of calm. This isn’t about positive thinking—it’s about taking responsibility for your mental well-being alongside your physical recovery.

10. Give yourself time

Healing takes time. Try to think in terms of months or even a year, rather than weeks. In my case, it took longer—partly due to the order in which I tried treatments, and partly because I went through pregnancy and early motherhood during recovery.

From survival to momentum: continuing the path toward recovery

Writing these four texts wouldn’t have been remotely possible for me just three months ago. It would have taken me forever to piece together even a single coherent sentence. Not to mention, the sharp lights in the library, where I write and people making noise would have sent me into a dizzy spiral after just 30 minutes—especially since I was writing around lunchtime, which is early in the day for me when my symptoms flare more intensely than in the evening, when my circulation is better.

I have been writing this between September and November 2025, going to the library 2–3 times a week, combined with going to the gym, picking up my son from kindergarten, playing with him, making dinner, and putting him to bed. I’ve also had a few weekends being social with friends. For someone with ME, this would be considered “getting your life back,” even though it still doesn’t measure up to a full day in a typical work schedule. These are big steps and a strong indication that my health will continue to improve over time.

I have so much more to share about my healing journey—topics like detox, infections, and genes. I’ve already started planning the next two texts mentally. If you’re reading this and have questions, or want me to go deeper into any of the topics I’ve already covered, please let me know in the comments. If you’ve had a similar journey, I would love to learn from you! And please share this if you know someone struggling with ME, POTS, or fibromyalgia.

I also have a few more things I’ll be adding to my treatment plan in the coming weeks that I’m super excited about. I truly believe these could make a huge difference in my recovery, and I’ll be writing about them after a few months of trying, so stay tuned—I think this could be a game-changer for those of us with ME.

If you found this work helpful or if any of this has resonated with you, you can support my writing by subscribing to my Substack or buying me a coffee here: https://buymeacoffee.com/krismartens Every contribution helps me continue researching and sharing what I learn.

If you’ve made it to text four, thank you so much for your time. I hope this information brings value to your own journey and motivates you to take steps toward building your own treatment plan.

Thank you,

Kristin

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From Rehabilitation to Motherhood

After a year of rehabilitation for craniocervical instability (CCI) and repairing damaged neck tissue with extracorporeal shock wave therapy (ESWT), I had eliminated several of my most debilitating symptoms — sleep apnea was gone, my arms and feet no longer felt heavy, and some of the constant neuromuscular tension finally began to ease. I could handle the physical aspects of daily life in a way that had once felt impossible.

At 37 years old, despite being advised to wait, I decided to get pregnant. I was terrified of losing my chance to have a child. After so many years of illness and loss, I couldn’t bear the thought of losing that, too.

I’ll admit, I was disappointed that I wasn’t functioning at a higher level by then. But I held on to hope — believing I would continue improving throughout pregnancy. I managed to keep up my three-day functional strength training routine all the way to week 39. I had also heard stories of people with ME who improved after giving birth, so I went into labor feeling both excited and cautiously optimistic.

Unfortunately, that wasn’t my experience.

My energy level didn’t completely crash — to my relief — but my back and body entered a new, alarming state. I needed a wheelchair for the first two days after giving birth. New inflammation flared up in my muscles, leaving some areas too weak and others too tight. The imbalance made walking painful and difficult.

In those first few weeks, I tried to ignore it. I wanted to protect that precious bubble of early motherhood. But soon, nerve pain began building in my knees and spread through my entire body. I didn’t want to believe it was happening — I couldn’t bear the idea of adding more symptoms to an already long list. Pain medication was prescribed, autoimmune disease was ruled out, and I was told that if it didn’t improve, fibromyalgia might be my next diagnosis.

An Unexpected Email

One day, an email from ACRIUS Stiftelsen landed in my inbox — completely unexpected. They’re an organization that approaches ME from a different angle, seeing it as a spine-related condition, sometimes rooted in structural issues or injuries. Back in 2020, when I was deep in research mode, they were actually one of the places I had looked into. I even sent an email expressing interest and received some information at the time.

But my gut back then told me to choose a more established clinic — somewhere bigger, more recognized, somewhere that relied on MRI imaging and had public-system credibility.

And now, years later, here they were again.

The email said they were offering a six-week treatment program in Spain and wondered if I might be interested. The dates matched exactly with the trip we had already planned — a getaway to somewhere warm during my boyfriend’s paternity leave. I was in so much pain at that point that I wanted to sign up immediately, just to have a shred of hope to hold onto for the coming months.

Still, I felt guilty — like I was dragging my family once again into another “maybe this will cure me” experiment.

But we went.

Arriving in Spain

The treatment center was just a 12-minute walk from our rented apartment — though even that distance felt almost impossible. My nerves felt pinched throughout my entire body. My hips and lower back were completely stiff, my brain fog was thick, and my vision felt grainy and unstable. I remember walking slowly down that sunlit Spanish street, half-wondering if I was even really there.

After giving birth, walking had become one of my biggest triggers for ME symptoms. Still, I was hopeful — this center promised a completely different approach to rebuilding the nervous system and spine.

I arrived with a six-month-old baby, and I was the only participant who hadn’t been physically examined in advance to confirm whether I was a good candidate. Their main criteria for treatment were misaligned hips and atlas — the top vertebra of the spine. According to their model, CCI and ME-like symptoms often begin with a misalignment in the hips, which then travels upward and distorts the atlas. Over time, this can create pressure on nerves — especially the vagus nerve — disrupting autonomic function and triggering systemic inflammation.

One surprising discovery was that several people there had mothers with hip dysplasia. That detail stuck with me, because my mother has that as well. The power of being in group rehabilitation lies in these shared observations — patterns that help connect the dots.

Although it’s not proven, it looks like there is a chance that this structural bias — such as a slight tilt in the hip — is something that can happen during birth. Over time, this kind of asymmetry might gradually irritate nearby nerves and contribute to symptoms.

It also made me question whether this could explain why some of my symptoms resemble those seen in Ehlers-Danlos Syndrome (EDS). Both conditions involve connective-tissue differences, which can lead to hypermobility and weak ligaments, so I looked into whether there might be a shared underlying factor.

During my research, I found that two collagen-related genes — COL1A1 and COL1A2 — appear in the literature for both hip dysplasia and certain types of EDS. These genes help build type-I collagen, an important structural protein that supports connective tissues, ligaments, and joint stability.

Why These Genes Matter

Changes in COL1A1 or COL1A2 can contribute to joint instability, increased ligament looseness, and weaker connective tissue support. When these features are present from birth, a baby may be more susceptible to developmental dysplasia of the hip (DDH), mild hip asymmetry, or effects from fetal positioning during birth.

If a parent has had DDH, their child may inherit a tendency toward joint laxity or a structural predisposition. However, this does not always lead to symptoms. Often, a genetic tendency only becomes relevant when it interacts with other factors — such as fetal position, the size of the baby, or the conditions of the pregnancy and birth.

It’s important to understand that hip asymmetry at birth isn’t always caused by genetics. Sometimes, it can result from how the baby is positioned in the womb, limited space during pregnancy, or a difficult birth. These factors can put uneven pressure on a newborn’s hips, leading to mild asymmetry even without any genetic predisposition.

While some people with ME may indeed have more fragile connective tissue, and I might be one of them, I’m proof that it’s possible to reverse neurological dysfunction through targeted rehabilitation and that nobody is doomed due to their genes.

Whether your ME symptoms started after an injury or a viral illness, the path toward recovery tends to follow the same principles for everyone. The first step is obtaining the correct diagnosis, which could include conditions such as cranio-cervical instability (CCI), Chiari malformation, or thoracic outlet syndrome (TOS). From there, it’s important to develop a plan that includes strength training, gentle micro-stretching, and therapies aimed at balancing the nervous system. In my experience, many ME symptoms arise from low vagal tone and an overactive nervous system. When the parasympathetic system is underactive, the body can remain in a prolonged “fight or flight” state, which over time amplifies symptoms.

How Nervous System Dysregulation Can Trigger MCAS and Affect the Lymphatic System

When low vagal tone causes the nervous system to misinterpret normal sensations as threats, it can trigger mast cell activation (MCAS). Activated mast cells release histamine and other inflammatory chemicals, which increase fluid in tissues and make blood vessels more permeable. The lymphatic system must then work harder to remove this fluid and inflammatory mediators. If lymph flow is slowed — due to inflammation, muscle tension, or tissue congestion — these substances linger, causing swelling, pressure, and prolonged flare-ups. This creates a cycle in which nervous system dysregulation, mast cell activation, and lymphatic overload reinforce each other. Supporting vagal tone, calming mast cells, and improving lymphatic drainage can help the body break this cycle and promote healing.

This connection also helps explain why many of us experience food sensitivities or environmental reactions. Rather than being solely a problem with gut flora or the food itself, these sensitivities often stem from dysregulation higher up in the nervous system. Injuries or other triggers can disrupt nervous system function, which in turn affects immune responses and can make the body react more strongly to foods or environmental factors.

Making Sense of It All

I’m sharing this because I want to give context — not just for my story, but for others who feel lost in their symptoms. So many people walk around feeling “crazy” because no one connects their neurological signs to something structural.

If you look at the twelve cranial nerves, you can trace almost every ME symptom back to nerve dysfunction or inflammation. The scientific justification for much of what these clinics do already exists within conventional neurology — it’s just not applied to ME.

Even if no cure existed 13 years ago when I got sick, having a professional confirm that numbness, burning pain, tingling, and weakness were neurological would have given me clarity — and spared years of self-doubt. Instead, most of us are told: “Nothing’s wrong, but you fit the ME criteria.”

After Spain

After six weeks in Spain, I wasn’t healed — but the nerve pain that had started after childbirth was reduced, and within two months, all the new “fibro-like” pain disappeared. I began feeling more connected to my legs, and my lower back finally started responding. For years, I had trained my glute muscles in the gym without results. What I needed wasn’t more strength — it was targeted stretching and nerve-release work to give the nervous system space to heal.

This theory of misalignment felt like the missing piece of my puzzle, and learning about it was absolutely incredible. My curious, searching nature had been longing for this answer, and I finally felt in my bones that I was on the right path. I learned that doing these stretches consistently for at least a year could start showing real results. The thought of this gave me so much hope and excitement for what 2025 could bring.

Treating ME Like an Injury — With MCAS and the Nervous System in Mind

Over time, I’ve come to believe that many cases of ME behave less like a mysterious illness and more like a complex injury to the nervous system — an injury that becomes overwhelmed by inflammation, stress, and structural vulnerability.

When someone already has underlying issues — such as mild spinal misalignment, compressed nerves, or more fragile connective tissue — the system is more sensitive to additional stressors. A viral infection, trauma, or period of burnout can then overload the nervous system and create a state of chronic neuroinflammation. This combination affects energy, pain levels, cognition, digestion, circulation, and sensory processing all at once.

This framework also helps clarify how ME and MCAS interact. When the vagus nerve is underactive and the body is stuck in “fight or flight,” the nervous system starts misreading normal signals as danger. Mast cells become more reactive, releasing histamine and inflammatory chemicals that increase tissue irritation and swelling. The lymphatic system struggles to clear that excess fluid, which adds pressure on nerves and prolongs flare-ups.

In other words, the nervous system, immune system, and connective tissue are all talking to each other — and all three influence how severe symptoms become.

Treating ME as an injury means taking all of this into account: supporting nerve function, calming the system, improving alignment and fascial balance, reducing inflammation, and creating conditions where the body finally feels safe enough to heal.

Looking Forward

This model of misalignment, nerve irritation, and autonomic overload finally made sense of my experience, connecting CCI, ME, MCAS, POTS, and previously unrelated symptoms.

Seeing ME as a multi-layered injury has shifted my approach: supporting the nervous system, reducing inflammation, and giving the body space to heal. This perspective brings hope — recovery is not impossible, even after years of dysfunction, and we are not defined by our genetics or past health struggles. With patience, precision, and the right guidance, the body has an incredible capacity to adapt and recover.

Every small improvement is proof that healing is possible.

To follow the next chapter of my journey, including the ups and downs of rehabilitation in 2025 and a sudden breakthrough in recovery, stay tuned for Part 3.

I first became seriously ill in the autumn of 2012. At the time, I was living in Copenhagen, doing an internship at an architecture firm while studying interior architecture in London. Life felt like it was at its peak — I was motivated, inspired, and moving forward. I already had some health issues, but I was still functioning. The beast hadn’t swallowed me whole just yet.

A few months after moving there, I started experiencing sudden, extreme dizziness and the sensation that the ground was rising up beneath me. Around this time, I was riding my bike home from work when the wheel slipped in the rain and I fell on my back — relieved that I hadn’t hit my head. I wasn’t in pain and didn’t think much of it. But my health was declining, and in fact, my long-lasting symptoms had started even before that.

Then everything collapsed. Within a single week, my nervous system gave out, my energy disappeared, and around forty new symptoms appeared. It felt like a rave was happening inside me — electric sensations, tinnitus, pins and needles, blurred vision -my brain was on fire.

Before I get to that turning point, it’s important to explain the health struggles that had quietly built up in the years leading to it.

Early Symptoms Before ME

Even in my late teens, I dealt with food sensitivities. Nights were the worst — I often woke with acid reflux or even brief episodes of respiratory arrest. Eating and sleeping, the two things that should have restored me, often left me feeling worse.

By the age of nineteen, I had gained a lot of weight and felt stuck. At that time, twenty years ago, information about food intolerances or anti-inflammatory diets wasn’t widely accessible.

I was fortunate to meet a homeopath who suggested I cut out wheat, dairy, sugar, and processed foods. That advice changed everything.

The constant mucus in my throat disappeared, my breathing improved, my allergies calmed down, and I lost twelve kilos. It felt like shedding an old skin — finally emerging as a truer version of myself. Looking back, I realize this one intervention probably saved me from a much steeper decline. The next six years of my life were made possible by that turning point.

From then on, my health required strict discipline: eating clean, minimizing inflammation, and practicing daily yoga stretches. Any lapse triggered numbness in my hands and feet, weak muscle signals, and overall fragility.

By twenty-five, new symptoms appeared — rashes, worsening allergies, and unexplained reactions. I begged my doctor for help and was sent to an allergy specialist. Their solution? Six daily antihistamines — but no real answers. Today, I know this was most likely MCAS (Mast Cell Activation Syndrome). I often wonder how different things might have been if it had been recognized back then.

Being Diagnosed

I was diagnosed with POTS in 2016 and ME in 2018. The delay highlights how slow and fragmented the medical system can be in recognizing complex conditions.

While ME is complex, POTS should have been identified much sooner. I had to research it myself and request a referral to a cardiologist for a tilt table test, the standard diagnostic procedure. During the test, blood pressure and heart rate are monitored with an EKG while the patient is gradually tilted upright to simulate standing. The patient remains in that position for approximately 45 minutes. A positive result is indicated by a significant drop in blood pressure and a sharp increase in heart rate.

Standing — particularly in the morning — was extremely difficult. My heart rate would rise to around 130 bpm, and I experienced dizziness, lightheadedness, and near-fainting.

POTS occurs when the autonomic nervous system does not properly constrict blood vessels upon standing. Blood pools in the lower body, reducing blood flow to the brain. The heart compensates by increasing its rate, causing symptoms such as dizziness, brain fog, fatigue, and fainting.

Receiving a measurable diagnosis was valuable because it provided a concrete basis for further investigation. Following patient reports and scientific research that aligned with my symptoms, I repeatedly found evidence pointing to the neck as a contributing factor.

Treating CCI Without Surgery

Fast forward several years. In 2019, a Swedish study from Karolinska Institutet and the Bragée Clinic revealed striking findings among ME/CFS patients:

• 50% had hypermobility

• 80% showed cervical spine obstruction

• 83% had signs of increased intracranial pressure

By then, I was already aware of possible connections between CCI (cranio-cervical instability), Chiari malformation, and ME. What frustrated me was the lack of safe treatment options. The only widely discussed solution was invasive, expensive surgery abroad — a fusion of the skull and cervical spine (C0–C2) using screws, rods, and bone grafts. While it could stabilize the spine, it came at the cost of mobility, with no guaranteed success.

I wasn’t willing to take that risk. Instead, I searched for professionals who could diagnose and treat CCI without surgery. A friend eventually recommended a rehabilitation center experienced with ME and cervical spine injuries.

Finally, in August 2022, I received a diagnosis: CCI and a small Chiari malformation.

The center guided me through advanced imaging (MRI and CT scans in London) and built a personalized rehabilitation plan. Slowly and carefully, I began stabilizing my spine through targeted functional exercises and extracorporeal shock wave therapy (ESWT).

Improvements Within Months

Within months of starting the program, I noticed remarkable changes:

• Nighttime breathing stoppages disappeared

• Nerve signaling improved

• I could lift objects with less dizziness

• Oxygen uptake increased

• My arms and feet felt lighter

• Spinal inflammation decreased

For the first time in years, I felt hope. This approach gave me a way to heal without invasive surgery — and it restored parts of my life I thought were gone forever.

Pregnancy, Rehabilitation, and Fighting for Motherhood

My biggest goal was to get well enough to carry a baby. This illness had taken so much from me, and I was willing to do anything to become a mother. At 37, I felt time was running out.

After a year of rehabilitation, I became pregnant. Doctors advised me to wait at least two years, but I knew I would never forgive myself if I waited too long and lost my chance. My life depended on the rehabilitation I had invested so much money, energy, and hope into — so I treated it as if my survival truly depended on it.

I kept up my four-day workout routine all the way to week 39 of pregnancy. It was one of the hardest things I have ever done. I have never been more dedicated, more frustrated, or more exhausted. Working out while pregnant is hard enough. Working out while pregnant and having extreme fatigue is close to impossible. But nothing can stop a chronically ill woman determined to heal and become a mother.

We’ve been through processes that have shaped us differently — we are built out of endurance.

You might wonder: How is it even possible to exercise if you have POTS and ME?

Here’s what finally moved the needle for me. After a decade of trial and error, I found a supplement protocol that actually worked. The key was high-dose vitamin B1 combined with other vitamins. I took 600 mg a day, right before my workouts — dosed according to my weight. I’ll share more about this protocol elsewhere. For me, it wasn’t a miracle cure, but it gave me energy, calmed my nervous system, and eased the pressure in my head. For others with ME, I’ve even heard of this protocol leading to near-symptom-free lives, which is mind-blowing.

The second game-changer was starting extremely small. Micro-movements and gentle strength training for my back and arms, paired with ESWT, allowed my body to finally flush out metabolic waste — the closest English word for the Norwegian slaggstoffer. Basically, all the toxic build-up that makes life with ME feel like living in a poisoned, hungover body.

Many of us with ME have damaged nervous systems, weak tissue, and cells and organs that struggle to clear toxins. Add MCAS on top of that, and you get a toxic storm so overwhelming that simply existing in your body can feel like a horror movie.

But once inflammation started to go down, something shifted. Circulation improved, oxygen delivery increased, and movement became possible. In the first years of my illness, I literally felt like a mummy — wrapped too tightly, struggling to breathe. Every time I moved, I became dizzy, my nervous system went into overdrive, and my pulse shot up. But once I got some of the inflammation under control, my body could finally tolerate movement at a higher frequency.

Reflections and What I’ve Learned

I’ve tried every diet, detox, and juice fast imaginable, but nothing reduced inflammation like this approach. Most people with ME and POTS cannot tolerate exercise — and if done incorrectly, it can even be dangerous.

It’s frustrating that so little research exists on spinal injuries and their connections to these conditions. I believe many patients wouldn’t be in this situation if chiropractors and physiotherapists were properly educated about ME, POTS, CCI, and Chiari malformations.

These conditions tested every part of me — physically, mentally, and emotionally. But through careful investigation, targeted rehabilitation, and persistence, I’ve found a path toward stabilization, recovery, and hope.

Share ME,POTS&CCI in remission.

Thirteen Years of Illness, Hope, and Healing

It is time for me to begin sharing this journey. For the past thirteen years, people have encouraged me to do so, but the truth is, it has been too painful—too overwhelming—to put into words.

And besides, what do I know about writing? I have dyslexia; words have never been where my natural talent lies.

Yet, as I have grown to love Substack, I’ve discovered a quiet urge to write—to finally give voice to what I have uncovered during more than a decade of searching, suffering, and learning.

If I had the means, I would have turned this into a documentary. But instead, I will use the tools I have and focus on sharing my story, my discoveries, and the insights that have shaped my path.

Why I’m Sharing

My aim is not to write beautifully for its own sake, but to share truthfully. To connect with others. To learn, to exchange experiences, and to find inspiration.

More than ever, I feel we are standing at the threshold of a breakthrough—on the verge of a deeper understanding of this disease, and of the complex layers of conditions that so often accompany it.

About Me

My name is Kristin. I am 39 years old and from Norway. I am the mother of a one-year-old son, and the past thirteen years of my life have resembled something out of a horror film.

Yet today, my life is finally good and stable. This transformation has only been possible because I left no stone unturned in my pursuit of healing from ME, POTS, and CCI.

The Lonely Journey

Over the years, the internet has been both a lifeline and a labyrinth.

With the rise of social media, people living with chronic illnesses—especially those without established cures—have leaned on the internet for information, comfort, and community. In return, we are often bombarded with conflicting solutions and advice.

Before COVID-19, ME was a hidden epidemic—a silent health crisis. To much of society, and especially to healthcare professionals, we were the outcasts—dismissed and forgotten.

In response, we sought knowledge where we could: in forums, in patient stories, and in the private clinics willing to treat the mysterious conditions that conventional medicine often ignored.

But what weighs heaviest in those online spaces is not the information—it is the suffering.

The grief and despair echo through Facebook groups like a chorus of trapped voices—like zombies in cages, left behind. To outsiders, this might sound dramatic. But for those of us who lived it, the imagery is tragically accurate: an entire community crying out for survival, yet unheard.

My Approach

I have tried almost every treatment imaginable. Healing became my life’s mission.

I have spent years silently observing these groups, following science, drawing connections between illnesses, and filling over ten notebooks with research, notes, and protocols.

I have attempted everything—from nervous-system rewiring to different Lyme disease treatments. And yes, I would have swallowed a frog if it promised a cure.

That is how desperate this illness makes you—because it is not just about life or death, but about the unbearable state of existing without truly living.

Now, I want to share the insights I have gained—what has helped, what has failed, and what I wish I had known sooner. Writing helps me process these years of illness, even with cognitive challenges and fatigue slowing me down.

I hope my story will guide those trapped in this web of misinformation and endless pressure to heal “perfectly”—whether through diets, gut protocols, or every other supposed cure.

A Call to the Community

Are you ready to climb out of this hole with me?

I will do my best to share this information clearly, take you through the steps I’ve taken, and offer insights from my personal story—in the hope that my experience can be a mirror for those in similar situations.

I was diagnosed with ME and POTS through the public health system, and fibromyalgia was also considered. But after a decade of research, I finally discovered the root cause of my problems—many of which I had struggled with since childhood.

I’ve now written four texts on Substack to guide you through a small part of this journey, focusing on the connection between the neck and spine in ME.

I hope you’ll subscribe and follow along as I continue sharing my journey, piecing everything together, and finding a way out of this web.