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Diseases similar to CFS/ME


Senior Member
I thought it would be useful to have a thread with diseases that are similar in their symptoms to ME/CFS (Canadian Criteria including fatigue, cognitive problems, lymph nodes) . This might be useful for those that have been wrongly diagnosed with CFS/ME as well as for treatment similarities.
Symptoms L = lymph noses, A = arthritis like, F = fatigue, G = gastro, C = cognitive, D = adrenal, N = neuro, I = allergies/ histamine probably not complete/ accurate now

I came up with the following:

Autoimmune Disorders
MS (N, A, F, G, C)
Ulcerative colitis (G)
Reiters syndrome (A)
Hughes syndrome (often next to me/cfs) (C, L,N,D)
Psoriatic arthritis (A)
Systemic lupus erythematosus (N, A, F, G, C)
Allergies (I,F,D,C)
Ankylosing Spondylitis
hashimoto's and Hashimoto's Encephalopathy (the latter is VERY similar to CFS, but treatable)
Wegener's granulomatosis
Inflammatory bowel disease
Behcet's syndrome
Sjogren syndrome
Autoimmune collagen-vascular diseases
Chronic inflammatory diseases
Crohn's disease
Connective tissue disease (e.g. Dermatomyositis or Polymyositis)
Adult-onset cystic fibrosis
Occult malignancy
Polymyalgia rheumatica
Giant cell arteritis

Nutritional deficiencies
inability to converge thiamine
b12 deficiency

Lyme disease
Fungal disease
Viral infections
parasitic infection in the nervous system (e.g. gnasthostomiasis)
Parasite infection
* Hookworm infection
* Amebiasis
* Giardiasis
* Helminthic infestation
Persistent infectious mononucleosis
Chronic brucellosis
Subacute bacterial endocarditis
mycoplasma infection

Organ disease
Chronic heart failure (type of Heart failure)
Chronic obstructive pulmonary disease
Chronic renal failure
Chronic pulmonary disease
Chronic kidney disease
Chronic liver disease
Chronic heart disease (see Heart symptoms)

endocrinology disorder
Adrenal insufficiency
Endocrine disease
Addison disease
Cushing syndrome
Diabetes mellitus

Heavy metal toxicity (e.g. lead)
Vibroacoustic Disease
Environmental toxins (agent orange, etc)
radiation poisoning

neuro disease
Neuromuscular disease (e.g. Myasthenia gravis)

Please add your suggestions and I will update the list


Senior Member
I know someone diagnosed with CFS that actually had Ankylosing Spondylitis. Probably not typical but it did happen.


Senior Member
Thank you guys I have updated, and also included Hashimoto's Encephalopathy and Psoriatic arthritis

can someone make this a sticky; i think it is quite important that we optimize this list, it can maybe get some people CURED. You dont want to hang out in the dark cave that is ME/CFS if not necessary..

it would be great if we could find some distinguishing symptoms/ tests for each disease. some kind of chart would be ideal.
also if we would mention the cfs-like symptoms for each disease; e.g. pain, fatigue, cognitive problems, lymph nodes, neuropathy, allergy symptoms, stomach problems, adrenal stuff etc
I dont have time for this now tho.


Senior Member
This is very good, useful list, Leaves. Thanks for compiling it.


Senior Member
Hi Leaves, great work!!!! Moderators please sticky this!!!!

Heres some more for the list unfortunately there are a vast number of illnesses that can cause these kinds of symptoms.

Wilsons disease
Post Polio syndrome
Hep c
Acute intermittent Porphyria
Porphyria cutanea tarda
ALAD Porphyria
Variegate Porphyria
Heriditary coproporphyria
Vitamin D deficiency
Athletes over training syndrome
Copper overload from hormone replacement therapy
Brain tumours, including astrocytomas, gliomas
Transverse Myelitis
Sleep apnoea
Mitochondrial myopathies
Autoimmune collagen-vascular diseases
Chronic Carbon monoxide poisoning
Vibroacoustic Disease (VAD)
Chronic obstructive pulmonary disease
Acute Disseminated Encephalomyelitis (ADEM)
Chiari Malformation
Devic's disease, Devic's syndrome or neuromyelitis optica (NMO)
Mitochondrial myopathies
Subacute bacterial endocarditis
Ulcerative colitis
Helminthic infestation
Chronic antidepressant use
Crohn's disease
Connective tissue disease
Inflammatory bowel disease
Adult-onset cystic fibrosis
Kawasaki disease
Post-infectious polymyositis

Some of these come from these sources



All the best

free at last

Senior Member
This is useful in one sense but highly confusing in another, but thats by virtue of how many different conditions can overlap with similar symptoms, I myself have found two particulaly interesting out of the list Recently. one has to be careful to blame the ME diagnosis on something else. when its possible the ME can lead to the other conditions, as secondary illnesses,

but its difficult in the uk to get tested, for conditions that may be related. i could suggest to a GP in the uk, two of these conditions that mat apply to me ive been thinking a lot about, but would likely get told its probably. not worth pursuing once the word CFS is seen in the medical records. very difficult and frustrating. The second list is even more confusing. like a needle in a haystack. Helpful agreed. But very bewildering.

free at last

Senior Member
Exactly heapsreal. its a waste basket diagnosis, to get the medical proffession off the hook to explain a myriad of similar looking symptoms in patients, that they can find no cause for.

what if different viral infections can lead to these similar symptoms in patients, do we all have the same illness ?

Or different illnesses that can lead to similar places.

Is there really ME/CFS or a condition that can come about in many different ways that unites many people in symptoms

is xmrv ME ? Is it Herpes virus ( or both ) is it auto immune disease ? is it different retroviruses MLVs, Is it a brain dysfunction caused by different viral or immune insults, on and on. Ive always belived we are not all suffereing the same illness. clearly even onset can differ markedly on this forum. I know the canadian criteria says you do, or do not have ME. If certain symptoms are ticked or are not, But that still doesnt explain the differences, even if many many things are shared in us. So confusing and always has been


iherb 10% discount code OPA989,
australia (brisbane)
i think our symptoms vary due to what co-infections we have and possibly auto-immune problems which then disrupts our biochemistry in many different ways, but i think they stem from immune supression(my money is on NK dysfunction) possibly caused by the one 'thing' MLVs maybe. This is how i think we get many different symptoms and also the length of time and severity plays a big part, the longer we have immune suppression the more chance we have of getting co-infections.



Senior Member
Northern Ca. USA
Great lists. Don't want to miss a treatable diagnosis. I would just add putting an asterisk in front of those diseases having PEM/PENE as a primary symptom, would narrow the differential list significantly for me/cfs.


Senior Member
Great lists. Don't want to miss a treatable diagnosis. I would just add putting an asterisk in front of those diseases having PEM/PENE as a primary symptom, would narrow the differential list significantly for me/cfs.

Hi, Tristen.

I agree. Look for PEM/PENE and then run the methylation pathways panel. If PEM/PENE is present, and there is a partial block in the methylation cycle, I would say that ME/CFS is very likely the diagnosis.

Best regards,



Senior Member
Hi, Tristen.

I agree. Look for PEM/PENE and then run the methylation pathways panel. If PEM/PENE is present, and there is a partial block in the methylation cycle, I would say that ME/CFS is very likely the diagnosis.

Best regards,


Hi Rich,

What is the best test to take to show a partial block in the methylation cycle?



Senior Member
Hi Free at Last, sorry to be bewildering, its just one of those facts of medicine, theres something like 14,000 different medical conditions, and only a limited number of symptoms that humans can have, so every disease always has symptoms that overlap with a lot of other diseases, unfortunately, there are a lot of diseases that have similar symptoms to ME.

You are completely right, people need to be acutely aware of the possibility of developing other diseases as well as ME, and if they start developing new symptoms get to a doctor straight away.

I really feel sorry for all you people in the UK, with the way that you are being denied access to testing, where I live New Zealand the problem is more incompetent doctors who havent got a clue what theyre doing, and a very underfunded health system. It may take a while, but you can still find doctors who are happy to run tests, theyre not ordered not to by the government like they are in the UK.

Im not 100% up to date on all the things that have been tried in the way of advocacy in the Uk, But has anyone made any use of this? http://www.rcpe.ac.uk/journal/issue/journal_40_4/newton.pdf Its a report by a group of NHS doctors showing that 40% of people who had been diagnosed as having CFS were found to have been misdiagnosed and had other serious diseases and sometimes fatal ones like cancer, I would have thought that if this report was sent to every media outlet in the UK, there would be a reasonable chance that it would get published and it could turn into quite a scandal!!! This would then put pressure on the government to act, and make doctors aware of what was going on; it would also help expose Wessely for the idiot he is forcing misdiagnosed patients to have CBT. Have a read of it and see what you think.

This next idea may seem like an extreme solution, but as I see it the people in the UK are in an extreme situation. If people ever find themselves in a situation where they have a lot of certainty that they have been misdiagnosed and that they know what the disease they have been misdiagnosed with is. Tell the doctor in no uncertain terms that if you die from the disease that they wont test you for, that your family know about it, and will sue their arse off if you die!!
Heres the story of one UK patient saving her life by doing this.


All the best!!


Senior Member
Hi Rich,

What is the best test to take to show a partial block in the methylation cycle?


Hi, NeilK.

The Methylation Pathways Panel. It costs $295 in the U.S., including the blood samples shipping to the lab. It requires an order from a physician or a chiropractor. It's available from the Health Diagnostics and Research Institute in New Jersey (contact info pasted below, as well as a guide to interpretation). As I recall, you live in New York, and the lab does not have New York state certification. Some others from New York have ordered the panel through physicians in New Jersey or Connecticut. The panel is also available from the European Laboratory of Nutrients in the Netherlands. I understand that the cost is higher there in U.S. dollar equivalent.

Best regards,


Methylation Pathways Panel

This panel will indicate whether a person has a partial methylation cycle block and/or glutathione depletion. I recommend that this panel be run before deciding whether to consider treatment for lifting the methylation cycle block. I am not associated with the lab that offers this panel.

The panel requires an order from a physician or a chiropractor. The best way to order the panel is by fax, on a clinicians letterhead.

Available from:

Health Diagnostics and Research Institute
540 Bordentown Avenue, Suite 2300
South Amboy, NJ 08879
Phone: (732) 721-1234
Fax: (732) 525-3288

Lab Director: Elizabeth Valentine, M.D.

Dr. Tapan Audhya, Ph.D., is willing to help clinicians with interpretation of the panel by phone, or you can use the guide below.

May 19, 2011

Interpretation of Results of the Methylation Pathways Panel

Richard A. Van Konynenburg, Ph.D.
Independent Researcher

Disclaimer: The Methylation Pathways Panel is offered by the European Laboratory of Nutrients in the Netherlands and the Health Diagnostics and Research Institute in New Jersey, USA. I am not affiliated with these laboratories, but have been a user of this panel, and have written these suggestions at the request of Tapan Audhya, Ph.D., Director of Research for the Health Diagnostics lab, for the benefit of physicians who may not be familiar with this panel. My suggestions for the interpretation of results of the panel are based on my study of the biochemistry involved, on my own experience with interpreting panel results as part of the analysis of a fairly large number of cases of myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) over the past four years, and on discussion of some of the issues with Dr. Audhya. I am a researcher, not a licensed physician. Treatment decisions based on the results of applying this panel and its interpretation to individual cases are the responsibility of the treating physician.

Application: In addition to being useful in analyzing cases of ME/CFS, this panel can also be usefully applied to cases of autism and other disorders that involve abnormalities in glutathione, methylation and the folate metabolism.

The panel includes measurement of two forms of glutathione (reduced and oxidized), S-adenosylmethionine (SAMe), S-adenosylhomocysteine (SAH), adenosine, and seven folate derivatives.

According to Dr. Audhya (personal communication), the reference ranges shown on the lab reports for each of these metabolites were derived from measurements on at least 120 healthy male and female volunteer medical students from ages 20 to 40, non-smoking, and with no known chronic diseases. The reference ranges extend to plus and minus two standard deviations from the mean of these measurements.

Glutathione (reduced): This is a measurement of the concentration of the
chemically reduced (active) form of glutathione (abbreviated GSH) in the blood
plasma. The reference range is 3.8 to 5.5 micromoles per liter.

Glutathione plays many important roles in the biochemistry of the body, including serving as the basis of the antioxidant enzyme system, participating in the detoxication system, and supporting the cell-mediated immune response, all of which exhibit deficits in CFS. The level of GSH in the plasma is likely to be more reflective of tissue intracellular glutathione status than the more commonly and more easily measured red blood cell or (essentially equivalent) whole blood glutathione level, which is about three orders of magnitude greater, because red blood cells are normally net producers of glutathione. Also, knowledge of the level of the reduced form, as distinguished from total (reduced plus oxidized) glutathione, which is more commonly measured, is more diagnostic of the status of glutathione function.

In order to be able to approximate the in vivo level of reduced glutathione when blood samples must be shipped to a lab, it is necessary to include special enzyme inhibitors in the sample vials, and these are included in the test kit supplied by these two laboratories.

Most people with chronic fatigue syndrome (PWCs), but not all, are found to have values of GSH that are below the reference range*. This means that they are suffering from glutathione depletion. As they undergo treatment to lift the partial methylation cycle block, this value usually rises into the normal range over a period of a few months. I believe that this is very important, because
glutathione normally participates in the intracellular metabolism of vitamin B12, and if it is low, a functional deficiency of vitamin B12 results, and insufficient methylcobalamin is produced to support methionine synthase in the methylation cycle. In my view, this is the mechanism that causes the onset of ME/CFS. This functional deficiency is not detected in a conventional serum B12 test, but will produce elevated methylmalonate in a urine organic acids test. In my opinion, many of the abnormalities and symptoms in ME/CFS can be traced directly to glutathione depletion.

Anecdotal evidence suggests that PWCs who do not have glutathione depletion do have abnormalities in the function of one or more of the enzymes that make use of glutathione, i.e. the glutathione peroxidases and/or glutathione transferases. This may be due to genetic polymorphisms or DNA adducts on the genes that code for these enzymes, or in the case of some of the glutathione peroxidases, to a low selenium status.

Glutathione (oxidized): This is a measurement of the concentration
of the oxidized form of glutathione (abbreviated GSSG) in the blood
plasma. The reference range is 0.16 to 0.50 micromoles per liter.

Normally, oxidized glutathione in the cells is recycled back to reduced glutathione by glutathione reductase, an enzyme that requires vitamin B2 and NADPH. If this reaction is overwhelmed by oxidative stress, the cells export excess GSSG to the plasma. In some (but not all) PWCs, GSSG is elevated above the normal
range, and this represents oxidative stress. It is more common in CFS to see this level in the high-normal range. This value may increase slightly under initial treatment of a partial methylation cycle block.*

Ratio of Glutatione (reduced) to Glutathione (oxidized): This is not shown explicitly on the panel results, but can be calculated from them. It is a measure of the redox potential in the plasma, and reflects the state of the antioxidant system in the cells. The normal mean value is 14. PWCs often have a value slightly more than half this amount, indicating a state of glutathione depletion and oxidative stress. This ratio has been found to increase during treatment of a partial methylation cycle block.*

S-adenosymethionine (RBC): This is a measure of the concentration of S-adenosylmethionine (SAMe) in the red blood cells. The reference range is 221 to 256 micromoles per deciliter.

SAMe is produced in the methylation cycle and is the main supplier of methyl (CH3) groups for a large number of methylation reactions in the body, including the methylation of DNA and the biosynthesis of creatine, carnitine, coenzyme Q10, melatonin and epinephrine. This measurement is made in the red blood cells because the level there reflects an average over a longer time and is less vulnerable to fluctuations than is the plasma level of SAMe.

Most PWCs have values below the reference range, and treatment raises the value.* A low value for SAMe represents a low methylation capacity, and
in CFS, it usually appears to result from an inhibition or partial block of the enzyme methionine synthase in the methylation cycle. Many of the abnormalities in CFS can be tied to lack of sufficient methylation capacity.

S-adenosylhomocysteine (RBC): This is a measure of the
concentration of S-adenosylhomocysteine (SAH) in the red blood cells. The reference range is 38.0 to 49.0 micromoles per deciliter.

SAH is the product of the many methyltransferase reactions that utilize SAMe as a source of methyl groups. In CFS, its value ranges from below the reference range to above the reference range. Values appear to be converging toward the reference range with treatment.

Sum of SAM and SAH: When the sum of SAM and SAH is below about 268
micromoles per deciliter, it appears to suggest the presence of
upregulating polymorphisms in the cystathionine beta synthase (CBS)
enzyme, though this may not be true in every case. For those considering following the Yasko treatment program, this may be useful information.

Ratio of SAM to SAH: A ratio less than about 4.5 represents low
methylation capacity. Both the concentration of SAM and the ratio of
concentrations of SAM to SAH are important in determining the
methylation capacity, because they affect the rates of the methyltransferase reactions.

Adenosine: This is a measure of the concentration of adenosine in the
blood plasma. The reference range is 16.8 to 21.4 x 10(-8) molar.

Adenosine is a product of the reaction that converts SAH to homocysteine. It is also exported to the plasma when mitochondria develop a low energy charge, so that ATP drops down to ADP, AMP, and eventually, adenosine. Adenosine in the plasma is normally broken down to inosine by the enzyme adenosine deaminase.

In some PWCs adenosine is found to be high, in some it is low, and in some it is in the reference range. I don't yet understand what controls the adenosine level in these patients, and I suspect that there is more than one factor involved. In most PWCs who started with abnormal values, the adenosine level appears to be moving into the reference range with methylation cycle treatment, but more data are needed.

5-CH3-THF: This is a measure of the concentration of 5L-methyl
tetrahydrofolate in the blood plasma. The reference range is 8.4 to 72.6 nanomoles per liter.

This form of folate is present in natural foods, and is normally the most abundant form of folate in the blood plasma. It is the form that serves as a reactant for the enzyme methionine synthase, and is thus the important form for the methylation cycle. It is also the only form of folate that normally can enter the brain. Its only known reactions are the methionine synthase reaction and reaction with the oxidant peroxynitrite.

When there is a partial block in methionine synthase, 5L-CH3-THF drains from the cells into the blood plasma by the so-called methyl trap mechanism. As other forms of folate are converted to 5L-CH3-THF, this mechanism depletes the cells of folates in general.

Many PWCs have a low value of 5L-CH3-THF, consistent with a partial block in the methylation cycle. Most methylation treatment protocols include supplementation with 5L-CH3-THF, which is sold over-the-counter as Metafolin, FolaPro, or MethylMate B (trademarks), and in the prescription medical foods supplied by PamLab, including Deplin, CerefolinNAC and Metanx. There are some others on the market that include both racemic forms (5L and 5R) of this folate.

When methylation treatment is used, the level of 5-CH3-THF rises in nearly every PWC. If the concentration of 5-CH3-THF is within the reference range, but either SAM or the ratio of SAM to SAH is below the reference values, it suggests that there is a partial methylation cycle block and that it is caused by inavailability of sufficient bioactive B12, rather than inavailability of sufficient folate. A urine organic acids panel will show elevated methylmalonate if there is a functional deficiency of B12. I have seen this combination frequently, and I think it demonstrates that the functional deficiency of B12 is the immediate root cause of most cases of partial methylation cycle block. Usually glutathione is low in these cases, which is consistent with such a functional deficiency. As the activity of the methylation cycle becomes more normal, the demand for 5-CH3-THF will likely increase, so including it in the treatment protocol, even if not initially low, will likely be beneficial.

10-Formyl-THF: This is a measure of the concentration of 10-formyl
tetrahydrofolate in the blood plasma. The reference range is 1.5 to 8.2 nanomoles per liter.

This form of folate is involved in reactions to form purines, which form part of RNA and DNA as well as ATP. It is usually on the low side in PWCs, likely as a result of the methyl trap mechanism mentioned above. This deficiency is likely the reason for some elevation of mean corpuscular volume (MCV) and mean corpuscular hemoglobin (MCH) often seen in PWCs. This deficit may also impact replacement of cells lining the gut, as well as white blood cells.

5-Formyl-THF: This is a measure of the concentration of 5-formyl
tetrahydrofolate (also called folinic acid) in the blood plasma. The reference range is 1.2 to 11.7 nanomoles per liter.

This form is not used directly as a substrate in one-carbon transfer reactions, but it can be converted into other forms of folate, and may serve as a buffer form of folate. Most but not all PWCs have a value on the low side. It is one of the
supplements in some methylation protocols. It can be converted to 5L-CH3-THF in the body by a series of three reactions, one of which requires NADPH, and it may also help to supply other forms of folate until the methionine synthase reaction comes up to more normal activity.

THF: This is a measure of the concentration of tetrahydrofolate in
the blood plasma. The reference range is 0.6 to 6.8 nanomoles per liter.

This is the fundamental chemically reduced form of folate from which several other reduced folate forms are synthesized, and thus serves as the hub of the folate metabolism. THF is also a product of the methionine synthase reaction, and participates in the reaction that converts formiminoglutamate (figlu) into glutamate in the metabolism of histidine. If figlu is found to be elevated in a urine organic acids panel, it usually indicates that THF is low. In PWCs it is lower than the mean normal value of 3.7 nanomoles per liter in most but not all PWCs.

Folic acid: This is a measure of the concentration of folic acid in
the blood plasma. The reference range is 8.9 to 24.6 nanomoles per liter.

Folic acid is a synthetic form of folate, not found in nature. It is added to food grains in the U.S. and some other countries in order to lower the incidence of neural tube birth defects, including spina bifida. It is the oxidized form of folate, and therefore has a long shelf life and is the most common commercial folate supplement. It is normally converted into THF by two sequential reactions catalyzed by dihydrofolate reductase (DHFR), using NADPH as the reductant. However, some people are not able to carry out this reaction well for genetic reasons, and PWCs may be depleted in NADPH, so folic acid is not the best supplemental form of folate for these people.

Low values suggest folic acid deficiency in the current diet. High values, especially in the presence of low values for THF, may be associated with inability to convert folic acid into reduced folate readily, such as because of a genetic polymorphism in the DHFR enzyme. They may also be due to high supplementation of folic acid.

Folinic acid (WB): This is a measure of the concentration of folinic acid in the whole blood. The reference range is 9.0 to 35.5 nanomoles per liter.

See comments on 5-formyl-THF above. Whole blood folinic acid usually tracks with the plasma 5-formyl-THF concentration.

Folic acid (RBC): This is a measure of the concentration of folic acid in the red blood cells. The reference range is 400 to 1500 nanomoles per liter.

The red blood cells import folic acid when they are initially being formed, but during most of their lifetime, they do not normally import, export, or use it. They simply serve as reservoirs for it, giving it up when they are broken down.

Many PWCs have low values of this parameter. This can be caused by a low folic acid status in the diet over the previous few months, since the population of RBCs at any time has ages ranging from zero to about four months. However, in CFS it can also be caused by oxidative damage to the cell membranes, which allows folic acid to leak out of the cells. Dr. Audhya reports that treatment with omega-3 fatty acids has been found to raise this value over time in one cohort.

If anyone finds errors in the above suggestions, I would appreciate being notified at richvank@aol.com.

* Nathan, N., and Van Konynenburg, R.A., Treatment Study of Methylation Cycle Support in Patients with Chronic Fatigue Syndrome and Fibromyalgia, poster paper, 9th International IACFS/ME Conference, Reno, Nevada, March 12-15, 2009. (http://www.mecfs-vic.org.au/sites/w...Article-2009VanKonynenburg-TrtMethylStudy.pdf)


Senior Member
Thank you Rich as always.
I called the lab and they directed me to a Dr. in NJ.
I will get in touch with them.



Senior Member
I keep on wondering, if you have been diagnosed with an illness that causes the same symptoms as ME/CFS could you still have ME/CFS? I assume you can have both, but maybe not likely. I have been diagnosed with POTS by my ME/CFS specialist and that causes the same symptoms.
I keep on wondering, if you have been diagnosed with an illness that causes the same symptoms as ME/CFS could you still have ME/CFS? I assume you can have both, but maybe not likely. I have been diagnosed with POTS by my ME/CFS specialist and that causes the same symptoms.

Lots of people have POTS without ME, ME without POTS, or both together.

Some illnesses aren't like that, and the other diagnosis would replace ME.


Senior Member
That makes it very complicated! My specialist didn't say anything about it, I will ask him. I am being tested for other illnesses ATM and if they come out positive they explain a lot too. Anyway, I think from POTS alone people can be very ill. I have fibromyalgia as well, but some say that's connected to CFS. However, the fibro could be caused by other things as well.