DecodeME, blood markers, neuroinflammation and a sobering review of dietary supplements and supporting technology
Author: Jan Fredrik Poleszynski, Uno Vita AS
ME/CFS is not the same as being tired. It is a complex, biological multisystem condition in which exertion can trigger a delayed and disproportionate worsening of symptoms, called PEM - post-exertional malaise. New genetics from DecodeME and a large study of blood-based markers strengthen the understanding that the immune system, nervous system, pain regulation and metabolism may be involved. The findings are important, but they do not yet provide a simple blood test, a genetic test for diagnosis or a one-size-fits-all treatment.
This article goes deeper than our basic article on fatigue, chronic fatigue and ME/CFS. The aim is to explain the new biology in an easy-to-understand way and assess what the research actually says about nutrients, natural substances and supporting technology. The measures are referred to as support for normal body functions and symptom management - not as a cure for ME/CFS.
Briefly explained
- DecodeME found eight genetic regions, not eight "ME genes". Each variant has little effect, and the findings are currently published as a preprint.
- The signals point in particular to the immune response after infection and neurological processes, including chronic pain.
- A separate, peer-reviewed study found blood-based patterns consistent with chronic inflammation, insulin resistance and liver-related changes. No single marker could be used diagnostically.
- PEM and individual energy management are still the most important practical starting point.
- Dietary supplements and technology may be relevant as individually adapted support, but the documentation varies from direct clinical studies in ME/CFS to biological plausibility and research from other conditions.
ME/CFS is an exercise intolerance – not just low energy
Normal fatigue is usually improved by sleep, food and rest. In ME/CFS, a small physical, mental, social or emotional strain can cause a clear "crash" 12-48 hours later. The worsening may include fatigue, pain, feeling like the flu, sleep disturbance, headache, dizziness, brain fog and increased sensitivity to sound or light. This is PEM.
CDC and NICE recommend that activity is managed within the person's individual tolerance limit. Fixed exercise programs with automatic increases are not suitable for PEM and can worsen the condition. Pacing therefore does not mean passivity, but conscious distribution of physical, cognitive, emotional and social load.
DecodeME: The largest genetic study of ME/CFS
DecodeME is a large genome-wide association study, a so-called GWAS, developed in collaboration between researchers and people with ME/CFS. The researchers analyzed common genetic variants in up to 15,579 people with ME/CFS and compared them with around 260,000 control people of European genetic background.
The study identified eight genomic regions with statistically significant association with ME/CFS. It is crucial to understand what this means:
- A locus is an area of the genome, not necessarily a specific gene.
- The variants are common in the population and cause only small changes in risk.
- The findings cannot be used as an individual diagnosis or as a basis for choosing dietary supplements.
- The main analysis largely concerns people with a European genetic background.
- As of July 2026, the results were still published as a preprint and must be interpreted accordingly.
What do the genetic signals point towards?
The researchers prioritized several candidate genes near the signals. These are research hypotheses, not a ready-made causal model.
RABGAP1L
RABGAP1L is linked to intracellular transport and the cells' handling of bacteria and viruses. The region supports the interest in how cells respond to infection and regulate transport between endosomes, lysosomes and other structures inside the cell.
BTN2A2
BTN2A2 is involved in regulation of T cells. The gene codes for a signaling protein that can help dampen T-cell activation and affect the balance between different immune cells. A genetic difference in this area may be relevant to the balance between activation and downregulation of the adaptive immune system after an infection.
OLFM4
OLFM4 is expressed, among other things, in neutrophil granulocytes and is involved in the regulation of innate immunity and antimicrobial responses. The protein can both suppress inflammation and influence the immune system's ability to deal with microorganisms. The exact meaning of ME/CFS has not yet been clarified.
CA10
CA10 is highly expressed in the nervous system and is involved in synaptic organization. The DecodeME signal in this region overlapped with a known genetic signal for chronic pain in several places in the body. This makes the area particularly interesting in research into pain, sensory hypersensitivity and neurological symptoms.
Other possible candidates in or near the regions are linked to mitochondria, synaptic signaling and regulation of microglia. Because each locus can affect several genes, it is too early to say which gene is possibly causal.
The overall picture is nevertheless interesting: Genetic vulnerability appears to involve both immunological and neurological processes. It fits with the fact that ME/CFS often, but not always, occurs after an infection. Genetics show predisposition; it does not alone tell what triggered the illness in the individual.
The blood study: Biological patterns that are not just due to inactivity
In 2025, Beentjes, Khamseh, Ponting and colleagues published a peer-reviewed analysis of UK Biobank data. Up to 1,455 people with ME/CFS were compared with 131,303 control people. The researchers examined 3,237 molecular and cellular features and used statistical methods to distinguish direct disease associations from changes that could be due to low physical activity.
Hundreds of features distinguished the groups. A total of 116 were significant in both women and men. The pattern was consistent with chronic inflammation, insulin resistance and liver-related changes. Nine of 14 selected features were replicated in the US All of Us cohort, and the differences were stronger in people with PEM.
This is important, but must not be over-interpreted:
- The study shows group differences, not a complete diagnostic blood test.
- No single marker reliably distinguished between people with and without ME/CFS.
- Observational patterns do not automatically show what is the cause, consequence or treatment goal.
- The results support further research on combinations of markers and biological subgroups.
A possible biological chain
The research does not provide one universal explanation, but a careful working model can be described as follows:
- A person has a biological vulnerability that consists of many small genetic, immunological and environmental factors.
- An infection or other stress triggers an immune response.
- In some people, the interaction between the immune system, nervous system, autonomic regulation and energy metabolism is not fully normalised.
- Exertion produces a disproportionate response with PEM, pain, cognitive impairment, sleep disturbance and orthostatic intolerance.
- Persistent inflammation and metabolic patterns can help keep the system out of balance.
This is a model for research – not a proven chain in everyone with ME/CFS.
Neuroinflammation, headache and brain fog
Neuroinflammation means immune-related processes in and around the nervous system. Microglia, astrocytes, mast cells, signaling substances and the blood-brain barrier can be included.
The term is often used too broadly. In people with ME/CFS, there is not one routine test that can confirm "neuroinflammation", and a mechanistic finding in cell or animal studies is not the same as a documented clinical effect.
Nevertheless, the research track is relevant because many people have oppressive or migraine-like headaches, sensory overload, slow information processing, word-finding difficulties, failing short-term memory and pain amplification. The DecodeME signal near CA10 and enrichment of genetic signals in brain-related tissues provide further reason to study neurological mechanisms.
Dietary supplements and natural substances: What is directly documented?
No dietary supplement is approved as a cure for ME/CFS. A systematic review from 2025 found some positive signals, but concluded that the studies are small, heterogeneous and often methodologically weak.
It is therefore more honest to sort the substances according to level of evidence than to present a long "treatment list".
Level 1: Clinical studies directly in ME/CFS
Coenzyme Q10 and NADH
Coenzyme Q10 and NADH are part of the cells' energy metabolism and redox balance. Small randomized studies have reported improvement in some measures of fatigue, sleep, quality of life and biochemical markers.
The combination is among the better researched nutritional strategies in ME/CFS, but the documentation is still too limited to promise an effect. The studies have relatively few participants, and the results must be confirmed in larger, independent trials.
Oxaloacetate
Oxaloacetate is a natural intermediate in the citric acid cycle and participates in the cells' energy metabolism.
In the RESTORE ME study, 82 people were randomized to 2,000 mg oxaloacetate or control daily for three months. Fatigue was reduced more in the intervention group than in the control group.
The study was relatively small, had several dropouts in the control group and financial conflicts of interest. The result is promising, but needs independent replication before firm conclusions can be drawn.
L-carnitine and acetyl-L-carnitine
Carnitine helps transport fatty acids into the mitochondria. Older and small studies have shown possible signals for physical or mental fatigue, but the results are not sufficient for safe conclusions.
Acetyl-L-carnitine is particularly interesting for the nervous system and mental energy, but should not be presented as a documented treatment for ME/CFS.
D-ribose
D-ribose is a building block in nucleotides, including ATP. Open studies have reported improvements in energy, sleep, mental clarity and well-being.
Because the studies mainly lack a good placebo control, expectation effects, natural disease fluctuations and other simultaneous changes cannot be ruled out.
Probiotics, polyphenols and certain combinations
Some small studies have investigated the gut-brain axis, polyphenols, the microbiome or multi-substance mixtures. The results may provide a basis for new hypotheses, but are currently too uncertain for general recommendations.
Level 2: Indirect clinical support from pain, migraine or post-viral conditions
PEA – palmitoylethanolamide
PEA is an endogenous fatty acid amide that the body produces locally during stress, tissue damage and inflammation. The substance affects, among other things, PPAR-alpha and can modulate mast cells, microglia and pain pathways.
PEA is sometimes referred to as a local protection and regulation substance. It does not work in the same way as traditional painkillers, but can affect mechanisms involved in inflammation and sensitization.
Micronized and ultramicronized forms are best investigated because regular PEA has limited water solubility and uptake.
Clinical data are strongest in chronic and neuropathic pain. There is also interest in PEA for fibromyalgia, migraine and some post-viral symptoms. Direct, large ME/CFS studies are lacking.
Luteolin
Luteolin is a flavonoid found in, among other things, celery, parsley, chamomile, oregano, olives and some other plants.
Cell and animal studies show the influence of NF-kB, NLRP3, oxidative stress and microglia-related signaling pathways. Luteolin can also affect mast cells and certain inflammation-related signaling substances.
The combination PEA and luteolin has been investigated in some post-viral and neurological contexts. There is a biological justification for combining the substances, but the combination cannot be referred to as documented treatment of ME/CFS.
Magnesium
Magnesium contributes to normal energy metabolism, muscle function, electrolyte balance and normal functioning of the nervous system. It can be particularly relevant in the case of low intake or a documented deficiency.
Magnesium has also been investigated in migraine and may be relevant when headache is part of the symptom picture. However, this does not document an effect on ME/CFS itself.
Different forms of magnesium have different properties. Magnesium glycinate is often used when good tolerance and a calmer stomach are important. Magnesium malate is interesting in energy and muscle contexts, while magnesium threonate is marketed specifically for the nervous system. The documentation that one form is best in ME/CFS is insufficient.
Riboflavin and coenzyme Q10 in headaches
Riboflavin, vitamin B2, and coenzyme Q10 have both been investigated for migraine. If headache is a central part of the symptom picture, it should first be diagnosed and treated as a headache - not automatically attributed to "neuroinflammation".
Omega-3 fatty acids
EPA and DHA are included in cell membranes and form lipid mediators that participate in the regulation of inflammation. Omega-3 is also important for the normal structure and function of the nervous system.
Direct documentation for ME/CFS is scarce, but omega-3 may be relevant as part of the diet and with a low intake of fatty fish.
Level 3: Mechanistically interesting, but without good documentation in ME/CFS
PQQ – pyrroloquinoline quinone
In preclinical research, PQQ has affected signaling pathways linked to PGC-1-alpha and mitochondrial biogenesis. This makes the substance biologically interesting, especially together with CoQ10.
PQQ participates in redox reactions and is studied in connection with the number and function of the mitochondria. However, there is no solid clinical evidence that PQQ reduces PEM or treats ME/CFS.
PQQ should therefore be presented as mitochondrial nutritional support and an interesting research substance – not as a documented ME/CFS intervention.
NAC and glycine
N-acetylcysteine, NAC, is a precursor to glutathione, while glycine is involved in glutathione synthesis and many other processes.
The combination glycine and NAC, often called GlyNAC, has been investigated in other groups with oxidative stress, mitochondrial changes and age-related loss of function. The combination has not been sufficiently investigated in ME/CFS.
Alpha lipoic acid
Alpha-lipoic acid acts as a cofactor in mitochondrial enzyme complexes and participates in redox reactions. The substance can also help to regenerate other antioxidants.
Clinical documentation specifically for ME/CFS is lacking.
Creatine
Creatine is included in the cells' rapid energy buffer through the phosphocreatine system. It is important in muscles and brain and can be relevant in case of low muscle capacity or insufficient intake.
There is biological interest and research from other conditions, but not sufficient documentation for an effect on ME/CFS or PEM.
Taurine
Taurine affects cell membranes, osmoregulation, calcium handling, nervous system and mitochondrial functions. The substance is interesting for neurological and metabolic stress, but direct clinical documentation for ME/CFS is insufficient.
NAD precursors such as NR and NMN
Nicotinamide riboside, NR, and nicotinamide mononucleotide, NMN, can increase NAD-related metabolites in humans.
NAD is important for energy metabolism, DNA repair and redox systems. It is still unknown whether supplementation with NR or NMN provides clinical benefit in ME/CFS.
Curcumin
Curcumin is a polyphenol from turmeric and affects several inflammatory and redox pathways in laboratory studies, including NF-kB, Nrf2 and certain cytokines.
The uptake varies greatly between formulations. Piperine can increase absorption, but can also affect enzymes that break down drugs.
Direct ME/CFS data are insufficient. Curcumin should therefore be referred to as general support for normal inflammation and antioxidant mechanisms, not as treatment of the disease.
Quercetin
Quercetin is found naturally in, among other things, onions, apples, berries and capers. The substance can affect Nrf2, NF-kB, mast cells and inflammasomes in preclinical studies.
There is clinical research from other conditions and some interest in post-viral symptoms, but the documentation for ME/CFS is not sufficient.
Resveratrol
Resveratrol is found, among other things, in grape skins, berries and peanuts. The substance affects sirtuins, AMPK, redox balance and mitochondrial signaling pathways in laboratory studies.
Clinical results in humans vary, and there is no good documentation for the treatment of ME/CFS.
Boswellia
Boswellic acids from virak affect, among other things, 5-lipoxygenase and leukotriene-related signaling pathways.
The documentation primarily applies to certain pain and inflammation conditions, not ME/CFS. Boswellia may be relevant in connection with specific muscle or joint complaints, but should not be presented as a general ME/CFS intervention.
Melatonin
Melatonin is a hormone that regulates the circadian rhythm. It also has antioxidant and immune-related properties in preclinical studies.
Melatonin may be relevant for a specific sleep disorder, but a higher dose is not necessarily better. It can cause drowsiness, vivid dreams, headaches or drug interactions.
The goal should be better sleep regulation - not the highest possible dose.
Rhodiola rosea
Rhodiola has been investigated for stress-related fatigue, mental strain and reduced work capacity. The results cannot be easily transferred to ME/CFS.
In ME/CFS, a stimulating experience can cause the person to do more than the energy limit allows. This can increase the risk of "push-crash".
Ashwagandha
Ashwagandha has been investigated for stress, sleep and non-specific fatigue. The substance can affect sedation, blood pressure, blood sugar, thyroid gland and immune-related processes.
The documentation for ME/CFS is insufficient, and use should be assessed individually.
Ginseng, schisandra and eleutherococcus
These plants are traditionally used for low energy, stress and reduced stamina. Evidence from non-specific fatigue must not be confused with documentation of PEM-dominated ME/CFS.
The stimulating effect can mask the body's energy limit without increasing the real biological capacity.
Lion's mane and medicinal mushrooms
Lion's mane, Hericium erinaceus, contains compounds that are studied in connection with nerve growth, cognition and neurological functions.
Beta-glucans from mushrooms can influence immunological responses. However, direct clinical data in ME/CFS are insufficient.
French oak extract
Standardized extracts of French oak have been examined for various forms of fatigue and oxidative stress. There are interesting signals, but results from non-specific fatigue or other patient groups cannot automatically be transferred to ME/CFS.
Ginkgo and cistanche
Ginkgo biloba affects blood flow, antioxidant mechanisms and neurological signaling pathways. Cistanche is traditionally used for exhaustion and reduced vitality.
Certain combination studies may be interesting, but the documentation for clearly diagnosed ME/CFS is limited.
Ginger and rosemary
Ginger and rosemary contain polyphenols and terpenes that affect inflammation and redox pathways in laboratory studies.
They can be good parts of a varied diet, but should not be referred to as treatment for ME/CFS.
Wasabi and isothiocyanates
Isothiocyanates activate, among other things, Nrf2-related defense mechanisms. Some small studies have investigated wasabi extracts and fatigue, but the documentation is currently weak.
Probiotics and the gut–brain axis
The intestinal microbiome can influence the immune system, metabolites, intestinal barrier and signals to the nervous system.
Some small studies have investigated probiotics in ME/CFS, but different strains of bacteria have different properties. Results from one product or one strain cannot be generalized to all probiotics.
[Image 5 - mitochondria: A detailed mitochondrion with energy flow through the inner membrane, surrounded by neutral molecular structures.]
Vitamins and Minerals: Correct Deficiency Before Advanced Protocols
In the case of prolonged fatigue, a medical examination should come before comprehensive supplement regimes.
Among other things, it may be relevant to examine blood status, ferritin, vitamin B12, folate, vitamin D, metabolism, liver and kidney function, HbA1c and celiac disease based on clinical assessment.
Vitamins and minerals can contribute to normal body functions:
- B vitamins contribute in various ways to energy metabolism and the nervous system.
- Vitamin C contributes to normal energy metabolism and protection of cells against oxidative stress.
- Vitamin D contributes to the normal functioning of the immune system.
- Magnesium contributes to normal energy metabolism, muscle function and nervous system.
- Zinc and selenium contribute to normal functioning of the immune system and to the protection of cells against oxidative stress.
- Iron contributes to normal oxygen transport and energy turnover, but should not be used in high doses without documented need.
More is not always better.
High doses of vitamin B6 over time can cause neuropathy. Iron can be harmful if used incorrectly. Magnesium can cause stomach problems and must be considered especially in case of reduced kidney function. Long-term high intake of zinc can contribute to copper deficiency.
A safe way to assess grants
- Clarify diagnoses, deficiencies and medicines.
- Define one target, such as sleep, headache, orthostatic discomfort or cognitive load.
- Change one thing at a time.
- Start low and rate slowly, because some people with ME/CFS are very sensitive.
- Before symptom and activity log, including response 24-72 hours after the change.
- Stop if there is clear deterioration.
- Do not use a temporary energy boost to exceed your endurance limit.
Possible interactions must be considered.
CoQ10 may affect warfarin treatment. Curcumin, resveratrol, ginkgo and omega-3 may be relevant for bleeding risk. Piperine can affect enzymes that break down drugs. Adaptogens can affect blood pressure, blood sugar, sedation, metabolism or immunomodulating treatment.
Supporting Technology: Interesting, but for now
Uno Vita works with several technologies that are relevant to the lighting environment, recovery and well-being. In the case of ME/CFS, the technology must be subordinated to pacing and individual tolerance.
Red and near-infrared light – photobiomodulation
Photobiomodulation, PBM, uses red and near-infrared light.
Preclinical research and studies in other groups show the influence of, among other things, cytochrome c-oxidase, redox signals, microcirculation and inflammation-related signaling pathways. There is research into muscle fatigue and certain areas of pain, but good documentation specifically for ME/CFS is very limited.
When testing, one should start with a short time and a low dose, avoid unnecessary heat stress and watch for delayed worsening of symptoms.
More light is not automatically better. PBM often has a biphasic dose response, where both too low and too high a dose can produce less of the desired effect.
PEMF – pulsed electromagnetic fields
PEMF affects tissue with a time-varying magnetic field. The technology has been investigated for, among other things, pain, bone healing and certain musculoskeletal disorders.
Claims about the influence of mitochondria, calcium signals and inflammation are interesting, but direct evidence in ME/CFS is insufficient.
People with a pacemaker or other electronic implant must follow the manufacturer's contraindications and medical advice. The same applies to pregnancy, epilepsy and serious illness.
Molecular hydrogen – H₂
Hydrogen-rich water and hydrogen inhalation are studied in connection with redox and inflammation signals.
Clinical studies exist in various diseases and in healthy subjects, but the results are heterogeneous. Molecular hydrogen has not been documented as a treatment for ME/CFS.
Hydrogen is flammable. Inhalation requires equipment designed for safe gas production, concentration control and ventilation. Oxygen or hydrogen should never be handled with improvised equipment or near sources of ignition.
What the technology must not do
Technology must not become a new burden.
If rigging, transport, heat, light, sound or the treatment itself triggers PEM, the measure is incorrectly dosed, regardless of how interesting the mechanism is.
In severe or very severe ME/CFS, even seemingly mild measures may be too much.
The foundation that cannot be replaced
Pacing and activity management
Map which physical, mental, social and emotional activities trigger deterioration. Plan breaks before crossing the border.
Pacing should protect the available capacity and reduce the risk of repeated crashes.
Sleep and circadian rhythm
Investigate sleep apnea, restless legs and other sleep disorders if suspected. Daylight and routines must be adapted to light sensitivity and energy level.
Unrefreshing sleep in ME/CFS does not necessarily disappear even if the length of sleep improves, but specific sleep disturbances should still be treated.
Orthostatic intolerance
Dizziness, palpitations, weakness or worsening brain fog in an upright position should be evaluated medically.
Fluid, salt and compression are not right for everyone, especially not in the case of high blood pressure, kidney or heart disease.
Nutrition and fluids
The goal is tolerable and nutrient-dense food, enough protein and a stable supply of energy - not a rigid "perfect diet".
In the case of nausea, mast cell problems, intestinal complaints, swallowing difficulties or extensive food intolerances, a clinical nutritionist can be useful.
Pain and headache
Headaches should be classified. Migraines, drug overuse, tension headaches, sleep problems and neck pain need different measures.
New, sudden or unusually severe headaches must be evaluated medically.
Environment and sensory load
Light, sound, temperature, screen and social activity can cost energy. Fencing is a biological adaptation, not a sign of a lack of motivation.
[Image 7 – pacing: A person plans the day calmly with a journal, heart rate monitor, water, food and natural light to stay within their energy limit.]
Suggestions for a careful, individual way of working
Phase 1 – Map
Record activity, pulse if useful, sleep, food intake, medicines and symptoms. Look especially for deterioration 12–48 hours after strain.
Phase 2 – Stabilize
Reduce "push-crash", simplify everyday tasks and treat identified deficiencies or co-morbidities.
Phase 3 – Choose a goal
Choose sleep, pain, headache, orthostatic intolerance or a documented deficiency - not "all ME/CFS" at once.
Phase 4 – Test one support at a time
Use a low starting load and sufficient observation time. Consider both immediate response and any delayed PEM.
Phase 5 – Keep only what provides net benefit
A measure that provides short-term energy, but triggers a crash later, is not a real improvement.
Frequently asked questions
Does DecodeME show that ME/CFS is genetic?
The study shows a polygenic genetic component. This means that many common genetic variants slightly affect the risk. Genetics is not destiny, and the results explain only part of the biological vulnerability.
Can a genetic test tell which supplements I should use?
No. The DecodeME findings are group findings and have not been validated as a clinical genetic test or as a basis for personal choice of dietary supplements.
Is there now a blood test for ME/CFS?
No. The blood study found promising patterns at the group level, but no single marker reliably distinguished between people with ME/CFS and controls.
What are the best researched supplements?
CoQ10 combined with NADH and oxaloacetate has some direct clinical data, but the studies are still too few and small for one agent to be generally recommended. Documented deficiencies should be corrected first.
Is PQQ documented against ME/CFS?
No. PQQ is interesting because of mitochondrial signaling pathways, but good clinical ME/CFS studies are lacking.
Can PEA and luteolin help against neuroinflammation?
PEA and luteolin have mechanistic and indirect clinical support for pain and some neurological or post-viral conditions. Direct documentation of ME/CFS is insufficient.
Can red light, PEMF or hydrogen cure ME/CFS?
No. None of the technologies has been documented as a cure. They can possibly be tried as low-load support during safe use, with pacing and delayed response as important control points.
Why should you start low?
ME/CFS can cause unusual sensitivity to activity, stimuli, drugs and supplements. Low starting load makes it easier to detect both benefit and deterioration.
Can an energizing product make you tolerate more activity?
Not necessarily. A substance can increase the experience of energy without increasing the body's real stress tolerance. If the person uses the energy lift to do more and gets PEM later, the measure has not provided a real net benefit.
Conclusion
DecodeME and the new blood study move ME/CFS research in a clear biological direction.
Genetic signals link risk to immune response, nervous system and pain regulation, while blood-based patterns point to inflammation and metabolic dysregulation.
The findings are important, but they are not a complete diagnostic model and do not provide a basis for matching one gene with one dietary supplement.
The most responsible strategy remains to protect against PEM, investigate other causes and comorbidities, correct documented deficiencies, and carefully test support.
CoQ10 combined with NADH and oxaloacetate has some direct clinical documentation. PEA, luteolin, PQQ, polyphenols, omega-3 and mitochondrial cofactors are interesting at different levels of evidence, but must be mentioned precisely.
PBM, PEMF and molecular hydrogen should be understood as research and wellness technology – not as documented treatment of ME/CFS.
The aim is not to push the body to perform more. The aim is to reduce unnecessary strain and create the best possible conditions for stability, regulation and quality of life.
Important information and reservations
The article is intended as general professional information and does not replace medical assessment, diagnosis or treatment.
ME/CFS can overlap with other serious conditions. Seek medical attention in case of new or rapidly increasing fatigue, unexplained weight loss, persistent fever, chest pain, difficulty breathing, fainting, new neurological symptoms, blood in stool or urine, or other alarm symptoms.
Dietary supplements can cause side effects and interactions. Pregnant and breastfeeding women, children, people with kidney or liver disease and people using medicines should consult a qualified healthcare professional.
Uno Vita AS does not claim that dietary supplements or wellness technology can prevent, treat or cure ME/CFS.
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