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Oct 3 2026
Natural substances against ME/CFS

When I started work on my website, almost 4 years ago, I was very sceptical about natural drugs. Over the years, I had tried a lot of different alternative approaches to alleviate my symptoms, and nothing had helped until I received a Fabry-specific treatment. That convinced me that real symptoms should be treated with real medications. However, the events that have unfolded over the past few years have again changed my perspective. With events I mean that my treatment was cancelled for reasons that have nothing to do with science, and then I found that galactose, which is sold as a nutritional supplement, works better than my Fabry-specific treatment. Today, I still think that most nutritional supplements and herbal medications are ineffective, but there might be some gems that are hidden amongst the countless preparations that are on offer.

Pharmaceutical science doesn’t move as fast as it should. There are many people that need help today, but drug development is a slow and expensive endeavor. New drugs that enter the market are increasingly expensive. This is already a problem for the German public health system. In less developed countries, access to certain treatments, like Fabry-specific treatment, is nigh impossible. Therefore, I’m scouring scientific literature for substances that are cheaper and readily available. Nutritional supplements have a number of advantages compared to the experimental chemicals that are used in some scientific experiments: they have been tested to be safe for human consumption and are available without a prescription. The active substances of a number of nutritional supplements have been well characterized. Especially chinese researchers are trying to put traditional chinese medicine on a scientific footing. This might sound far-fetched, but it’s not much different from modern drug development in the western world. Pharmaceutical companies often have large compound libraries of substances that are tested for medicinally relevant properties. Chinese researchers do the same, only using substances that have a long history of traditional use.

Of course, nutritional supplements have a number of drawbacks compared to prescription drugs. Between a proven physiological effect and a practical use for patients, there are many steps. These have to be elucidated before a drug may enter the market, but for nutritional supplements, these are often poorly characterized. Bioavailability and relevant concentrations are just two of them. Pharmacokinetics are often unknown. Additionally, there’s a risk of interference with prescription drugs. Practically, preparations containing the same active substance may contain completely different concentrations, so patient experience reports should always mention the concentration of their preparation in addition to dose and frequency.

Lastly, if I’m trying to find a natural substance that would help ME/CFS patients (and other patients affected by conditions as described in my August 4 blog post), what does “helping” constitute? I’m writing under the assumption that ME/CFS is caused by ER stress, a disruption of a cell’s metabolism caused by protein misfolding. When too many misfolded proteins are produced, due to genetic mutations or viral infections, the degradation mechanism are overwhelmed, leading to the formation of aggregates of misfolded proteins. The progressive acculumation of these aggregates causes a persistent inflammation that in turn causes of many of the symptoms associated with ME/CFS. For more information, watch my video. From my experience with Fabry patients, the restoration of proper protein folding means that the degradation mechanisms for misfolded proteins are no longer overwhelmed. As a consequence, existing aggregates of misfolded proteins are slowly broken down. This process triggers occasional bouts of increased inflammation. So when I’m looking for a natural substance for the treatment of ME/CFS, I’m not looking for something that allows patients to get up out of their beds after a day or two. Instead, I’m looking for something that removes the cause of the chronic inflammation from the body. This is a slow and unpleasant process that only leads to a gradual improvement of symptoms, interspersed with occasional bad days.

Looking for substances that reduce the effects of ER stress, I initially found two papers, one about the treatment of ER stress in the context of Alzheimer’s disease using mainly natural substances, and one about the treatment of ER stress in the context of Parkinson’s disease using mainly chemical compounds. Because of the reasons mentioned above, regarding availability and safety for human consumption, I have mostly focused on the first of those two papers. One substance that stood out is quercetin. Quercetin has been reported to improve ME/CFS symptoms. An extensive description of quercetin can be found here. However, these sources do not mention the mechanism of action, so while there is some recognition that quercetin has a beneficial effect for ME/CFS patients, it is likely still poorly understood why it has such an effect. Here, I would like to propose quercetin’s modulation of ER stress as the relevant mechanism of action. Quercetin has a poor bioavailability, but a combination with bromelain or a liposomal formulation might enhance its uptake.

The above paper mentions other substances, including schisandrin, ginsenoside and resveratrol (see also here and here.

A substance that is not included in the above paper is harpagoside, the active substance of devil’s claw. This substance is found to have a positive effect on inflammation. It also reduced mitochondrial dysfunction in an articially induced Parkinson’s disease model. Additionally, this substance might have a direct beneficial effect on ER stress.

There are many more natural substances that pique my attention. For example, miglustat may alleviate symptoms in Pompe disease. There are natural extracts, mainly from mulberry leaves, containing miglustat. Could these improve the condition of Pompe patients with specific missense mutations?

There is so much yet to discover in the world of natural medicine. Initially, I was sceptical, but now I think: “It is improbable, considering how many natural substances have been characterized, that none of these substances should have a beneficial effect on ME/CFS.” Many preparations are still likely to benefit the vendor more than the buyer. However, it’s an interesting challenge to find the relevant ones.

Fabrienne 0 Comments
Sep 4 2026
Galactose treatment for Fabry disease

While reviewing the video scripts of my galactose videos, I noticed that they lack structure. I was putting out information as I gathered it, but that means that patient experiences and technical details ended up together in each of my three videos. So in this post, I’ll try to summarize the most important information in a more coherent fashion. I think it’s obvious to most that I was the one who came up with the whole oral galactose idea, even though, in my videos, I put a bit differently, to make it absolutely clear that whatever I say about galactose does not constitute medical advice and is no replacement for a consultation with a physician. Even though I now feel safe to say that the idea was mine, that caveat remains in place for this blog post too: whatever I say about galactose does not constitute medical advice and is no replacement for a consultation with a physician. Note, however, that people who are affected by galactosemia should refrain from taking oral galactose.

Galactose is a sugar that has a very similar structure to one of the available Fabry medications: Galafold. Galafold is an oral Fabry treatment that works as a pharmacological chaperone. A chaperone is a small molecule that aims to improve the production of a patient’s own enzyme. This is a different approach to enzyme replacement therapy (ERT), which, as the name suggests, aims to completely substitute a patient’s own enzyme.

Here are a few differences between chaperone therapy and ERT. As a small molecule, chaperone therapy can pass the blood-brain-barrier. As an oral therapy, it doesn’t require wounds that can pose an infection risk. The risk of allergic reactions is much less for chaperone therapy, and there is no risk for an immune resistance. However, chaperone therapy doesn’t work for all Fabry mutations. Mutations that cause a complete loss cannot be salvaged and have to be substituted using ERT. Chaperone therapy is mainly used for missense mutations that cause a moderate loss of enzyme function (amenable variants). Some of these genetic variants are very common (affecting up to half a percent of the general populace), and some have been declared benign. However, recently it has been proven that ER stress is in additional cause for Fabry disease. This secondary cause of Fabry disease was overlooked when these variants were declared benign.

Many people who are affected by these common Fabry variants do not receive treatment, including me. I started self treatment using galactose (there are two papers about galactose treatment for Fabry disease, one in cell cultures and one with a single patient). Initially, I used 0.1 gram per kilogram of body weight. That amounts to single doses of e.g. 6 grams for a 60 kilogram person. I took at least four of such doses, or sometimes up to six, a day. At least an hour before and after each dose, I didn’t eat or drink, except water. The reason: the body prefers glucose of galactose, so if glucose is present in the body, galactose isn’t absorbed as effectively.

Galactose needs to enter to blood stream to work. However, when ingested, a share of that galactose is turned into glucose in the liver, making galactose less effective. The workaround I used: galactose can be absorbed into the blood stream by the oral mucosa. So by leaving it in the mouth for a few minutes, galactose uptake can be greatly improved. This process is further enhanced by adding a pinch of salt to the galactose, allowing the SGLT1 sugar transporters to work more effectively.

Lately, I have been making galactose lozenges. That means that I mix galactose, one percent salt and water to create a viscous mass. Then I pour that mixture into silicon baking molds for candy, and let the water evaporate. With the molds I use, that yields galactose lozenges of 4 grams each. These dissolve very slowly in the mouth, yielding a continuous benefit over longer periods of time.

There are some experiences I want to mention. Initially, the body (including digestion) may need to adapt to galactose treatment, so it’s better to start it slowly. Galactose doesn’t solve every problem instantly. Some symptoms, like brain fog and exhaustion, improved quickly (within days or weeks) and still keep improving after three years. Other symptoms, like food intolerances and inefficient sweating only improved after years of treatment. Occasionally (every few months), I have a few days with flu-like symptoms, and on such days I really need to take things slowly. My theory is that aggregates of misfolded proteins keep dissolving and cause an immune reaction. On good days, I might feel like I can do lot, but I still need to take things slowly, or else I will have some really bad days afterwards. Galactose doesn’t replace pacing. My guideline: I can do the same as I did before treatment and feel much better, or I can do a lot more and feel equally bad as I did before treatment.

Fabrienne 0 Comments
Aug 19 2026
Quality problems of medical research

When I first read that my genetic variant is supposedly benign, I was shocked. “That’s an unfortunate mistake”, I thought. But since, I have read many more medical scientific papers, and it’s not just a mistake, it’s one of many signs of the poor state of medical scientific writing. Before Fabry hit, my field of interest was historical linguistics. In that field of research, no new data can be generated, and new insights are mainly gained from combining the same sources in ever new ways. From this background, I have identified a number problems in medical scientific research. Two of them pose a systematic challenge.

1. The extrapolation trap. Sometimes, no distinction is made between solid conclusions and tentative conclusions that are partially based on assumptions. Regarding my GLA-variant D313Y, there’s the following chain of extrapolations. First, the association between Gb3 deposits and Fabry disease is turned into a causal association. Next, that causal association becomes a singular exclusive pathomechanism. Only then can a variant that does not trigger that pathomechanism be considered benign. The final extrapolation is that, assuming that that specific genetic variant is benign, the Fabry symptoms in patients with that variant must have different a cause. Every time an extrapolation is presented as a fact, that moves the interpretation of data further away from the actual data. In the end, it might lead to a complete disconnect between the two.

2. A miraculous multiplication of sources. Conclusions, including tentative conclusions that are treated as facts, are repeated in review papers. Then, those review papers are cited in other review papers. In the end, there appears to be a large body of literature supporting certain views, without a correspondingly large amount of data to back them up. This effect distorts the relative reliability of specific statements. Certain positions are echoed over an over again (like the assumption that my genetic variant is benign), and other positions, that might be better supported by available data (like the fact the ER stress is a pathomechanism for Fabry disease) disappear from scientific discourse again and again. Which positions are repeated and which vanish is likely partially due to reseacher’s bias. Data which fits exisiting models is repeated, other data ignored. This introduces an element of subjectivity, which has no place in science. Apart from that, it’s the data that doesn’t fit existing models that can really broaden our understanding of the subject matter at hand, so that’s what we should be focusing on.

Other problems include nonsense citations. In this paper, the quote “However, it was clear that such a high dosage of galactose is not practicable in patients with Fabry disease” is in no way backed up by the source that is mentioned. Sometimes, the problem is simple nonsense. In this paper, the quote “AGALopathy is thus not FD, which is based on an enzyme deficiency resulting in intracellular Gb3 accumulation. Thus, AGALopathy cannot be successfully treated with ERT.” is also not backed up by the source mentioned, but even without consulting the original source, the statement is obvious nonsense. Another problem is that research papers are sometimes created to fulfill certain quota, without adding any new insights. The sheer amount of available publications can sometimes make it difficult to assess the robustness of the data underlying given statements, especially in view of the second problem mentioned above.

The peer review process doesn’t work as intended. To prevent each of the above points from happening, there’s a peer review process. Even if most academic researchers write well, all it needs is one or two reviewers who themselves adhere to subpar standards to publish a paper.

By and large, medical research reminds me of archaeology around 1900. Everyone was racing to find something grand spectacular, sometimes dragging of parts of temples or even entire temples from faraway places to Europe. Modern archaeology, on the other hand, involves sifting through endless piles of dust. Even small finds can rewrite history. Similarly, in medicine, there seem to be people who strive for a breakthrough through original research. Claiming that the most common GLA variant is benign sure is a spectacular headline, but in the end, it’s an overinterpretation of data that harms the very people medical research set out to save.

Fabrienne 0 Comments
Aug 4 2026
The extent of the ER stress problem

In my last video, I proposed endoplasmic reticulum stress (ER stress) as a possible cause for ME/CFS and long COVID. In that same video, I presented a list of other diagnoses that may be linked to ER stress. One of my next goals is mapping the total extent of the ER stress problem. My first conclusion: that list in my video was clearly too short.

There appears to be a whole family of diagnoses that are linked through ER stress. However, even a comprehensive review of ER stress in disease pathogenesis doesn’t come close to listing all of the associated diagnoses. So far, I have found

(From the above paper): Cancer, cardiovascular diseases (atherosclerosis, ischemia/reperfusion injury, myocardial infarction, heart failure), neurodegenerative diseases (Alzheimer’s disease, Parkinson’s disease, Huntington’s disease), metabolic diseases (insulin resistance, type 2 diabetes, obesity), autoimmune diseases (rheumatoid arthritis, multiple sclerosis, inflammatory bowel disease).

Additional autoimmune diseases are systemic lupus erythematosus and Sjögrens syndrome.

Another case of an overreacting immune system is mast cell activation syndrome (MCAS).

The pathogenesis of endometriosis also involves ER stress.

Then, there’s genetic diseases like Fabry disease, Ehlers-Danlos syndrome, cystic fibrosis and sickle cell anemia.

ER stress plays a role in a number of eye diseases like glaucoma, diabetic retinopathy, age-related macular degeneration, retinitis pigmentosa, achromatopsia, cataracts, uveal disease, ocular surface diseases and myopia.

Then there are problems which are commonly considered psychological, like autism and depression.

Additionally, ER stress is worsened by viral infections, some bacterial infections and aging. Microplastic, too, might exacerbate ER stress.

This is merely the starting point of my new research. There are likely many more genetic diseases that are related to ER stress. For example, there’s a group of genetic diseases that are termed endoplasmic reticulum storage diseases, including alpha-anti-trypsin-deficiency (AATD) and hereditary hypofibrinogenemia with hepatic storage (HHHS). Are these linked to ER stress, too?

All in all, ER stress appears to be one of the major causes of disease, especially in the modern world. Common symptoms appear to be: fatigue, brain fog, inflammation and the consequences of cell death of the affected cell types. Some of these diagnoses may be risk factors for other diagnoses within this disease family. In some cases, we might be dealing with polygenic phenotypes that do not follow Mendelian inheritance patterns. Polygenic inheritance might even mean that the exact diagnosis within this disease family changes between a parent and a child (I would like to introduce the term “Fabriennian inheritance”). The link between Ehlers-Danlos syndrome and autism is already well established, but even this research paper doesn’t consider ER stress as a possible link.

Overall, the total scope of the ER stress problem would put it on one level with bacterial infections, viral infections and cancer. Still, there is no coordinated research. In the case of Fabry disease, the problems arising from ER stress are not taking seriously, despite being definitely proven. That’s why it’s important to raise awareness for this problem.

Fabrienne 0 Comments
Jul 30 2026
I’m starting a blog

I’m starting a new project. Sometimes it takes a lot of time, before I can publish a new video. That doesn’t mean I’m doing nothing. From now on, I’ll publish new findings and conclusions here.

In my last video I explained why I think that ER stress (endoplasmic reticulum stress) is (part of) the cause for ME/CFS. ER stress refers to a disturbance of a cell’s metabolism that is caused by protein misfolding. Protein misfolding always happens, so it’s not necessarily a problem. But a number of factors can make this problem so much worse that several processes of a cell’s metabolism may be disrupted. Examples for such factors are viral infections and genetic mutations. Causes of ER stress, from my experience with Fabry disease, are brain fog, exhaustion and inflammation. Additional problems may arise when cells start dying because of ER stress. Even though this connection is not proven, I consider ER stress to be a likely cause for small fibre neuropathy. The video, which includes many scientific sources, can be found here:

At the moment, I’m working on three subjects: how many health problems are related to ER stress, what can be done about it, and why is medical research so slow. In the month since I published this video I already gathered many new facts. By and by I will publish them here.

Thanks for reading and have a great day, Fabrienne

Fabrienne 0 Comments