Page Synopsis: Xyrem, for instance appears promising. This page is a 'kitchen sink' where I put all the CFS players in the game on the page, unranked. The therapies I recommend have their own pages. This exhaustive list is for therapies to try if the other (paged) therapies fail. Also it may educate you to find medicine more specific to your condition. All that to say, this page is extremely long and perhaps not required reading

Skill Level  5

Relevance:4 Technical Level:3

With all the medicines to try, surely something must help as other patients have been helped


page 32

page 34


Intravenous Cyclophosphamide in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome. An Open-Label Phase II Study


Results: The overall response rate by Fatigue score was 55.0% (22 of 40 patients). Fatigue score and other outcome variables showed significant improvements compared to baseline. The SF-36 Physical Function score increased from mean 33.0 at baseline to 51.5 at 18 months (all patients), and from mean 35.0 to 69.5 among responders. Mean steps per 24 h increased from mean 3,199 at baseline to 4,347 at 18 months (all patients), and from 3,622 to 5,589 among responders. At extended follow-up to 4 years 68% (15 of 22 responders) were still in remission. Patients positive for HLA-DQB1*03:03 and/or HLA-C*07:04 (n = 12) had significantly higher response rate compared to patients negative for these alleles (n = 28), 83 vs. 43%, respectively. Nausea and constipation were common grade 1–2 adverse events. There were one suspected unexpected serious adverse reaction (aggravated POTS) and 11 serious adverse events in eight patients.


Conclusion: Intravenous cyclophosphamide treatment was feasible for ME/CFS patients and associated with an acceptable toxicity profile. More than half of the patients responded and with prolonged follow-up, a considerable proportion of patients reported ongoing remission. Without a placebo group, clinical response data must be interpreted with caution. We nevertheless believe a future randomized trial is warranted

Preclinical evaluation of the abuse potential of Pitolisant, a histamine H3 receptor inverse agonist/antagonist compared with Modafinil


Histamine H3 autoreceptors control histamine synthesis and release from tuberomamillary neurons, a brain system involved in the control of wakefulness, attention, learning and other cognitive functions (Schwartz et al., 1991; Haas and Panula, 2003; Lin et al., 2011). Therefore the use of H3 receptor inverse agonists, a class of compounds reversing the high constitutive activity of the native receptors (Morisset et al., 2000), appears as a useful therapeutic approach to enhance wakefulness in states of excessive daytime sleepiness such as narcolepsy, obstructive sleep apnoea or Parkinson's disease (Lazewska and Kiec-Kononowicz, 2010; Kuhne et al., 2011; Leurs et al., 2011).


The first compound of this class to be introduced in the clinics, PitolisantINN (formerly named tiprolisant, BF2.649, [1-{3-[3-(4-chlorophenyl)propoxy]propyl}piperidine, hydrochloride]), a potent and highly selective non-imidazole histamine H3-receptor inverse agonist (Ligneau et al., 2007b), constitutes a promising tool for the treatment of narcolepsy as shown in an animal model of this pathology, the orexin−/− mouse as well as in clinical trials (Lin et al., 2008, Schwartz, 2011). Dopamine-releasing agents currently used to fight against daytime somnolence in narcolepsy comprise amphetamine derivatives, sodium oxybate and Modafinil which both suffer, to a variable degree, from abuse liability



Colloidal silver

Drink a quart of colloidal silver a day for 30 days and you can get rid of most anything that is a virus. 10 days is enough for almost everything, but when a threat is very serious 30 days will make sure


Very Severely Ill "ME/CFS" Patient Gets a New Diagnosis, New Treatment Approach & Major Improvement | Health Rising's Chronic Fatigue Syndrome (ME/CFS) and Fibromyalgia Forums



Therapeutic Treatment of Long Covid as applied to chronic fatigue syndrome

1) BC 007

2) Tollovid

3) Extracorporeal Apheresis

4) Ivermectin

5) ct38

7) Transcranial Direct Current

8) Long COVID: Latest on Research and Treatments

9) and


1) BC 007

1a) Further patients benefit from drug against Long COVID › Friedrich-Alexander-Universität Erlangen-Nürnberg


1b) Berlin Cures...? Could BC 007 Help With Long COVID and ME/CFS?


1c) BC 007 Long Covid 2022


1d) bc 007 chronic fatigue syndrome


1e) BC 007 - AdisInsight


1f) Seite nicht vorhanden - Universitätsklinikum Erlangen


1g) BC 007: New drug combats fatigue | In Good Shape - The Health Show | DW | 06.03.2022


1h) BC007_miracle_in_need_of_explanation_141221.pdf


2) Tollovid

2a) Tollovid chronic fatigue syndrome


2b) Case Study #2: PASC (Long COVID) and its resolution with Tollovid®


2c) Tollovid ™ Maximum Protection Natural Dietary Supplement for Immune Support : Health & Household


2d) Fenben LAB Fenbendazol 444mg, Purity >99%, by Fenben Lab, Certified Third-Party Laboratory Tested, Analysis Report Included, 90 Caps: Industrial & Scientific


2e) Todos Medical Releases Preliminary Data From IRB-Waived Tollovid® Market Research Study in Acute and Long COVID :: Todos Medical Ltd. (TOMDF)


2f) Tollovid™ + Long COVID: Exploring Viral Persistence


2g) Todos Medical Reports 2nd Long COVID Case Study and


3) Extracorporeal Apheresis

3a) Chronic post-COVID-19 syndrome and chronic fatigue syndrome: Is there a role for extracorporeal apheresis?


3b) extracorporally filtered and cleaned with the use of Heparin, which is then removed again before the blood is being fed back into the body. The Heparin binds to various inflammation inducing components in the blood plasma


3c) Apheresis


4) Ivermectin

4a) FLCCC Alliance (Front Line COVID-19 Critical Care Alliance, Long Covid therapy protocol including Ivermectin


I-RECOVER Long COVID Treatment

Long Haul COVID Syndrome (LHCS)—commonly known as long COVID—is characterized by prolonged malaise, headaches, generalized fatigue, sleep difficulties, hair loss, smell disorder, decreased appetite, painful joints, dyspnea, chest pain and cognitive dysfunction.


Up to 80% of patients experience prolonged illness after COVID-19. Long COVID is not only seen after COVID infection but is also being observed in some people who have received vaccines (likely due to monocyte/microglia activation by the spike protein from the vaccine). Long COVID may persist for months after the acute infection and almost half of patients report reduced quality of life.


Patients may suffer prolonged neuropsychological symptoms, including multiple domains of cognition. A puzzling feature of long COVID is that it is not predicted by initial disease severity; it frequently affects mild-to-moderate cases and younger adults who did not require respiratory support or intensive care.


The symptom set of long COVID is, in the majority of cases, very similar to chronic inflammatory response syndrome (CIRS)/myalgic encephalomyelitis/chronic fatigue syndrome. An important differentiating factor from CIRS is the observation that long COVID continues to improve on its own, albeit slowly in the majority of cases.


Another important observation is that long COVID includes more young people compared to severe COVID, which affects older people or persons with co-morbidities.


Long COVID is highly heterogeneous and likely results from a variety of pathogenetic mechanisms. Furthermore, it is likely that delayed treatment (with ivermectin, etc.) in the early symptomatic phase results in a high viral load (high spike protein load), which increases the risk and severity of long COVID.


The approach outlined in the I-RECOVER: Long COVID Treatment Protocol is a consensus based on a collaboration led by Dr. Mobeen Syed (“Dr. Been”), Dr. Tina Peers, and the FLCCC Alliance. The approach should be individualized according to the patient’s clinical signs and symptoms.


As with all FLCCC protocols, aspects may change as scientific data and clinical experience in this condition evolve. Thus it is important to check back frequently to receive notification of any protocol changes




5) ct38

5a) Clinical trial provides preliminary evidence of a cure for myalgic encephalomyelitis / chronic fatigue syndrome (ME/CFS) and Long Covid


5b) AXA1125 ct38 New “Long Covid” Treatment Looks to Improve Patient Feeling and Function


7) Successful Treatment of Post-COVID Symptoms With Transcranial Direct Current Stimulation


8a) Long COVID: Latest on Research and Treatments


8b) Long Covid patients, in search of relief, turn to private company


8c) A systematic review of nutraceutical interventions for mitochondrial dysfunctions in myalgic encephalomyelitis/chronic fatigue syndrome - PMC


8d) Successful treatment of prolonged COVID-19 with Bamlanivimab in a patient with severe B-Cell aplasia due to treatment with an anti-CD20 monoclonal antibody: A case report - PubMed


8e) Long COVID treatment protocol - Google Search


8f) Treatment for COVID | Johns Hopkins Medicine


8g) Treating patients with long COVID


8h) 11 things doctors have learned about long COVID


8i) Can Long COVID Be Treated? - The Atlantic


8j) Successful treatment of prolonged COVID-19 with Bamlanivimab in a patient with severe B-Cell aplasia due to treatment with an anti-CD20 monoclonal antibody: A case report - ScienceDirect


8k) One U.K. trial is transforming COVID-19 treatment. Why haven't others delivered more results? | Science | AAAS


8l) Frontiers | Case Report: Neutralization of Autoantibodies Targeting G-Protein-Coupled Receptors Improves Capillary Impairment and Fatigue Symptoms After COVID-19 Infection


9) and



9b) Health Rising's Chronic Fatigue Syndrome (ME/CFS) and Fibromyalgia Forums


9c) Chronic Fatigue Syndrome (ME/CFS) Research | Health Rising's Chronic Fatigue Syndrome (ME/CFS) and Fibromyalgia Forums


9d) Treatment | Health Rising's Chronic Fatigue Syndrome (ME/CFS) and Fibromyalgia Forums


9e) Health Rising's Chronic Fatigue Syndrome (ME/CFS) and Fibromyalgia Forums


9f) Recovery Stories | Health Rising's Chronic Fatigue Syndrome (ME/CFS) and Fibromyalgia Forums


9g) Health News | Health Rising's Chronic Fatigue Syndrome (ME/CFS) and Fibromyalgia Forums


9h) General Discussion | Health Rising's Chronic Fatigue Syndrome (ME/CFS) and Fibromyalgia Forums







Endotherapia GEMSP

Endotherapia (GEMSP) as a customized treatment for ME/CFS


mentioned alongside Rituximab in this paper from Molecular Neurobiology as a potential treatment for ME/CFS. Early trials have shown good results in MS (1), ALS (2), and RA (3) without toxicity. Followup showed continued benefit in MS patients (4)


Endotherapia is a subligual tablet with a blend of fatty acids, antioxidants, aminco acids, and radical scavengers customized to one's immunological blood work, brain imaging, and symptoms. It's delivered via poly-L-lysine (which allows for better cell permeability). The end result is a reduction in oxidative stress and inflammation, and an improvement in neuroprotection.


I can see this treatment fitting in well with the "refill the tank" step of Dr Naviaux's proposed 3 step protocol.


Endotherapia was developed by professor Michel Geffardat at the IDRPHT in France.


Here is a breakdown of the ingredients used in Endotherapia by disease. The first article suggests using the MS preparation (GEMSP) for ME/CFS. I imagine it would be further customized based on the individual.

xclick here to close and return to reportclick for full size, click 'x' button to closeingredients used in Endotherapia



More on Endotherapia


From "The Emerging Role of Autoimmunity in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/cfs)"

Endotherapia is an immunopathological strategy addressing pathology which seems to underpin chronic incurable diseases whose etiology is multifactorial.


It involves the combination of an evaluation of circulating immunoglobulins directed against specific neo-epitopes that created ROS elevation.


GEMSP is a preparation of numerous small molecules, including fatty acids, anchorage molecules, antioxidants, radical scavengers, amino acids, ligated to linear chain of poly-L-lysine (PLL) which are non-immunogenic and inhibit inflammation and O&NS processes. Each individual linkage affords significant advantages.Importantly, it prevents metabolic degradation of the linked molecules and enables a long half-life and confers stability on the various linked chemical entities. Membrane permeability is increased and the induction of various viral and bacterial components. These features combine to induce neuroprotection.


Full article

And "Endotherapia: A New Frontier in the Treatment of Multiple Sclerosis and Other Chronic Diseases"

Endotherapia is a new biomedical and therapeutic approach for the treatment of chronic diseases, including autoimmune, neurodegenerative, and proliferative diseases. It is based on a pathophysiological concept that takes into account genetic predisposition and immunological events, together with bacterial and environmental factors.


It includes: a) clinical aspects, paraclinical exams (Magnetic Resonance Imaging, MRI),and biological examination, allowing an exact diagnosis of the disease; b) the identification of specific circulating antibodies in the serum of patients suffering from chronic diseases; and c) the use of therapeutic tools,such as small compounds linked to poly-L.Lysine(PLL), whose physiological actions are well known.Here, we focus on two specific aspects of Endotherapia:1) the identification of circulating antibodies as a means to follow up on chronic pathology and 2) the therapeutic drugs used against those pathologies [MS, amyotrophic lateral vv(ALS), and rheumatoid arthritis (RA)


Full article


An ALS patient who traveled from Australia to France for the treatment reports good results:

For me, I am now entering into week 12 of my Endotherapy medication. I take it 3 times a day. In terms of results, I was advised (based on previous patients) not to expect to notice too much in the first 3 months. So, I impatiently complied with the regime.

So far so good...

Within myself I can definitely say that I feel as though any progression of the disease has slowed considerably. I could almost say that it's likely at a stand-still (but I'm trying not to get too excited too early). Energy levels are rising and very rarely do I need to rest during the day. My friends and family - especially some I haven't spoken to in a while- have commented on many occasions that my speech is a lot clearer and has picked up speed. I have noticed this also, however it is not yet consistent. On occasions where I am exhausted my language reverts back to a mild and sometimes moderate speech deficit (slurred, slow, and mispronounced in nature - comparable to my prior baseline). On the up side, every other day feels like I've gained a little more of my ‘self’ back


GcMAF is a naturally occurring substance in the human body which destroys pathogens by activating macrophages. The acronym stands for Gc (a vitamin D binding protein) Macrophage Activating Factor.


In the early 1990s, Dr. Nobuto Yamamoto, director of the Division of Molecular Immunology and Immunotherapy at the Socrates Institute for Therapeutic Immunology in Philadelphia, Pennsylvania, discovered a substance that inhibited tumor production in mice. Throughout the 1990s Dr. Yamamoto continued his research, expanding it to cases of cancer in humans. But it wasn't until 2008 that Dr. Yamamoto published his groundbreaking study on breast cancer. In this study, weekly injections of GcMAF were given to 16 breast cancer patients. Within three months the tumors were eradicated, with no recurrence over the next four years.


Subsequent studies with GcMAF used for colorectal and prostate cancer yielded similar results. In all cases the tumors disappeared with no recurrence. The rationale behind the success of GcMAF is that when the naturally occurring Gc protein is destroyed by cancer cells (more specifically by an enzyme called nagalase) it hamstrings the immune system's ability to make sufficient tumor-destroying macrophages. The result is an immunosuppressed state which allows the cancer to spread. Injecting GcMAF into cancer patients restores the compromised immune system, which then successfully combats the cancer. CFS Treatment Guide Verrillo/395


The implications for other immune compromised patients are enormous. In 2009 Dr. Yamamoto published a study demonstrating that after fewer than 18 weekly administrations of GcMAF, HIV infection was also completely eradicated. According to the study, "no recurrence occurred and their healthy CD + cell counts were maintained for 7 years."


Given the spectacular results of the Yamamoto studies one would have expected to have seen front-page spreads in the New York Times. However, apart from Reuters, the news agencies barely took notice. As of today, no clinics in the U.S. are using GcMAF as a treatment for cancer. Several prominent CFS/ME physicians, however, have begun using GcMAF for patients who test high in nagalase.


Dr. Kenny De Meirleir treated 108 of his CFS/ME patients with weekly administration of GcMAF. This group of patients showed high amounts of nagalase, which Dr. De Meirleir notes can be produced by intestinal bacterial infections as well as herpes and retroviral infections. (Dr. Chia also points out that nagalase can be elevated as a result of enteroviral infections, which produce small intestinal bacterial overgrowth (SIBO) leading to subsequent immune system dysregulation.) After an average of 15 weeks of treatment, 68 of the 108 patients reported significant improvement in fatigue, sleep, pain, cognitive impairment, orthostatic intolerance, and digestive disturbances. (See below for a link to Dr. De Meirleir's presentation.)


Because GcMAF causes an increase in immune system activation, Dr. De Meirleir recommends starting with a very low dose of GcMAF. Some CFS/ME patients have undiagnosed infections which could lead to Immune Reconstitution Inflammatory Syndrome (IRIS). Once the immune system is stimulated, symptoms due to co-infections can worsen. Of Dr. De Meirleir's 108-patient cohort, 20-30% of them experienced IRIS.

Dr. Cheney has also begun to treat patients with GcMAF, as well as with a natural yogurt probiotic MAF (MAF 314) developed by Professors Ruggiero and Pacini in Italy. GcMAF demonstrated a response rate of 79% (15 out of 19 patients), which is similar to Dr. De Meirleir's results. The oral MAF 314 demonstrated a response rate of 76% over a period of only 28 days.


There are several protocols currently in use. Most CFS physicians begin with 0.20 - 0.25 ml via injection (IM) weekly. Dr. Cheney starts his severely ill patients at a much lower dose administered sublingually, then gradually increases the dose. Typically, the full course of treatment is 8-20 weeks. In order to be effective, GcMAF requires adequate levels of vitamin D. Patients should be tested for vitamin D levels prior to beginning treatment. (Optimal ranges fall between 42 and 60). Patients should also be tested for nagalase levels before treatment and on a monthly basis after beginning GcMAF.


Physicians may recommend concurrent antiviral treatment with Nexavir if the viral load is high. Artesunate may also be prescribed, as well as adjunctive supplementation with B vitamins. CFS Treatment Guide Verrillo/396


Anti-inflammatory drugs, such as corticosteroids (prednisolone, prednisone, etc.) and NSAIDs (ibuprofen, aspirin, etc.) should be avoided while taking GcMAF as these will interfere with the treatment. Morphine analogs (oxycodone, tramadol, etc.), beta blockers, and cytotoxic medications (Sendoxan, Vepesid, Taxol, etc.) should be avoided. Aspartame and carrageenan, two food additives, can also block GcMAF.


GcMAF is contraidicated for patients with MS.


GcMAF is an experimental drug, which means not much is known about its effects on the CFS/ME population other than the few studies performed by Drs. De MeirLeir and Cheney. As with other medications, patients report a wide range of responses, from feeling significantly worse to an almost miraculous recovery of strength and energy. Frequently, a patient will notice improvement over the first six weeks, and then experience a decline. This may be due to exhaustion of vitamin D reserves. For this reason, continuing supplementation with vitamin D may be advised.


 Drs. Cheney, Enlander and De Meirleir are currently using GcMAF with their CFS/ME patients. The price for 2.2 ml of GcMAF (about 8 doses at .25 per dose) is roughly $1000 ($800 euros). Because of the risk of IRIS, it is not recommended that CFS/ME patients take GcMAF without the supervision of a knowledgeable physician. MAF 314 can be obtained from Dr. Cheney's clinic for $3500. Dr. Enlander is currently developing a less expensive form of probiotic MAF (MAF 378) in New York. The test for nagalase levels can be ordered by physicians from Health Diagnostics. It costs $65. GcMAF must be refrigerated



Health Diagnostics and Research Institute (formerly Vitamin Diagnostics, Inc.)

South Amboy Medical Center

540 Bordentown Ave., Suite 2300

South Amboy, New Jersey 08879

Telephone: (732) 721-1234

Fax: (732) 525-3288

Testing for nagalase.




Clos de Balade 21

1140 Evere




BGLI Bio Group Laboratories

Tel: 31-3576-00-176 (GMT+2) (Netherlands)

Website: (There is a contact form on the site) CFS Treatment Guide Verrillo/397



Dr. Kenny De Meirleir's talk on GcMAF and its use in treating CFS/ME:

Dr. Cheney's GcMAF studies:

Excellent information on GcMAF, including where to find clinics in Europe that use GcMAF, patient forums, and purchasing information:

European lab that offers testing for nagalase:

Phoenix Rising forum threads on GcMAF discussing Kenny De Meirleir's use of GcMAF, where to purchase, and how to obtain testing for nagalase:


Patient thread on MAF 314:

"Who Responds to GcMAF." Very technical discussion of gene types

Good article about cancer and GcMAF by Bill Sardi

Another good follow-up article by Bill Sardi:

Cancer and GcMAF:

Professor Ruggiero's website on GcMAF and MAF 314

“Compassionate Use Treatment of CFS with GHP (GcMAF)” Dr. Paul Cheney, Sept. 2011.

Dr. Cheney's pilot study of GcMAF.



A Cheney patient blog about her experience with GcMAF. This blog is very detailed, with information about dosage, testing and patient responses.

Cheney patient blog on GcMAF



Yamamoto N, Suyama H, Yamamoto N, Ushijima N. “Immunotherapy of metastatic breast cancer patients with vitamin D-binding protein-derived macrophage CFS Treatment Guide Verrillo/398

activating factor (GcMAF).” Int J Cancer. 2008 Jan 15;122(2):461-7. (Abstract)

Yamamoto N, Suyama H, Koga Y. “Immunotherapy of metastatic colorectal cancer with vitamin D-binding protein-derived macrophage-activating factor, GcMAF.” Cancer Immunol Immunother. 2008 Jul;57(7):1007-16. (Abstract)

Yamamoto N, Suyama H, Yamamoto N, “Immunotherapy for Prostate Cancer with Gc Protein-Derived Macrophage-Activating Factor, GcMAF.” Transl Oncol. 2008 Jul;1(2):65-72. (Abstract)

Yamamoto N, Ushijima N, Koga Y. “Immunotherapy of HIV-infected patients with Gc protein-derived macrophage activating factor (GcMAF).” J Med Virol. 2009 Jan;81(1):16-26.




Epogen is human erythropoietin, a glycoprotein that controls red blood cell production in bone marrow.


Epogen has been approved for treating anemia caused by kidney failure or chemotherapy, and after certain types of surgery in order to decrease the need for blood transfusions. Epogen has also been used to treat orthostatic hypotension, a condition in which blood pressure drops upon standing, causing light-headedness, dizziness or fainting.


Dr. Hugh Calkins, a cardiologist at Johns Hopkins, has observed that CFS/ME is closely associated with neurally-mediated hypotension (NMH). He found that 90% of CFS/ME patients have some form of NMH. This observation was independently confirmed by Dr. David Streeten who discovered that among two groups of patients with orthostatic intolerance (OI), one had an abnormally low volume of red blood cells, and another had low plasma circulation. As it turned out, both of these were people with CFS/ME. Dr. Streeten treated these patients using protocols and medications for OI, including Florinef, beta-blockers and epogen to raise standing blood pressure. It wasn't until he was contacted by Dr. Bell, whose CFS/ME patients were exhibiting the same symptoms, that Dr. Streeten realized he had successfully treated a group of CFS/ME patients. Since that time, most doctors in the CFS/ME community have incorporated NMH treatments into their protocols.


In an important study conducted at the University of Miami, Hurwitz et al observed that 60-70% of CFS/ME patients show below normal red blood cell volume. The authors concluded that “the findings indicate that lower cardiac volume levels, displayed primarily by subjects with severe CFS, were not linked to diminished cardiac contractility levels, but were probably a consequence of a co-morbid hypovolaemic condition.” This study was significant because it proved that diminished blood volume was pervasive among CFS/ME patients. Unfortunately, while Procrit increased red blood cell volume, fatigue and exercise intolerance did not improve in the treated group.


Very few CFS/ME doctors use Procrit. Dr. Shoemaker treats his patients with 8,000 units of Procrit twice a week for five doses and then decreases the dosage to 4,000 to 6,000 every three to five days. This rather intensive protocol has not gone without criticism from doctors who point out that the “off label” use of Procrit for non-anemic patients is risky.


Procrit is by no means a proven treatment for the correction of low blood volume in CFS/ME. In fact, even weeks after correcting low red blood cell volume in CFS/ME patients, Hurwitz et al noted that there was no corresponding reduction in symptoms. Procrit includes a boxed warning that “ESAs [Erythropoiesis-Stimulating Agents ] increase the risk of death, myocardial

CFS Treatment Guide Verrillo/389

infarction, stroke and thrombosis.” Needless to say, CFS/ME patients should give careful thought to the possible risks before embarking on a protocol that includes Procrit.


Safety update from the makers of Procrit:

CFS/ME Forum review of treatments for NMH in CFS/ME:

Fall 2002 CFIDS Chronicle Q&A with Dr. Hurwitz about Procrit.


Hurwitz, Barry E., Virginia T. Coryell, Meela Parker, Pedro Martin, Arthur LaPerriere, Nancy G. Klimas, George N. Sfakianakis and Martin S. Bilsker. “Chronic fatigue syndrome: illness severity, sedentary lifestyle, blood volume and evidence of diminished cardiac function.” Clinical Science (2010) 118, (125–135) (Printed in Great Britain)



Xyrem (Sodium Oxybate)

XyremXyrem ( gamma-hydroxybutyric acid or GHB


a neurochemical involved in regulating metabolism which is also able to affect sleep. Sodium oxybate is the active ingredient in Xyrem. Xyrem has been approved to treat narcolepsy (severe daytime sleepiness) and cataplexy (sudden muscle weakness).


Zyrem was developed by the Office of Orphan Products Development (OOPD) – a department of the FDA dedicated to producing drugs for rare conditions.  Acquired by Jazz Pharmaceuticals in the US in 2005 Xyrem is currently approved to treat narcolepsy. Currently undergoing Phase III trials for fibromyalgia (FM), Xyrem is also being studied in CFS, Parkinson’s, schizophrenia, essential tremor and others.


Xyrem May Work in ME/CFS/FM Because..

It is able to reduce the frequency of abnormal brainwaves (called alpha intrusions) that appear to impair deep sleep in many CFS and fibromyalgia patients. It is also one of the only drugs known to improve both sleep and reduce pain. Xyrem may enhance the activity of two neurotransmitters, dopamine and serotonin, both of which may be deficient in ME/CFS as well as growth hormone production. The highest concentrations of GHB are found in two areas of the brain; the hypothalamus and basal ganglia, that are of interest to CFS and FM researchers.


ME/CFS Physicians Report

Dr. Teitelbaum flatly states “Xyrem is the most effective way known to increase deep sleep and raise growth hormone”. Dr. Peterson reported that to his ‘amazement’ Xyrem helped with both sleep and pain in his  patients with sleep disorders. Drs. Ross and Marion Hauser call it ‘probably one of the safest and most effective sleep aids that we know of.” They believe it may enhance growth hormone levels. Dr. Klimas notes that Xyrem it induces ‘slow wave’ sleep – the type of sleep most ME/CFS patients have the most trouble achieving.


Chronic Fatigue Syndrome and Fibromyalgia Studies

Currently in Phase III Clinical Trials for FM, Xyrem has been the focus of several extensive studies.A large 2012 trial found that from 42-50% of patients reported a greater than 30% reduction in pain.  A 2011 trial containing over 500 patients found that from 55-60% of patients experienced a 30% drop in pain and significantly reduced fatigue and sleep disturbances. Subjective sleep quality was increased in a 2009 FM study.


A 2010 Spitzer retrospective study found that 60%  and 75% of 118 CFS/FM patients experienced significant reductions in pain and/or fatigue. Two studies have found improved sleep and about a thirty percent reduction in fatigue and pain scores in fibromyalgia. Of particular interest was Xyrem’s abiity to reduce the frequency of anomalies observed in both FM and ME/CFS during sleep called alpha intrusions. Alpha intrusions involve the appearance of unusual high frequency brainwave patterns that are believed to disrupt deep sleep.



Dr. Teitelbaum recommends 9 cc’s (4.5 grams) at bedtime and then about 4 hours later if needed. Xyrem is fast acting and should be taken in bed.


Side Effects

Xyrem can be habit forming. Patients in clinical trials reported confusion (2.5%), depression (3.5%), incontinence at some point (7%), sleepwalking (4%). Headache (22%), nausea (21%) and dizziness (17%) and others were also found.



Do not take other sleep enhancing substances (alcohol, pain medication, muscle relaxants, sedative hypnotics, etc.) when taking Xyrem. Xyrem should be discontinued gradually. Rinse well with water and swallow after taking as Xyrem can damage tooth enamel.



GHB is known as the GHB is known as the date rape drug because of its ability to induce amnesia when combined with alcohol. It can only be obtained from a special compounding pharmacy. According to Dr. Staud, Xyrem’s cost is now up to about $30,000 a year.  Jazz Pharmaceuticals has hiked the price up 220% since 2008 and some analysts expect another 70% boost by 2014.


Pain. 2011 May;152(5):1007-17. Epub 2011 Mar 11.Sodium oxybate reduces pain, fatigue, and sleep disturbance and improves functionality in fibromyalgia: results from a 14-week, randomized, double-blind, placebo-controlled study.Russell IJ, Holman AJ, Swick TJ, Alvarez-Horine S, Wang YG, Guinta D; Sodium Oxybate 06-008 FM Study Group.


Pain Pract. 2010 Jan-Feb;10(1):54-9.Treatment of the narcoleptiform sleep disorder in chronic fatigue syndrome and fibromyalgia with sodium oxybate. Spitzer AR, Broadman M.


Arthritis Rheum. 2009 Jan;60(1):299-309. Sodium oxybate relieves pain and improves function in fibromyalgia syndrome: a randomized, double-blind, placebo-controlled, multicenter clinical trial. Russell IJ, Perkins AT, Michalek JE; Oxybate SXB-26 Fibromyalgia Syndrome Study Group.


Scharf MB, Baumann M, Berkowitz DV, J Rheumatol. 2003 May;30(5):1070-4. The effects of sodium oxybate on clinical symptoms and sleep patterns in patients with fibromyalgia.


Jacob Teitelbaum, MD., 2007. From Fatigued To Fantastic 3rd. ed., Avery Publishing.’


Sodium oxybate [Xyrem] for the treatment of Fibromyalgia – Source: Expert Opinion on Pharmacotherapy, Jun 16, 2011. by Roland Staud


Wikipedia: Xyrem



Xyrem (sodium oxybate), also known as the “date rape drug,” is a central nervous system depressant. Chemically, Xyrem is the equivalent of gamma hydroxobutyric acid (GHB), a naturally occurring substance found in the central nervous system. Xyrem's use for medical purposes is highly restricted. The only approved use of Xyrem is for narcolepsy, a rare condition in which people suddenly fall asleep during the day. In 2010 the makers of Xyrem, Jazz Pharmaceuticals, submitted a New Drug Approval to the FDA for fibromyalgia. Approval was denied. Xyrem is currently listed as an “orphan drug” (a drug used for rare conditions).


USES IN ME/CFS: Xyrem has sometimes been used for treating the intractable insomnia experienced by many patients. Because of its potential for illegal use, physicians and patients who wish to use Xyrem must be registered with Jazz Pharmaceuticals. Registration includes a precise set of instructions for how to take Xyrem. These include not getting up after ingestion and using the bathroom before ingestion. Side effects include nausea, dizziness, headache, vomiting, sleepiness, and bed-wetting (for those who did not use the bathroom first



Prescription Treatments for ME/CFS


It seems you are missing the most effective medication for CFS and Fibromyalgia which I believe is Xyrem. I’m sure it’s because 95% of us will have it denied by our insurance company because it’s so expensive because it’s not approved for our diagnosis. Without this medication I’m totally bedridden. My pain has improved by 95% and fatigue by about 60%. I still can’t work full time but I’m not housebound or bedridden. I worry every month that it will be taken away because my wonderful life that I have again would change for the worse again. I can’t wait until 2023 when it will be generic!



How did you get it approved? I thought it was only indicated for Narcolepsy. Can you tell me anymore about your experience. How’s your sleep?



Dear Hope, Xyrem is a name for GHB which is a precursor for among other things, GABA (gamma-butyric Acid) and you can buy GABA without problem. Now, GABA has low bioavalability but you kan make it into liposomes and take it nasally. Try it an compare it with the effect of Xyrem. Perhaps you can get the same effect with GABA

Treatment of the narcoleptiform sleep disorder in chronic fatigue syndrome and fibromyalgia with sodium oxybate


This study investigates the response of the underlying sleep disorder associated with Chronic Fatigue Syndrome (CFS) and fibromyalgia (FM) to treatment. We retrospectively reviewed 118 cases clinically consistent with CFS or FM, treated in a neurology practice. Abnormal findings on sleep studies and associated human leukocyte antigen markers, and a clinical pattern suggestive of narcolepsy, are present in a high proportion of patients. When considered appropriate based on the clinical picture and test results, treatment with sodium oxybate was offered to these patients. Sixty percent of patients treated with oxybate experienced significant relief of pain, while 75% experienced significant relief of fatigue. We postulate that the response to oxybate in CFS and FM suggests a disturbance of sleep similar to narcolepsy. These findings support this novel approach to intervention and further research. The inability to distinguish CFS and FM by testing and response to treatment suggests that they may represent variations of the same disorder or may be closely related disorders


Xyrem (Sodium Oxybate) for Fibromyalgia

Clinical trials on FMS have consistently shown that the drug can significantly improve sleep quality and reduce pain. A 2013 study (Spaeth) concluded that it had a good long-term safety profile as well.


A 2010 study (Spitzer) suggested it may be effective in ME/CFS as well, but this was the first study of this drug for ME/CFS


Treatment with Flumazenil (GABAA receptor antagonist)



Treatment with Flumazenil (GABAA receptor antagonist) (click to open) An antidote for hypersomnia | Emory University | Atlanta, GA]( Researchers at Emory University School of Medicine have discovered that dozens of adults with an elevated need for sleep have a substance in their cerebrospinal fluid that acts like a sleeping pill. The results are published in the journal [Science Translational Medicine]( "science translational medicine hypersomnia"). Some members of this patient population appear to have a distinct, disabling sleep disorder called "primary hypersomnia," which is separate from better-known conditions such as sleep apnea or narcolepsy. They regularly sleep more than 70 hours per week and have difficulties awakening. When awake, they still have reaction times comparable to someone who has been awake all night. Their sleepiness often interferes with work or school attendance, and conventional treatments such as stimulants bring little relief. "These individuals report feeling as if they’re walking around in a fog — physically, but not mentally awake," says lead author David Rye, professor of neurology at Emory University School of Medicine and director of research for Emory Healthcare’s Program in Sleep. "When encountering excessive sleepiness in a patient, we typically think it’s caused by an impairment in the brain’s wake systems and treat it with stimulant medications. However, in these patients, the situation is more akin to attempting to drive a car with the parking brake engaged.  Our thinking needs to shift from pushing the accelerator harder, to releasing the brake." In a clinical study with seven patients who remained sleepy despite above-ordinary sleep amounts and treatment with stimulants, Emory researchers showed that treatment with the drug flumazenil can restore alertness, although flumazenil’s effectiveness was not uniform for all seven. Alertness was gauged through the psychomotor vigilance test, a measurement of reaction time. Flumazenil is usually used in cases of overdose of benzodiazepines, a widely used class of sedatives such as diazepam (Valium) and zolpidem (Ambien). Evidence in the paper suggests that the sleep-inducing substance in patients’ cerebrospinal fluid is not a benzodiazepine drug, even though flumazenil counteracts it. Identifying the mysterious "somnogen", which appears to be produced by the body, could give scientists greater insight into how our brains regulate states of consciousness such as alertness and sleep. "Primary hypersomnias are disabling and poorly understood. This study represents a breakthrough in determining a cause for these disorders and devising a rational approach to therapy. Further research is required to determine whether or not the results apply to the majority of patients," says Merrill Mitler, a program director at the National Institute of Neurological Disorders and Stroke, part of the National Institutes of Health. The team of researchers involved in this effort includes Rye, Andrew Jenkins, assistant professor of anesthesiology, and Kathy Parker, previously at Emory and now at University of Rochester Medical Center. The paper describes how samples of patients’ cerebrospinal fluid (CSF) contain a substance that enhances the effects of the brain chemical GABA (gamma-amino butyric acid). GABA is one of the main inhibitory chemicals of the nervous system — alcohol, barbituates and benzodiazepines all enhance the effects of GABA. In the laboratory, the size of the effect on GABA receptor function is more than twice as large in the hyper-sleepy patients, on average, than in control samples. "In some of the more severely affected patients, we estimated the magnitude of the GABA-enhancing effect as nearly equivalent to that expected for someone receiving sedation for outpatient colonoscopy," Rye says. "This is a level of impaired consciousness that many subjects had to combat on almost a daily basis in order to live their usual lives." The ICSD-2 (International Classification of Sleep Disorders) terms this disorder "primary hypersomnia" and the proposed DSM-V describes it as "major hypersomnolence disorder." Its prevalence is unclear. The Emory team’s findings could potentially provide a biological definition and a treatment for an under-recognized sleep disorder. The patients in the group examined in the paper have received a variety of diagnoses, including idiopathic hypersomnia and narcolepsy without cataplexy. Cataplexy is a sudden loss of muscle tone, sometimes triggered by surprise or strong emotion, characteristic to narcolepsy. Other members of the group are simply considered "long sleepers" (more than 10 hours per day). In addition, the identity of the GABA-enhancing substance is not yet known, although Rye and Jenkins are devising strategies to pin it down. Based on its size and sensitivity to certain enzymes, it could be a peptide, similar to but not the same as the hormones oxytocin or hypocretin. In the laboratory, Jenkins and his colleagues have shown that the sleep-inducing substance can act on GABA receptors that are not sensitive to benzodiazepines. "Previous studies with flumazenil indicate that it does not have a wake-promoting effect on most people, so its ability to normalize vigilance in this subpopulation of extremely sleepy patients appears genuinely novel," Rye says. Other Emory authors include postdoctoral fellows Amanda Freeman and Jacqueline Fairley, data analyst Prabhjyot Saini, Donald Bliwise, professor of neurology, Michael Owens, professor of psychiatry and behavioral sciences, Lynn Marie Trotti, assistant professor of neurology, James Ritchie, professor of pathology and laboratory medicine and Paul Garcia, assistant professor of anesthesiology. Parker, Rye and Jenkins are co-inventors on patent rights held by Emory University. Emory and the inventors could potentially receive royalties derived from the intellectual property related to this research. The research was supported by the Woodruff Health Sciences Center Fund, the National Institute of Neurological Disorders and Stroke (NS055015 and NS050595) and the National Institute of General Medical Sciences (GM073959), James Sumner and the Arthur Williams Jr. Foundation. Reference:D.B. Rye, D.L. Bliwise, K. Parker, L.M. Trotti, P. Saini, J. Fairley, A. Freeman, P.S. Garcia, M.J. Owens, J.C. Ritchie and A. Jenkins. Modulation of vigilance in the primary hypersomnias by endogenous enhancement of GABA(A) receptors. *Science Trans. Med* 4, 161ra151 (2012).  |||How flumazenil's effects were discovered{nl}![](C:\Users\julie\Brains\U01\B02\3eda8a7f-9379-4b71-8eee-fef0c019e7e3/Notes/3246e316-0170-4723-9a3d-c69e4d311a9e.jpg)An Atlanta woman came to Emory’s sleep center in 2005. Her sleep requirements – up to 16 hours per day -- gradually increased so much that she needed to take leave of absence from her job. Stimulants (modafinil and amphetamines) prescribed by doctors had a temporary benefit. However, tolerance to these medications required increasing doses that made her uncomfortable, elevated her blood pressure and produced rebound sleepiness, such that she’d sleep for 30 or even 57 hours continuously.{nl}Analysis of her CSF revealed biological activity that enhances the effects of GABA. In the laboratory, her CSF’s GABA-enhancing effects were reversible with flumazenil.{nl}Based on these results, the Emory team reasoned that flumazenil could form a treatment for the Atlanta woman. She found that it made her feel awake for the first time in years, and long-term treatment with flumazenil has allowed her to return to work.{nl}Flumazenil is normally delivered intravenously. Working with manufacturer Roche, Emory investigators, led by Parker, obtained permission from the FDA for long-term sublingual delivery of flumazenil for the Atlanta woman.{nl}This success drove Rye and his colleagues to examine CSF samples from other sleep clinic patients, and then to study flumazenil’s effects in a small group of patients with similar symptoms.{nl}{nl}From: The sleep switch: hypothalamic control of sleep and wakefulness{nl}Clifford B. Saper, Thomas C. Chou and Thomas E. Scammell|   More than 70 years ago, von Economo predicted a wake-promoting area in the posterior hypothalamus and a sleep-promoting region in the preoptic area. Recent studies have dramatically confirmed these predictions. The ventrolateral preoptic nucleus contains GABAergic and galaninergic neurons that are active during sleep and are necessary for normal sleep. The posterior lateral hypothalamus contains orexin/hypocretin neurons that are crucial for maintaining normal wakefulness. A model is proposed in which wake\- and sleep-promoting neurons inhibit each other, which results in stable wakefulness and sleep. Disruption of wake\- or sleep-promoting pathways results in behavioral state instability.   During World War I, the world was swept by a pandemic of encephalitis lethargica, a presumed viral infection of the brain that caused a profound and prolonged state of sleepiness in most individuals. The victims could be awakened briefly with sufficient stimulation, but tended to sleep most of the time. A Viennese neurologist, Baron Constantin von Economo, reported that this state of prolonged sleepiness was due to injury to the posterior hypothalamus and rostral midbrain1. He also recognized that one group of individuals infected during the same epidemic instead had the opposite problem: a prolonged state of insomnia that occurred with lesions of the preoptic area and basal forebrain. von Economo further hypothesized that lesions of the posterior diencephalon could cause the disease we now call narcolepsy, in which individuals have a tendency to fall asleep at inappropriate times. Based on his observations, von Economo predicted that the region of the hypothalamus near the optic chiasm contains sleep-promoting neurons, whereas the posterior hypothalamus contains neurons that promote wakefulness.   In subsequent years, his observations on the sleep producing effects of posterior lateral hypothalamic injuries were reproduced by lesions in the brains of monkeys2, rats3 and cats4; and the insomnia producing effects of lateral preoptic–basal forebrain injuries were demonstrated in rats3 and cats5.   Injections of the GABA-receptor agonist muscimol into these areas in cats produced results similar to that of the lesions, suggesting that wakefulness is promoted by neurons in the posterior lateral hypothalamus and sleep by neurons in the preoptic area6. However, the basic neuronal circuitry that causes wakefulness was only clearly defined in the 1980s and early 1990s, and the pathways responsible for the hypothalamic regulation of sleep began to emerge only in the past five years. This article focuses on these hypothalamic switching mechanisms. Other recent publications are available that discuss the homeostatic and circadian control of sleep7, the contributions of brainstem cholinergic–monoaminergic interactions to rapid eye movement (REM)–non-REM (NREM) sleep oscillations8^–10^, and the role of the dopaminergic system in sleep regulation11. Our model of the hypothalamic switching circuitry provides an effector mechanism by which many of these other systems produce or prevent sleep.   The cholinergic and monoaminergic substrates of arousal In the years after World War II, Moruzzi, Magoun and many others contributed to identifying an ascending pathway that regulates the level of forebrain wakefulness12. Transection of the brainstem at the midpons or below did not reduce arousal, whereas slightly more rostral transections at a midcollicular level caused an acute loss of wakefulness. The wakepromoting outflow from this crucial slab of tissue at the rostral pontine–caudal midbrain interface was traced by anatomical and physiological techniques through the paramedian midbrain reticular formation to the diencephalon, where it divided into two branches. One pathway innervated the thalamus, and the second extended into the hypothalamus. Although this arousal system was termed the ascending reticular activating system, in fact its origins were identified only recently by the availability of modern neuroanatomical tracer methods combined with immunohistochemistry (Fig. 1).   The main origin of the thalamic projection from the caudal midbrain and rostral pons was identified as the cholinergic pedunculopontine and laterodorsal tegmental nuclei (PPT–LDT)^13–15^. This population of cholinergic neurons projects in a topographic fashion to the thalamus, including the intralaminar nuclei16^–18^, but also to the thalamic relay nuclei and the reticular nucleus of the thalamus. The reticular nucleus is thought to play a key role in regulating thalamic activity, and the cholinergic influence is thought to be crucial in activating thalamocortical transmission19.   Fig . 1. The ascending arousal system sends projections from the brainstem and posterior hypothalamus throughout the forebrain. Neurons of the laterodorsal tegmental nuclei and pedunculopontine tegmental nuclei (LDT and PPT) (blue circles) send cholinergic fibers (Ach) to many forebrain targets, including the thalamus, which then regulate cortical activity. Aminergic nuclei (green circles) diffusely project throughout much of the forebrain, regulating the activity of cortical and hypothalamic targets directly. Neurons of the tuberomammillary nucleus (TMN) contain histamine (HIS T), neurons of the raphé nuclei contain 5-HT and neurons of the locus coeruleus (LC) contain noradrenaline (NA). S leep-promoting neurons of the ventrolateral preoptic nucleus (VLPO, red circle) contain GABA and galanin (Gal).     The activity of the PPT–LDT neurons varies with different behavioral states. During wakefulness, when the cortical electroencephalogram (EEG) shows low-voltage fast activity, many PPT–LDT neurons fire rapidly (Table 1). As the individual goes to sleep, the EEG waves become slower and larger; during this period, few PPT–LDT neurons are active. Periodically during the night, the individual enters a very different state of active sleep, in which there are rapid eye movements (REM sleep), a loss of muscle tone, except for the muscles involved in respiration, and a low-voltage fast EEG, which resembles a waking state. The PPT–LDT are released from tonic monoamine-mediated inhibition and hence fire rapidly during REM sleep8^–10,20^.   If the thalamocortical system is activated in both wakefulness and REM sleep, what is the difference between these two states? One key distinction is the activity in the hypothalamic branch of the ascending arousal system (Fig. 1). Cell groups in the caudal midbrain and rostral pons that contribute to this projection include the noradrenergic locus coeruleus and the serotoninergic dorsal and median raphé nuclei, as well as the parabrachial nucleus21. Their axons run through the lateral hypothalamus, where they are joined by histaminergic projections from the tuberomammillary nucleus (TMN). Other neurons in the lateral hypothalamic area, some of which contain the peptide neurotransmitters orexin (also known as hypocretin)^22 ^or melanin-concentrating hormone23, join this projection, as do axons from the basal forebrain cholinergic nuclei (Fig. 1). Each of these pathways projects diffusely to the cortex of the entire cerebral hemisphere.    |||EEG                Fast, low voltage Slow, high voltage      Fast, low voltage{nl}Eye movement Vision related Slow, infrequent    Rapid{nl}Muscle tone   ↑↑                   ↑                          0{nl}LDT/PPT          ↑                       0                         ↑↑{nl}LC/DR/TMN   ↑↑                   ↑                          0{nl}VLPO cluster    0          ↑↑     ↑? VLPO extended     0            ↑?       ↑↑{nl}Orexin/hyprocretin ↑↑          0?                         0?{nl}^aFiring rates are as follows: two arrows = rapid firing, one arrow = slower firing, 0 = little or no firing. Question marks represent hypothesized firing patterns for which there is as yet no firm evidence. Abbreviations: DR, dorsal raphé nucleus; EEG, electroencephalogram; LC, locus coeruleus; LDT, laterodorsal tegmental nuclei; NREM, nonrapid eye movement; PPT,{nl}pedunculopontine tegmental nuclei; REM, rapid eye movement; TMN, tuberomammillary nucleus; VLPO, ventrolateral preoptic nucleus.|     The neurons in the monoaminergic cell groups have been closely studied for their relationship to behavioral state. Neurons in the locus coeruleus, the dorsal raphé nucleus and the TMN all fire at relatively characteristic rates, which are state dependent24^–27^. All three groups fire fastest during wakefulness, slow down with the EEG during NREM sleep, and nearly stop firing during REM sleep. Hence, the differences in the firing of the cholinergic and monoaminergic ascending arousal systems characterize and probably regulate the production of the different behavioral states (Table 1). ## The ‘off’ switch Because the firing of monoaminergic neurons is state dependent, understanding the sources of inputs to these cell groups provides a window into the mechanisms that regulate wakefulness. Sherin and colleagues have found two major inputs to the TMN core: (1) a population of diffusely distributed neurons in the lateral hypothalamic area; and (2) a dense cluster of neurons in the ventrolateral preoptic nucleus (VLPO cluster), surrounded medially and dorsally by a more diffuse extension from the nucleus (extended VLPO)^28,29^. Injections of an anterograde tracer have confirmed that the axons from the VLPO intensely innervate the cell bodies and proximal dendrites of the TMN, as well as less intensely innervating the dorsal and median raphé nuclei and the locus coeruleus29^,30^ (Fig. 2). The axons from the VLPO also terminate within the cholinergic basal forebrain and PPT–LDT groups, but do not appear to contact the cholinergic cell bodies.   Nearly 80% of the retrogradely labeled VLPO neurons contain both the GABA-synthesizing enzyme glutamic acid decarboxylase and the peptide galanin29. Electron microscopy confirmed that the VLPO terminals onto TMN neurons were immunoreactive for GABA and make symmetric synapses29. Because galanin and animals were sleep deprived for 9 or 12 hours, to dissociate Fos expression from the circadian cycle. These animals showed the same correlation of Fos expression in the VLPO and sleep. However, the animals that failed to fall asleep following deprivation showed little or no Fos expression in the VLPO. Similar results have since been obtained in mice, cats, degus and Nile river rats (S. Gans *et al.,*unpublished)^36,37^. Electrophysiological recordings have similarly identified sleep-active neurons in the VLPO region38^,39^. The rate of firing of VLPO neurons was nearly doubled during sleep compared with waking, and it doubled again during the deep sleep that followed sleep deprivation. The firing rate of VLPO neurons was not increased after sleep deprivation until the animals actually slept, so VLPO firing rates probably are not related to the degree of sleepiness, but instead the production of sleep itself.   The chemical identity of the sleep-active VLPO neurons has recently been determined by combining *in situ*hybridization for galanin with immunocytochemistry for Fos (S. Gaus *et al.*and J. Lu *et al.*, unpublished). In sleeping rats, 80% of the Fos-immunoreactive neurons in the VLPO cluster (and 50% in the extended VLPO) also contained galanin mRNA, and about half of the galanin mRNAcontaining neurons in both parts of the nucleus had a Fos-immunoreactive nucleus. Galanin-positive neurons of the VLPO were also sleep active in mice and cats (S. Gaus *et al.*, unpublished)^40. A galanincontaining cell group in the VLPO has also been identified in monkeys and humans (S. Gaus *et al.*, unpublished), so this system appears to be a uniform feature of mammalian brains. Is the VLPO necessary for sleep? To determine whether the VLPO neurons are necessary for producing sleep, Lu and colleagues produced small excitotoxic lesions in the lateral preoptic area by microinjecting ibotenic acid41. Although previous studies have demonstrated insomnia after injury to this region, these lesions injured fiber pathways3^,5^ ^or involved much of the preoptic area beyond the VLPO (Refs 42,43). In order to analyze the lesions, the numbers of remaining Fos-immunoreactive cell bodies in the VLPO cluster and the extended VLPO were compared with the changes in sleep behavior. In animals with more than 70% bilateral cell loss in the VLPO cluster, the amounts of both NREM and REM sleep two possible stable patterns of firing and a tendency to avoid intermediate states. Such properties would be very useful in sleep–wake regulation, as an animal that walked about while half asleep would be in considerable danger. GABA are known to inhibit both TMN and neurons of the locus coeruleus24^,31–33^, the descending projection from the VLPO is likely to be inhibitory in nature29^,34,35^. To determine the relationship between VLPO activity and sleep–wake behavior, the expression of Fos protein immunoreactivity was examined, as a marker of neuronal activity in the VLPO across the wake–sleep cycle28. The number of Fos-immunoreactive neurons in the VLPO correlated closely with the amount of sleep the animals experienced during the hour before death. Other were reduced by about 55% (Ref. 41). The loss of neurons in the VLPO cluster correlated closely with the loss of NREM (*r*=0.77), but did not correlate significantly with loss of REM sleep. However, the loss of Fos-immunoreactive neurons in the extended VLPO correlated closely with the loss of REM sleep (*r*=0.74), but did not show a significant correlation with the loss of NREM sleep. Conversely, when rats were exposed to a period of darkness during the day, a condition that doubles REM sleep time, there was a concomitant increase in Fos expression in the extended VLPO, but not the VLPO cluster (J. Lu *et al.*, unpublished). Anatomical studies have shown that the projections to the locus coeruleus, dorsal–median raphé, and the PPT–LDT arise predominantly from the extended VLPO, rather than the VLPO cluster (J. Lu *et al.*, unpublished)^30,44^. These observations suggest that the VLPO contains specific subregions that are specialized for the control of REM versus NREM sleep. ## The flip–flop and bistability The relationship between the VLPO and the major monoamine groups appears to be reciprocal. The VLPO is innervated by histaminergic axons from the TMN, noradrenergic terminals from the locus coeruleus and serotoninergic inputs from the midbrain raphé nuclei45. Recordings from individual VLPO neurons in hypothalamic slices show that they are inhibited by noradrenaline and by 5-HT (Ref. 46). No responses to histamine were recorded, but TMN neurons also contain GABA and galanin, which might inhibit the VLPO (Ref. 47). The model shown in Fig. 3 is based on the hypothesized mutual inhibition between the VLPO and the major arousal systems. Although the monoamine systems are emphasized, there might be other components of the arousal system that are not illustrated here, such as neurons in the lateral hypothalamic area, that would interact with the VLPO in a similar way. When VLPO neurons fire rapidly during sleep, they would inhibit the monoaminergic cell groups, thus disinhibiting and reinforcing their own firing. Similarly, when monoamine neurons fire at a high rate during wakefulness, they would inhibit the VLPO, thereby disinhibiting their own firing. This reciprocal relationship is similar to a type of circuit that electrical engineers call a ‘flip–flop’48. The two halves of a flip–flop circuit, by each strongly inhibiting the other, create a feedback loop that is bistable, with       Fig . 2 . The projections from the ventrolateral preoptic nucleus (VLPO) to the main components of the ascending arousal system. Axons from the VLPO directly innervate the cell bodies and proximal dendrites of neurons in the major monoamine arousal groups. Within the major cholinergic groups, axons from the VLPO mainly innervate interneurons, rather than the principal cholinergic cells. Abbreviations: LC, locus coeruleus; LDT, laterodorsal tegmental nuclei; PPT, pedunculopontine tegmental nuclei; TMN, tuberomammillary nucleus; VLPO, ventrolateral preoptic nucleus. The blue circle indicates neurons of the LDT and PPT; green circles indicate aminergic nuclei; and the red circle indicates the VLPO.   The self-reinforcing firing patterns of the flip–flop switch produce a degree of resistance to switching when one side is firing briskly. This stability avoids inappropriate changes in wake–sleep state when input signals to the VLPO and the monoaminergic cell groups fluctuate transiently over the course of the day. However, large scale influences, such as circadian sleep drive or accumulated homeostatic need for sleep might gradually shift the relative balance of mutual inhibition. When this pressure to change becomes great enough, the same feedback properties that allow the flip–flop circuit to resist change will suddenly give way and rapidly produce a reversal of firing patterns. The flip–flop switch therefore changes behavioral state infrequently but rapidly, in contrast to the homeostatic and circadian inputs, which change continuously and slowly. A crucial aspect of this bistable switch is that if the firing of neurons on either side is substantially weakened, the switch is less stable. For example, after lesions of the VLPO, the animals experience much more wakefulness, and the homeostatic drive for sleep might increase, forcing the balance in the circuit nearer to its transition point41. Thus, rats with VLPO lesions fall asleep more frequently, but because the self-reinforcing properties of the circuit are weaker, they switch back into wakefulness more frequently as well, with the result that both wake and sleep bouts are shorter after VLPO lesions. Fig . 3 . A model for reciprocal interactions between sleep\- and wakepromoting brain regions, which produces a flip–flop switch. Inhibitory pathways are shown in red, and the excitatory pathways in green. The blue circle indicates neurons of the LDT and PPT; green boxes indicate aminergic nuclei; and the red box indicates the VLPO. Aminergic regions such as the TMN, LC and DR promote wakefulness by direct excitatory effects on the cortex and by inhibition of sleep-promoting neurons of the VLPO. During sleep, the VLPO inhibits amine-mediated arousal regions through GABAergic and galaninergic (GAL) projections. Most innervation of the TMN originates in the VLPO core, and input to the LC and DR predominantly comes from the extended VLPO. This inhibition of the amine-mediated arousal system disinhibits VLPO neurons, further stabilizing the production of sleep. The PPT and LDT also contain REM-promoting cholinergic neurons. The extended VLPO (eVLPO) might promote REM sleep by disinhibiting the PPT–LDT; its axons innervate interneurons within the PPT–LDT, as well as aminergic neurons that normally inhibit REM-promoting cells in the PPT–LDT. Orexin/hypocretin neurons (ORX ) in the lateral hypothalamic area (LHA) might further stabilize behavioral state by increasing the activity of aminergic neurons, thus maintaining consistent inhibition of sleep-promoting neurons in the VLPO and REM-promoting neurons in the PPT–LDT. Unbroken lines represent neuronal pathways described in the text. Broken black lines indicate influences of specific regions on behavioral states. Abbreviations: DR, dorsal raphé nucleus; HIS T, histamine; LC, locus coeruleus; LDT, laterodorsal tegmental nuclei; PPT, pedunculopontine tegmental nuclei; REM, rapid eye movement; TMN, tuberomammillary nucleus; VLPO, ventrolateral preoptic nucleus.   ## S tabilizing the flip–flop A similar deficit on the waking side of the mutually inhibitory flip–flop circuit might produce abrupt and unstable fluctuations in behavioral state in the disorder known as narcolepsy. Individuals with narcolepsy experience frequent and unwanted transitions into sleep during wakefulness, and they tend to awaken more frequently from sleep as well. When placed in a quiet environment, they fall asleep and transition into REM sleep far more rapidly than unaffected individuals. At times, they experience fragments of REM sleep intermixed with wakefulness, such as loss of muscle tone while awake, a condition known as cataplexy. The origin of narcolepsy was not understood until a dramatic series of events that unfolded during the past three years. In 1998, two groups of investigators simultaneously discovered a family of peptide neurotransmitters that was made by neurons in the lateral hypothalamus. Sakurai and co-workers identified two peptides in a screen for ligands for orphan G-protein-coupled receptors, which they named ‘orexin A and B’, because the peptides appeared to promote feeding49. de Lecea *et al.*, meanwhile, described two hypothalamic-specific mRNAs coding for the same peptides, which they termed ‘hypocretins’because they were hypothalamic peptides with sequence similarity to secretin50.             However, when the full extent of the pathways containing the orexin/hypocretin peptides was revealed by immunocytochemistry51^–53^, it became clear that the orexin/hypocretin neurons, like the VLPO, innervated all of the components of the ascending arousal system (Fig. 4). Orexin 1 receptors were found in the locus coeruleus, orexin 2 receptors in the TMN and basal forebrain, and both types of receptors were found in the midbrain raphé nuclei and mesopontine reticular formation54^,55^. Because both receptors are mainly excitatory, these observations suggested that orexin/hypocretin might help maintain wakefulness by increasing the activity of the ascending arousal system. In 1999, Chemelli *et al.*produced orexin/hypocretin knockout mice53. These animals suffered intermittent attacks during the active (dark) period, in which they would suddenly fall onto their sides for a few minutes, then get up and resume their activities. Polysomnographic analysis showed that these periods of behavioral arrest consisted of episodes of atonia associated with an EEG that was consistent either with wakefulness (i.e. cataplexy) or REM sleep, findings that are suggestive of narcolepsy. Simultaneously, Nishino *et al.*found that canine narcolepsy was due to mutations in the gene for the type 2 orexin/hypocretin receptor56. The combination of these two findings provide overwhelming evidence that the loss of orexin/hypocretin signaling via the type 2 receptor is sufficient to produce the symptoms of narcolepsy. The absence of orexin in the hypothalamus and in the spinal fluid of humans with narcolepsy has subsequently been confirmed57^–59^. The orexin/hypocretin neurons probably play an important role in producing normal wakefulness. Kilduff and Peyron have hypothesized that these neurons might be active during wakefulness and REM sleep60, but we predict that these cells are predominantly wake active. Orexin neurons synthesize Fos protein during wakefulness, and the number of Fos-positive orexin-containing neurons correlates closely with the amount of wakefulness, whether it is naturally occurring, produced by sleep deprivation or caused by stimulant drugs, such as amphetamine or modafinil53^,61^. Extracellular recordings from neurons in the perifornical region, which contains the orexin/hypocretin cell bodies, confirm that cells in this area are predominantly wake active although some also fire during REM sleep (R. Szymusiak, unpublished). However, neither orexin-deficient animals nor narcoleptic humans have excessive amounts of sleep, but instead they have poor maintenance of both wakefulness and sleep, or dysfunctional switching. What, then, can be the role of the orexin/hypocretin neurons in maintaining behavioral state? Recent studies have shown that the orexin/hypocretin neurons might influence both sides of the flip–flop circuit by direct projections to both the monoaminergic and cholinergic arousal cell groups, and to the VLPO region. Orexin/hypocretin increases the firing of neurons in the locus coeruleus62, the dorsal raphé nucleus63 and the TMN (H. Hass, unpublished). Although VLPO neurons do not appear to contain orexin/hypocretin receptors53, injection of orexin/hypocretin into the preoptic area near the VLPO increases wakefulness and decreases both REM and NREM sleep64, suggesting a presynaptic mechanism of action (perhaps on monoaminergic axons). Orexin/hypocretin neurons therefore might act as a ‘finger’, pressing the flip–flop switch into the ‘wakeful’position, and preventing inappropriate switching into the ‘sleep’position. In the absence of such an influence, as seen in narcolepsy, the switch would be less stable, and more susceptible to sudden and inappropriate transitions. This model could also explain the rapid transitions into REM sleep, or fragments of REM sleep, that are seen in narcoleptics. The TMN, raphé nuclei and locus coeruleus contain orexin/hypocretin receptors54, and all three groups inhibit REM sleep10. In the absence of an excitatory orexin input, the weakened arousal influence and increased activity of the extended VLPO would allow earlier and more frequent transitions to the REM state. Interestingly, like the animals with VLPO lesions, destabilizing the switch in narcolepsy also results in more frequent awakenings from sleep. ## Concluding remarks Advances over the past five years have largely borne out the remarkable predictions of von Economo, which were made over 70 years ago on the basis of clinical observations. The occurrence of insomnia in individuals with lesions of the preoptic area and basal forebrain was almost certainly due to the involvement of the VLPO in these cases. The hypersomnolent individuals clearly had lesions of the ascending arousal pathways at the midbrain–diencephalic junction. And von Economo’s prediction that narcolepsy could be caused by lesions of the posterior diencephalon has been proven true by the recognition that this region contains the orexin/hypocretin neurons, the loss of which causes narcolepsy in humans. The recent progress in defining the components of the sleep switching system should allow us to understand better how slowly changing influences, such as homeostatic and circadian drives, can produce rapid and discrete changes in behavioral state.



Most common drugs used for CFS

  • Bromocriptine
  • Cerebrolysin
  • Citalopram
  • Donepizil
  • Erythropoietin
  • Memantadine
  • Methylphenidate
  • Milnacipran
  • Neuropeptide
  • Neurotrophic
  • Pioglitazone
  • Peptides



Suramin ( "Suramin is anti-purinergic drug usually used to treat African sleeping sickness and river blindness. Dr. Naviauw believes Suranim may be able to turn off the  "cell danger response" in ME/CFS and autism. A small Suramin autism trial was successful. ") (2)


  • Most common Drugs used for CFS (and CFS cofactors continued
  • Abilify (4);
  • Ampligen (16);
  • Amytriptyline (2
  • Anti-inflammatory (1);
  • Antivirals (17);
  • Ativan (1);
  • Baclofen (1);
  • Clonidine (2);
  • Cortene (5);
  • Cymbalta (4);
  • Dextromethorphan (7);
  • Doxepin (1);
  • Enbrel (1);
  • Flexeril (4);
  • Heparin (1);
  • Hormones (thyroid, testosterone, progesterone, estrogen, hydrocortisone) (4);
  • Hydrocortisone (Cortef) (1);
  • Intranasal (1);
  • Ivabradine (6);
  • IVIG (11);
  • Ketamine (7);
  • Klonopin (3);
  • Low Dose Naltrexone (26);
  • Lyrica (11);
  • Memantine (1);
  • Mestinon (2);
  • Metformin (2);
  • Mifepristone (4);
  • Nimodipine (4);
  • Opioid drugs (15);
  • Propanolol (3);
  • Quetiapine (1);
  • Rituximab (7);
  • Savella (5);
  • Stimulants (5);
  • Suramin (2);
  • Tomnya (2);
  • Xifaxin (2);
  • Xyrem (1);


Classes of Drugs


Several categories of drugs are used to treat ME/CFS. They include:


Antimicrobial drugs (includes antiviral, antibiotic)


Antidepressants (SSRIs/SNRIs and tricyclic)


Anxiety or anxiolytic agents


Nonsteroidal anti-inflammatory drugs (NSAIDs)


Blood-pressure medications


Experimental treatments


Anti-fungal drugs: Fluconazole, Itraconazole

Other drug treatments: Chelation, Cyclophosphamide, Prednisone, Trazodone, Tramadol


B-cell depletion: Rituximab

Immunomodulators and immunostimulants: Ampligen, Low dose naltrexone, Intravenous immunoglobulin, Staphylococcal vaccine, Interferon


Antivirals: Valganciclovir, Famciclovir, Valaciclovir, Acyclovir


Anti-inflammatory drugs: Sulfasalazine


Full list


Because all of these medications are used for off-label purposes (meaning they're not FDA approved specifically for ME/CFS), your insurance company may not cover them.



"Antimicrobial" refers to a variety of drug types, including antivirals, antibiotics, antifungals, and antiprotozoals. Researchers say this condition makes your body constantly act as if it's fighting an infection. While no specific virus or bacteria has been linked conclusively to ME/CFS, some research supports the possibility of the Epstein-Barr virus (which causes mononucleosis), human herpes virus 6 (HHV-6, which causes roseola) and enteroviruses.


Ampligen (rintatolimod)

This experimental drug was rejected by the FDA and is not yet on the market for any use. Ampligen works by jump-starting your body's natural anti-viral pathway and regulating levels of RNase L (a substance in your cells that attacks viruses), which can be high in people with ME/CFS. Studies show Ampligen is more effective and has far fewer side effects than other drugs in its class. Manufacturer Hemispherx Biopharma is continuing trials of other conditions, hoping to someday win approval.


Valcyte (valganciclovir)

The antiviral valganciclovir treats HHV-6, which multiple studies have found in a significant percentage of people with ME/CFS. Small studies have had encouraging results, but experts agree that larger and better-designed studies need to be done before they can draw reliable conclusions.


Because researchers haven't identified a particular infection that leads to this condition, doctors don't usually prescribe other antimicrobials for it, unless you have an active infection.



Just because antidepressants are a common treatment, it doesn't mean all the people taking them are depressed or have any kind of psychological condition. (While many people with the condition are clinically depressed, it's generally considered a resultof the symptoms and change in lifestyle and not a cause of the illness itself.) The most common types of antidepressants prescribed are SSRI/SNRIs and tricyclic agents.


SSRI/SNRI-Type Antidepressants


The reason antidepressants work is because they raise levels of important neurotransmitters that are low in some people with ME/CFS. These drugs are called selective serotonin reuptake inhibitors (SSRIs) or serotonin-norepinephrine reuptake inhibitors (SNRIs or NSRIs).


Serotonin helps process pain signals and is also important to your sleep-wake cycle, while norepinephrine (a type of adrenaline) is involved in the stress response and bursts of energy.


Examples of SSRIs and SNRIs are:


  • Cymbalta (duloxetine)
  • Prozac (fluoxetine)
  • Zoloft (sertraline)
  • Paxil (paroxetine)
  • Effexor (venlafaxine)
  • Desyrel (trazodone)
  • Wellbutrin (bupropion)
  • Tricyclic Antidepressants


Low doses of tricyclic agents sometimes improve sleep and relieve mild, widespread pain in people with ME/CFS. Some examples are:


  • Adapin, Sinequan (doxepin)
  • Elavil, Etrafon, Libitrol, Triavil (amitriptyline)
  • Norpramin (desipramine)
  • Pamelor (nortriptyline)


Be sure you're familiar with the side effects of any antidepressants you're taking, especially since many antidepressants come with a warning of heightened risk of suicidal thoughts and behaviors. If you decide to stop taking any of these drugs, talk to your doctor about how to properly wean off of them. Stopping cold turkey can lead to some potentially serious problems.



Doctors sometimes prescribe anti-anxiety drugs for those ME/CFS patients with panic disorder. They include:


  • Xanax (alprazolam)
  • Klonopin (clonazepam)
  • Ativan (lorazepam)


Common side effects of anxiety drugs include sedation, amnesia, insomnia, muscle cramps, and convulsions. Stopping them also can lead to withdrawal symptoms.



These drugs sometimes are used to relieve the pain and fever associated with ME/CFS. Several are available over-the-counter, including:


  • Advil, Bayer Select, Motrin Nuprin (ibuprofen)
  • Aleve, Anaprox, Naprosyn (naproxen)
  • Feldene (piroxicam)


Your doctor may also prescribe other types of NSAIDs, and it's important not to combine different drugs in this class. That can put you at greater risk of developing dangerous side effects, including kidney damage and gastrointestinal bleeding.

Blood Pressure


A form of low blood pressure called neurally mediated hypotension (NMH) is common in people with ME/CFS. It's caused by an abnormal interaction between the heart and the brain, even though both organs are normal and healthy. Also called the fainting reflex, NMH can cause dizziness and fainting and is sometimes diagnosed by what's called a tilt table test.


Some people with diagnosed NMH take a low-blood-pressure medication called Florinef (fludrocortisone), while others take the high blood-pressure medication Tenormin (atenolol). If you're on Tenormin, you'll probably need to be watched for low blood pressure and may be advised to increase your salt and water intake.


Source: 2013 Solve ME/CFS Initiative. All rights reserved. Treatment FYI


From: 'Medications for Chronic Fatigue Syndrome'






















Modafinil is used for: Improving wakefulness in patients with excessive sleepiness associated with narcolepsy or other sleep disorders. It may also be used for other conditions as determined by your doctor.


Modafinil is a wakefulness-promoting agent. Exactly how it works is not known, but it is thought to work by altering the natural chemicals (neurotransmitters) in the brain.



Lisdexamfetamine is used for:


Treating attention deficit hyperactivity disorder (ADHD). It is also used to treat binge eating disorder (BED). It may also be used for other conditions as determined by your doctor.


Lisdexamfetamine is an amphetamine. Exactly how lisdexamfetamine works is not known. It affects certain chemicals in the brain that may help improve attention span and behavior.



Amantadine is used for:


Preventing and treating certain types of flu. It is used to treat Parkinson disease and uncontrolled muscle movements caused by some medicines. It may also be used for other conditions as determined by your doctor.

 Amantadine is an antiparkinson and antiviral agent. How amantadine works against the flu is not known. It may block reproduction of the virus and decrease the ability of the virus to get into the cells. How amantadine works against Parkinson disease is not known. It may increase a certain chemical in the brain.



Duloxetine delayed-release capsules are used for:


Treating depression and generalized anxiety disorder. It is used for managing pain caused by fibromyalgia and diabetic peripheral neuropathy (DPN). Duloxetine delayed-release capsules are used for managing chronic musculoskeletal pain, including osteoarthritis and chronic low back pain. It may also be used for other conditions as determined by your doctor.


Duloxetine delayed-release capsules are a serotonin-norepinephrine reuptake inhibitor (SNRI). It works by restoring the balance of certain natural substances in the brain (serotonin and norepinephrine), which helps to improve certain mood problems and manage pa.



Armodafinil is used for:


Improving wakefulness in patients with excessive sleepiness from sleep apnea, narcolepsy, or shift work disorder. It may also be used for other conditions as determined by your doctor.


Armodafinil is a wakefulness-promoting agent. Exactly how it works is not known. Armodafinil affects certain chemicals in the brain that may affect sleep.


From: 'Amitriptyline for Fibromyalgia & Chronic Fatigue Syndrome'


Amitriptyline is a popular antidepressant that's available only in generic form in the U.S. It used to be sold under the brand name Elavil.

Amitriptyline is classified as a tricyclic antidepressant. For years, some doctors have considered it a front-line treatment for fibromyalgia( and chronic fatigue syndrome( However, this came about more from trial-and-error use than clinical studies.

Amitriptyline and other tricyclic drugs are thought to increase the amount of the neurotransmitters serotonin and norepinephrine that your brain can use. They do this by slowing down a process called "reuptake," which is when specialized cells absorb used neurotransmitters so they can be re-used elsewhere.


Other antidepressants, called reuptake inhibitors, use different mechanisms to achieve a similar effect.

Serotonin and norepinephrine are believed to be dysregulated in both fibromyalgia and ME/CFS.


Amitriptyline has a long history of use for ME/CFS, again despite a lack of clinical studies and because of real-world observations of improvement. Very little research has been done.


A 2012 study, however, did look at amitriptyline for ME/CFS and found that it was the only one among several antidepressants tested that inhibited mast-cell release of pro-inflammatory cytokines(, which are believed to play a role in ME/CFS.





For adults, a typical amitriptyline dosage can range from 40 mg up to 150 mg per day. It's generally divided into multiple doses.

It can take as long as a month for you to notice changes due to this medication.

Be sure to follow your doctor's instructions for taking this medication. If you want to quit taking it, don't just stop suddenly. Ask your doctor about the proper way to wean off of this drug.


There are many less common drugs such as scopolamine zantac360and choline


click links.html


\*This list not complete yet (please see 5 Treatment Protocols(brain://


Listing of therapies, protocols, drugs and supplements (in order of average effectiveness as reported by takers of a 'curetogether' poll)



Plus add items nopt listed from report


From: 'Treatments for ME/CFS'




# Prescription Treatments for ME/CFS


Azithromycin(– Azithromycin is an antibiotic that has antiviral and immunomodulatory properties. It may be effective against a broad range of bacteria, many of which have been linked to ME/CFS. A study found that 58 out of 99 ME/CFS patients had a decrease in symptoms while taking Azithromycin. Dr. De Meirleir and Dr. Nicholson are both advocates of this antibiotic and have used it on ME/CFS patients with some success.


Azithromycin is generally fairly low in side effects although sometimes causing stomach upset. It is normally taken 3 times a day (away from food) at a dosage of 500mg on each occasion.



Dr. Brewer’s Protocol(– This protocol involves patients taking either a nasal version of Amphotericin B or a compounded Nystatin that has to be atomised. Patients should also take a chelating PX. A pilot study by Dr. Brewer found that 56 out of 151 ME/CFS patients could not tolerate the Amphotericin B. 88 out of the remaining 94 patients (93.6%) had a reduction in symptoms. Approximately a third of these 88 CFS patients reached remission. Since this pilot study, Dr. Brewer has used a compounded and atomised Nystatin due to it being safer than the nasal Amphotericin B. The theory behind Dr. Brewer’s Protocol involves treating the sinus reservoirs of mycotoxins that may be causing ME/CFS symptoms.


Since replacing Amphotericin B with Nystatin, Dr. Brewer’s Protocol has become safer for patients, with followers of the protocol rarely reporting nasal side effects. Patients experiencing die-off symptoms range from 30-40% according to Dr. Brewer. The appropriate dosages of the compounded and atomised Nystatin and the chelating PX are provided by the compounding pharmacy.



Clonazepam(– This treatment is one of the most polarising ME/CFS treatments in existence. Clonazepam may benefit patients due to reducing the overstimulation of the brain and central nervous system. It also has potential effects as a sleep aid, neuroprotector and energy enhancer. Several ME/CFS specialists are advocates of Clonazepam under the right circumstances, such as Dr. Cheney. There are also many online reports of patients benefiting from Clonazepam.


The dark-side of Clonazepam involves countless ME/CFS patients’ online anecdotes stating that this drug has been the worst treatment they have ever tried as it has caused long term side effects. A dosage around the 0.5mg\- 1mg range is normally used on ME/CFS patients for sleep which is a lower amount than for other conditions. An even tinier dose is recommended by Dr. Cheney if the drug is used during the day with the motive of increasing the patient’s energy. Clonazepam shouldn’t be stopped suddenly and patients should gradually reduce the dose before ceasing treatment. The common side effects of Clonazepam include drowsiness and confusion. Some ME/CFS patients have reported other side effects such as a general worsening of their condition. As Clonazepam usage can be habit forming, patients often feel like they need to increase the dose to maintain efficacy which can be a dangerous process.



Dexedrine(– Dexedrine may benefit ME/CFS patients due to alleviating cognitive impairment, reducing fatigue and increasing energy. A small study found 9 out of 10 ME/CFS patients had reduced fatigue after taking Dexedrine in comparison to 4 out of 10 patients in the placebo group. Dr. Teitelbaum is a supporter of this treatment, believing that it increases energy and blood pressure. Dr. Goldstein has written that 1/3^rd of ME/CFS patients will improve as a result of taking stimulants and he has recommended amphetamine salts.


One of the risks of Dexedrine is that prolonged usage may lead to addiction. Dr. Goldstein has warned that if specific neurotransmitters are low in an ME/CFS patient, stimulants may increase ME/CFS symptoms. Dr. Rowe has recommended that ME/CFS patients begin with a 5mg dosage in the morning and if no improvement is noted, the dosage be increased to 10-15mg. Some patients may find that 5mg is too high for them to tolerate.



DHEA(– DHEA is a hormone produced by the adrenal glands. A study found that the majority of the Japanese ME/CFS subjects had DHEA deficiency. Several studies have found the use of oral DHEA and intravenous vitamin C to be useful in treating ME/CFS. Another study found normal DHEA levels in ME/CFS patients but low blood levels of a hormone that causes the adrenal glands to release DHEA.


Dr. Cheney has found that DHEA is more effective in less severe cases of ME/CFS and that sometime symptoms may worsen if severely ill patients take this treatment. Dr. Myhill recommends Pregnenolone as an alternative to DHEA. Some doctors have experienced success in prescribing lower doses of DHEA such as doses less than 10mg. Another ME/CFS specialist recommends 50mg every second day. Palpitations, hair loss, acne and an upset stomach are some possible side effects.



Fludrocortisone(– Fludrocortisone is a synthetically produced hormone. It may benefit ME/CFS patients with; hypotension, POTS, orthostatic intolerance or adrenal insufficiency. Its mechanism of action in ME/CFS patients could be due to; increasing blood volume, raising blood pressure and helping blood reach the bodies extremities. Three studies have been performed on ME/CFS patients taking Fludrocortisone with the ME/CFS patients’ level of improvement no better than the placebo group. According to Dr. Bell, Fludrocortisone is more likely to work on younger patients who are still somewhat active. Dr. Bell tries this treatment on almost all of his patients and says that it works well in approximately 25% of cases. If the drug doesn’t increase the ME/CFS patients’ activity levels by at least 50%, he stops the drug. Dr. Cheney believes that liquorice can have the same effect on patients as Fludrocortisone.


Many ME/CFS specialist recommend that Fludrocortisone dosages start at a very low amount such as a quarter of a 0.1mg tablet. Dr Rowe begins patients on a quarter of a tablet and if no side effects are noted, gradually increased this amount every 4-7 days to maximum of 2 tablets (0.2mg). Potassium and plenty of water should be used concurrently with this treatment. High blood pressure and depression are two possible side effects.



Gabapentin (Neurontin)(– Gabapentin is a anticonvulsant drug that may benefit ME/CFS patients due to reducing pain, increasing energy and improving sleep. Its mechanism of action may be its ability as a calcium channel blocker to reduce the excretion of certain neurotransmitters that cause pain and stimulate the brain. Anecdotally, a number of ME/CFS patients have gained extra energy as a result of taking Gabapentin however in some of these cases the extra energy has worn off. Dr. Goldstein lists Gabapentin amongst his five most favoured treatments for ME/CFS. Dr. Teitelbaum uses Gabapentin for its sleep effects and Dr. Enlander uses it for stopping the ‘abnormal impulses’ in ME/CFS patients’ brains. Three studies have found Gabapentin to be beneficial to Fibromyalgia patients in the areas of sleep enhancement and pain reduction.


Gabapentin is considered to be fairly safe with a Cochrane review finding that serious adverse effects were no more common in the Gabapentin group than the placebo group. Dizziness, somnolence, peripheral oedema and gait disturbance are the most common side effects. Dosages should begin at low levels and only be increased if tolerated. ME/CFS specialists tend to start patients at 100mg-800mg and if no side effects occur, the dose is gradually increased up to 2400mg-5000mg. These doses are the total daily dosages and should be split up into three dosages across the day.



Heparin (– Heparin is an anti-coagulant drug that may benefit ME/CFS patients who have hypercoagulation. A Heparin-ME/CFS study found all 9 patients gaining improvement with 5 noting significant improvement. Another paper refers to 60 ME/CFS/Fibromyalgia patients taking Heparin with an average improvement of 85%. Dr. Teitelbaum writes that Heparin helps about 50% of ME/CFS patients who haven’t benefited from any other treatment. It is imperative that ME/CFS patients have coagulation testing performed to determine Heparin suitability before commencing treatment.


Depending on what type of Heparin is used and what delivery method is chosen, the possible side effects of Heparin vary. If unfractionated Heparin is injected subcutaneously, regular blood tests to monitor treatment are a necessity. Heparin-induced thrombocytopenia is a potential side effect with this treatment although with Low Molecular Weight Heparin this is less likely to occur. A DEXA bone density test and liver and kidney function tests may be required before starting Heparin treatment. Sublingual Heparin and Low Molecular Weight Heparin are considered safer than unfractionated Heparin. Dr. Teitelbaum recommends those patients taking unfractionated Heparin start with 5000 unit injections twice a day and if blood tests are normal, the dose be gradually increased to a maximum of 8000 units twice a day.



Isoprinosine (Immunovir)(– Isoprinosine may benefit ME/CFS patients due to its effects as an antiviral as well as its various immunomodulatory properties. A study found that 6 out of 10 ME/CFS patients benefited by taking Isoprinosine. In those patients who improved, their CD4+, T-cells and natural killer cells dramatically increased. Dr. Sharp believes Isoprinosine is one of the most helpful, safest and cost effective drugs for ME/CFS patients.


Isoprinosone may increase uric acid levels and therefore shouldn’t be used by those with gout. ME/CFS specialists generally pulse the dosage of Isoprinosine so patients don’t develop a tolerance to the drug.



Low Dose Naltrexone (LDN)(– When used at low doses, Naltrexone causes the body to create more opioids which in turn may; relax the microglial cells, block pain, create endorphins and modulate the immune system. A small, pilot study on Fibromyalgia patients found that subjects experienced on average a 30% decrease in pain and fatigue while taking LDN. A second placebo controlled study on Fibromyalgia patients resulted in 32% of those taking LDN experiencing a significant reduction in pain as well as either a significant reduction in sleep problems or significant reduction in fatigue. Dr. Bihari reports that approximately 50% of ME/CFS patients are helped by LDN. Stories litter the internet of ME/CFS patients benefiting from this treatment.


LDN is considered one of the safest treatments for ME/CFS with few patients experiencing side effects. The most common side effect is sleep disturbance. The dosage used is normally in the 1.5mg-4.5mg range. LDN is generally taken at night before falling asleep.



Magnesium Injections(– A study found low red blood cell magnesium levels in ME/CFS patients. After intramuscular magnesium sulphate injections, 12 out of the 15 ME/CFS patients improved compared to 3 out 17 patients receiving the placebo improving. A study determined that despite normal magnesium blood levels, Fibromyalgia patients had low intracellular levels of magnesium. Dr. Myhill has found approximately 70% of her ME/CFS patients improving after receiving magnesium injections.


Magnesium injections can cause temporary pain at the injection sight. High doses may cause diarrhea. Intramuscular injections are generally given once or twice a week.



Melatonin– Melatonin is a hormone whose primary role as an ME/CFS treatment is to aid sleep. One study found that it improved ME/CFS patients’ ability to function and that it enhanced patients’ quality of life. Another study concluded that it reduced patients’ fatigue levels. Dr. Wright states that over 60% of his ME/CFS patients produce undetectable levels of Melatonin. As well as improving quality of sleep, this treatment may be beneficial due to its anti-inflammatory and antioxidant effects.


The most common side effects of Melatonin are morning drowsiness and headaches. These side effects may dissipate if the dose is decreased. Melatonin is listed in this section under the ‘prescription treatments’ umbrella due to a prescription being required to gain it in Australia despite formulations with negligible amounts of Melatonin being available over the counter. Other countries may have differing laws regarding prescription requirements to gain Melatonin. Some doctors use doses as low as 0.5mg while most doctors recommend doses in the 3-9mg range. It is normally taken at night, before sleep.



Myers’ Cocktail (– The Myers’ Cocktail is an intravenously administered mixture of supplements including; magnesium, calcium, vitamin C, B vitamins and sometimes further ingredients. A study on Fibromyalgia patients receiving this treatment found that most of the subjects noted improvements however the placebo group that received a saline solution also improved. Intravenous saline solution is considered by some to be an effective treatment for ME/CFS/Fibromyalgia hence it is conceivable that both groups did improve. The authors noted that both groups experienced “strong symptomatic relief.” Dr. Teitelbaum is an advocate of Myers’ Cocktails and believes they can provide ME/CFS patients with more energy. Dr. Majid Ali had found that 15 grams of intravenous vitamin C (an ingredient in Myers’ cocktails) can fix the abnormal shapes of ME/CFS patients’ blood cells and hence improve blood flow.


Some patients feel sleepy immediately after a Myers’ cocktail for a short period of time. If the patient feels excessive warmth, dizziness, nausea or a headache during the Myers’ cocktail IV, they should notify the physician. The dosages of the individual ingredients within a Myers’ cocktail vary and are at the physician’s discretion.



Nexavir (Kutapressin)(– Nexavir is a porcine liver extract that is administered via subcutaneous or intramuscular injection. Studies have found that Nexavir can inhibit EBV in vitro and HHV-6 replication in vitro by greater than 90%. A study of 270 ME/CFS subjects found that a staggering 96% of patients receiving more than 40 Kutapressin injections reached remission or near remission status. 71% of patients receiving 11-40 injections obtained remission or near remission levels. If an ME/CFS patient had high EBV-EA-IgG titres, they were more likely to improve in this study. A final Kutapressin study contained 130 ME/CFS patients with 85% noting significant improvements. 43% of patients reached remission while a further 42% of patients gained near remission status (they had a few residual symptoms). Dr. De Meirleir had found 67% of his ME/CFS patients responding to Nexavir in comparison to 17% receiving the placebo improving. Dr. Cheney, Dr. Enlander, Dr. Teitelbaum and Dr. Lapp have all been advocates of Nexavir or an analogous version of Nexavir.


Out of the 400 patients across both Kutapressin\- ME/CFS studies, only 1 person experienced new symptoms and a deterioration of function following Kutapressin injections. Some physicians are reluctant to prescribe antivirals including Valtrex or Famvir due to side effects and therefore prescribe Nexavir as a safer alternative. Nexavir is contraindicated in those allergic to pork or liver products. It shouldn’t be used by those taking MAO inhibitors. The most common dosage is 2mls administered daily although some patients start with a lower dose.



Nimodipine (– Nimodipine is a calcium channel blocker that is used to improve cognitive function or reduce pain in other illnesses. Dr. Goldstein found that Nimodipine improved ME/CFS patients’ cerebral blood flow (monitored through SPECT scans) and indeed this is the treatment’s primary usage in ME/CFS patients. Dr. Goldstein has labelled Nimodipine as one of the most useful treatments for both ME/CFS and Fibromyalgia. Dr. Mason Brown has found that Nimodipine helps 20% of ME/CFS patient quickly, another 20% over 6 months and the remaining patients to varying degrees. A report on Nimodipine usage in ME/CFS patients found that 9 out of 13 experienced enhanced mental clarity or improved general functioning.


Possible side effects of Nimodipine include; hypotension, nausea, headache, bradycardia, skin rash and peripheral edema. Specialists generally recommend starting at a low dose (some patients begin with as little as 1/16^th of a tablet). The maximum dose normally recommended for ME/CFS patients is 30-60mg taken 2-3 times a day.



Oxytocin (– This treatment is a neurotransmitter hormone whose most effective delivery method is widely considered to be injection, followed by nasal spray and finally tablets. The ME/CFS patients most likely to respond to Oxytocin are those with cold extremities. Dr. Flechas states that many ME/CFS symptoms are similar to those that an Oxytocin deficiency would cause. Dr. Goldstein found approximately 20% of his patients benefiting from Oxytocin injections and in those patients who do benefit, the improvement is dramatic. As well as Dr. Goldstein, the ME/CFS specialists; Dr. Lapp, Dr. Flechas and Dr. Teitelbaum all use Oxytocin injections on their ME/CFS patients.


Possible side effects of Oxytocin include; headache, weight gain, irregular heartbeat, nausea and dizziness. Intramuscular injections are sometimes given at 10 units and sublingual Oxytocin has been used by Dr. Cheney at 10 units up to a maximum of three times a day. Oxytocin should not be used by those who are pregnant.



Pentoxifylline(– Pentoxifylline belongs to a class of drugs called xanthine derivatives and its most common usage is to improve cerebral and peripheral blood circulation. It may also benefit ME/CFS patients by reducing; the cytokine IL-2, lowering NF-Kappa B and downregulating the cytokine TNF-alpha. All three facets of the immune system are thought to be high in ME/CFS patients and potentially contributing to symptoms. Pentoxifylline also has antiviral and further immunomodulatory properties. Dr. Leslie Simpson has noted that Pentoxifylline is useful at reducing cognitive problems and dizziness in ME/CFS patients.


Pentoxifylline should not be taken by those who cannot tolerate stimulants. It should also be avoided by those with a peptic ulcer or at risk of haemorrhaging. The drug hasn’t been well studied in ME/CFS patients but in other illnesses is considered safe and well tolerated at 1200mg per day. The standard dose of Pentoxifylline for various non ME/CFS illnesses is 400mg three times per day.



Rifaximin (Xifaxan)(– Rifaximin is an antibiotic that may benefit ME/CFS patients due to eradicating small intestinal bacterial overgrowth (SIBO). SIBO involves healthy bacteria in the large intestine being transferred to the small intestine thus causing gastrointestinal symptoms. Dr. Pimentel found 100% (42/42) of Fibromyalgia patients testing positive to SIBO compared to 20% of controls. The degree of pain experienced by Fibromyalgia patients in this study correlated strongly with the amount of hydrogen seen on the lactulose breath test. Rifaximin may also help ME/CFS patients as it balances gut flora. In vitro, 90% of the 536 strains of anaerobic bacteria tested were inhibited in vitro. Anecdotally, a reasonable number of ME/CFS patients have improved whilst on Rifaximin although many patients have had their symptoms return upon stopping the drug. Interestingly, some ME/CFS patients with no gastrointestinal symptoms improve. Dr. De Meirleir, Dr. Teitelbaum, Dr. Peterson and Dr. Myhill all use Rifaximin on their ME/CFS patients with some only using it after positive test results.


Rifaximin is generally well tolerated and only 0.4% of subjects in a traveller’s diarrhea study had to discontinue treatment due to side effects. The most common side effects are gastrointestinal. Long term usage of Rifaximin increases the chances of building resistance to the drug. Some specialists recommend a slightly lower dose of 550mg taken 2 times per day for 8 days. Other specialists recommend doses up to 550mg be taken 3 times per day for 14 days. It is recommended that probiotics are taken after Rifaximin usage.



Sleep Aids(– In the attached link I examine the various prescription sleep drugs that the ME/CFS specialists recommend. Dr. Cheney, Dr. Teitelbaum, Dr. Klimas, Dr. Lapp, Dr. Myhill and Dr. Enlander all have certain sleep inducing and sleep enhancing drugs that they try on their patients in a specific order.



Vitamin B12 Injections(– Despite often having normal B12 as determined by a blood test, ME/CFS patients commonly have low B12 levels in their brain. High levels of B12 being injected can ensure that sufficient B12 crosses the blood-brain barrier. B12 may also benefit ME patients by acting as a scavenger of nitric oxide, a compound that may contribute to ME/CFS symptoms. A poll found that 50%\-80% of Dr. Lapp and Dr. Cheney’s ME/CFS patients improved to some degree after taking B12 injections. A study found that ME/CFS patients were much more likely to respond to B12 injections if they had more frequent injections, a higher dose of B12, tried the treatment for longer and were taking oral folic acid. The study also found that the concentrated (5mg/ml) methylcobalamin form of B12 tended to be more effective than the hydroxocobalamin form (1mg/ml). Some specialists prefer the cyanocobalamin form of B12 as it is more stable. If an ME/CFS patient doesn’t respond to B12 injections, they may respond to oral folic or folinic acid. B12 is also available over-the-counter in a sublingual form however this isn’t necessarily as effective as the injectable versions. ME/CFS specialists inevitably opt for injectable B12 over other forms. Dr. De Meirleir, Dr. Lapp, Dr. Teitelbaum and Dr. Cheney are amongst a number of ME/CFS specialists to use this treatment.


When taking high doses of B12, a vitamin B complex is recommended to be taken concurrently. Although considered to be a fairly safe treatment, B12 may cause a temporary weakness in some patients. Dosage, type of B12, frequency of injection and method of injection vary depending on the physician’s preference.




# Over-the-Counter Treatments for ME/CFS (Non Prescription)


Artesunate(– Artesunate is a derivation of the herb artemisia and commonly used in the non-ME/CFS realm for its anti-malarial properties. It may benefit ME/CFS patients due to its potential anti-herpesvirus and anti-CMV effects. Using Artesunate, Dr. Cheney has doubled his number of ME/CFS cures and 75% of patients have shown some level of improvement using this treatment. Part of Dr. Cheney’s protocol involves the Artesunate being used concurrently with the herb wormwood.


Some ME/CFS patients taking Artesunate have reported dizziness or tiredness. Dr. Cheney recommends the brand Hepasunate be taken on three days of the week. As opposed to swallowing the capsule, he encourages patients to place half the contents of the capsule under their tongue for a period of a minute followed by swishing it around their mouth and spitting the remnants out.



Benfotiamine and Allithiamine(– These are alternate versions of high dose thiamine that may be better absorbed. Anecdotally, many patients have improved as a result of these treatments. Studies have shown that a thiamine deficiency can causes similar symptoms to ME/CFS and these symptoms can be resolved (especially fatigue) after treatment with high doses of thiamine. See ‘Thiamine\- High Dose’ for more information about thiamine and ME/CFS.


Theoretically, these treatments should be avoided by those who have cancer. Few side effects have been reported by those taking Benfotiamine and Allithiamine. It is difficult to determine a standard quantity for these ‘high dose’ treatments as patients have tried a wide range of doses. Anecdotally, ME/CFS patients online have commonly taken either 50-200mg of Allithiamine or 300-600mg of Benfotiamine.



Biotin(– Biotin deficiency has many shared features with ME/CFS. Several anecdotal accounts are online that mention Biotin greatly benefiting ME/CFS patients. High dose Biotin is currently being studied, with some promising results, as a treatment in progressive multiple sclerosis.


Biotin is normally a fairly safe treatment with few side effects noted. The dosages used by ME/CFS patients have often been in the 300mcg-1000mcg range. A neurologist from Massachusetts recommended that an ME/CFS patient take; 100mg of B1 (twice a day), 100mg of B2 and the high dosage of 5000mcg of Biotin for treating post-exertional malaise. This treatment benefited the patient.



Butyrate(– Butyrate may improve ME/CFS patients’ gut symptoms by creating T-cells in the digestive system. It may reduce cognitive symptoms, lower inflammation and enhance the immune system. Studies have shown that butyrate may be beneficial in treating ulcerative colitis and Crohn’s disease symptoms.


Butyrate is low in side effects and 1-2 capsules are usually taken with each meal.



Coenzyme Q10– Coenzyme Q10 is a treatment that when taken with L-Carnitine, has superior effects. These treatments both enhance mitochondrial function and hence may benefit ME/CFS patients. The active version of Coenzyme Q10, Ubiquinol is often preferred. A study found a close association between levels of Coenzyme Q10 and severity of ME/CFS. Dr. Lapp has found that about half of his patients benefit from Coenzyme Q10 generally by around 10%\-15%. A University of Iowa study rated Coenzyme Q10 as the leading treatment for ME/CFS with 69% of patients reporting it as beneficial. A study with 20 ME/CFS patients (80% of those deficient in Coenzyme Q10) found 90% had a reduction or complete disappearance of symptoms after 3 months of taking Coenzyme Q10.


There is a theory that taking Coenzyme Q10 as two doses throughout the day can increase its efficacy. There also exists a sublingual version of Coenzyme Q10. Alongside the energy boost that Coenzyme Q10 may provide, it occasionally causes insomnia. Those with diabetes or other types of hypoglycemia should be wary of Coenzyme Q10 as it can reduce blood sugar levels. The daily dose that is used generally varies from 50mg to 300mg.



Cordyceps Sinensis and Shiitake Mushroom(– Cordyceps Sinensis may enhance the immune system. A study on healthy subjects found ‘CordyMax’ increased aerobic capacity, reduced fatigue and lowered diastolic blood pressure. Another treatment that is similar to Cordyseps Sinensis is Shiitake mushroom which may increase interferon levels and have antiviral and immunomodulatory benefits. Anecdotally, numerous ME/CFS patients have reported more energy after taking versions of Shiitake mushroom supplements. A Japanese study that used injected ‘Lentinan’ taken from Shiitake mushroom on ME/CFS subjects found patients’ natural killer cell function increased. Recovery of the majority of patients studied took several months. Another study injected Lentinan into ME/CFS patients and found that 6 months of injections was required to normalise natural killer cell activity. Lentinan doesn’t get absorbed orally hence has to be given as an injection. Maitake and Reishi are another two of the many types of mushroom supplements used by ME/CFS patients. A study found that oral Maitake and oral Shiitake mushroom in combination significantly increased natural killer cell function in mice.


Most people that take Cordyceps Sinensis experience no side effects however rarely diarrhea and nausea can occur transiently. In the aforementioned study, subjects took 333mg of Cordymax three times per day with meals. Shiitake mushroom supplements may cause gastrointestinal symptoms or a rash. Shiitake mushroom supplements are sometimes used at daily doses between 400mg-1500mg, with this total daily dose broken up into smaller doses taken several times a day.



Curcumin(– Curcumin is a derivation of turmeric. A study found that curcumin benefited mice with ‘CFS.’ Dr De Meirleir has recommended this treatment to some patients. It may reduce cognitive impairment, improve HPA axis dysfunction and have anti-inflammatory and antioxidant properties. A study found that when Curcumin is supplemented with either; olive oil, stearic acid or choline, the brain and blood absorption levels of Curcumin dramatically increase.


Side effects from Curcumin usage are rare however if they do occur are generally of a gastrointestinal nature. Dosages used generally fall within the 500mg-1000mg range. Those with illnesses other than ME/CFS have ventured up to 8 grams of Curcumin a day. The absorption levels of the specific type of Curcumin used are relevant when determining a dosage.



D-Ribose(– This treatment may improve mitochondrial function and supply the body with energy. A pilot study found that 66% of ME/CFS patients significantly improved while taking D-Ribose. A follow up study involved 203 ME/CFS and Fibromyalgia patients that completed three weeks of treatment. The patients’ experienced: an average energy increase of 61%, a 37% improvement in well-being, a 30% increase in mental clarity, a 29% enhancement in sleep and a 16% reduction in pain.


D-Ribose shouldn’t be used by those with gout as it may raise uric acid levels. Side effects can include nausea, headache and sleepiness. In the above D-Ribose studies, patients took 5 grams of D-Ribose, three times per day. It may be wise to start at a lower dose, to gauge any potential side effects.



Energy Revitalization System(– This formulation contains a broad range of nutrients including a B vitamin complex. It also contains various amino acids, choline, malic acid and biotin. It was developed by Dr. Teitelbaum and it is claimed that it can replace taking 30 tablets in the one formulation. A number of the ingredients probably aren’t of a high enough dosage to have a therapeutic effect on some patients although other parts of this formulation contain reasonable dosages. Many ME/CFS specialists recommend that patients take a multi-vitamin tablet including Dr. Cheney who labels a quality multi-vitamin as “essential.” Energy Revitalization System isn’t a multi-vitamin tablet but rather a powder containing eclectic ingredients targeted at improving patients’ energy.


A small number of patients taking this treatment experience gastrointestinal symptoms. The typical dosage is one scoop (20.3 grams) per day.



Epicor(– Studies have shown that Epicor may improve natural killer cell function (which is almost inevitably low in ME/CFS patients) up to 4-fold. A similar substance, beta-glucan, may regulate other parts of the immune system too. A study that induced mice with ‘CFS’ found that beta-glucan significantly improved the symptoms of the mice.


Epicor and beta-glucan are considered to be fairly safe supplements. The standard dosing of Epicor and beta-glucan ranges from 200mg to 3000mg.



Essential fatty acids (EFA)– Essential fatty acids include such substances as; flaxseed oil, evening primrose oil and fish oil. The first study to examine EFA usage in ME/CFS patients provided patients with both omega-3 and omega-6, resulting in 85% of the patients showing at least moderate improvement. A second study on ME/CFS patients taking EFA found 90% of patients experiencing a reduction in symptoms. Another study that provided patients with eicosapentaenoic acid (EPA) found that all four patients improved while the same patients didn’t respond to a placebo.


Heartburn and gastrointestinal symptoms are some of the most common side effects of fish oil. The recommended dosing of EFA varies depending on what type of EFA product is being used. Fish oil is often used at 3000-4000 mg per day.



Far Infrared Sauna(– A study on 13 ME/CFS patients using a Far Infrared Sauna found two patients dramatically improve. The other 11 ME/CFS patients had a reduction in physical symptoms, lower levels of pain and reduced fatigue. Another study monitored the effects of Far Infrared Saunas on 10 ME/CFS patients. Average fatigue levels reduced on a 10 point scale from 6.7 to 4.8.


It is recommended to hydrate after a Far Infrared Sauna session with electrolytes. Also, many people shower when a session is completed to remove the excess sweat from their body. The Far Infrared Sauna user should also be cognisant of the signs of heat stroke. ME/CFS patients that do trial this therapy should start off for only a short period of time in the Far Infrared Sauna before gradually increasing the time period if they don’t experience side effects. Some patients slowly build up to having a maximum 15-30 minute session per day.



Fucoidan(– There is limited information online pertaining to ME/CFS patients taking Fucoidan. Despite this, over 850 studies on Pubmed detail many effects that may potentially benefit ME/CFS patients. These include; immune modulation, antiviral, anticoagulant and anti-inflammatory effects. A study found that Fucoidan reduced the amount of fatigue experienced by cancer patients.


Fucoidan is widely considered to be a safe treatment. Some people have experienced transient diarrhea while taking this treatment. Anticoagulants shouldn’t be used while a patient in on Fucoidan. Studies have found that the efficacy of Fucoidan is largely dose dependant. An osteoarthritis study determined that 1000mg per day had a much better effect on subjects that 100mg per day. Fucoidan has been largely untried by the ME/CFS patient community hence appropriate doses are hard to establish.



Germanium(– A 1988 paper reported that Dr. Greenberg found 25% of his ME/CFS patients showing “substantial clinical improvement” as a result of taking 300mg of Germanium a day. Dr. Maslin in the same paper found 150mg-300mg daily was sufficient to provide significant relief from ME/CFS symptoms in the majority of his patients and found 20% of patients to be non-responders. Dr. Anderson found half of his patients responding favourably to Germanium with doses for some patients needing to be as high as 1 gram.


If patients are keen to take high doses of Germanium, they should have regular tests to monitor kidney function. It may be wise for ME/CFS patients to start Germanium at a low dosage and gradually build up to 300mg per day. As the above specialists’ reports indicate, some patients may need high doses, up to 1 gram a day to experience the effects of this treatment. The safer, medicinal form of Germanium is known as organic Germanium-132, the inorganic form is not recommended for supplemental use.



Hawthorn(– Dr. Cheney has been an advocate of Hawthorn and did recommend its use in tandem with the prescription injectable, Nexavir. Hawthorn may improve the heart’s ability to pump blood around the body. Dr. Cheney trialled it on some of his patient and noted that it improved their cardiac output.


In low doses, Hawthorn is non-toxic. Side effects are fairly uncommon but may include; nausea, headaches and palpitations. Doses used generally fall between 200mg-1000mg.



Inosine(– The supplement, Inosine, is the active ingredient in prescription medication ‘Isoprinosine.’ A study on the prescription version of this treatment found benefits in 6 out of 10 ME/CFS patients. Dr. De Meirleir believes the supplement Inosine is as effective as the prescription formulation. Inosine is antiviral and an immunomodulator. Dr. Sharp has labelled its prescription cousin as “One of the safest, most cost effective and helpful drugs at our (ME/CFS doctors’) disposal.”


Inosine is fairly low in side effects although some patients have experienced insomnia and headaches. Inosine can raise uric acid levels so shouldn’t be taken by those with gout. ME/CFS patients commonly take inosine at a dosage of 500mg three times a day but only on five days of the week. The treatment isn’t taken on 2 consecutive days each week such as the weekend. A pulsing dosing structure of this treatment is recommended so the patient doesn’t build up a tolerance to the Inosine.



IP-6 (Inositol Hexaphosphate)(– The main mechanism of this supplement is to increase natural killer cell activity which is inevitably low in ME/CFS patients. Dr. Conley reports that he has used IP-6 to increase natural killer cell function in dozens of cases of ME/CFS. He notes one patient who went from being unable to work to working a 32-40 hour a week job as a result of taking IP-6. A related treatment that some patients use is Inositol. Inositol may be useful against insomnia and depression.


IP-6 is generally low in side effects with the most common being gastrointestinal. It is recommended that this supplement be taken on an empty stomach and twice a day. Some ME/CFS patients start with a lower dose of IP-6 such as 500mg and gradually increase this dosage to a total daily dose between 2-8 grams. The dose is taken at two separate occasions each day.



L-Carnitine– This amino acid could potentially benefit ME/CFS patients due to improving mitochondrial function. Acetyl-L-Carnitine may be better absorbed by the body than standard L-Carnitine. When taken in tandem with Coenzyme Q10, the positive effects may be magnified. A research centre found that out of 150 ME/CFS patients taking L-Carnitine, 69% noted an improvement in symptoms. A study found 12 out of 18 ME/CFS patients noting a statistically significant reduction in fatigue as a result of taking L-Carnitine. Another study found that 59% of ME/CFS patients taking Acetyl-L-Carnitine improved, 63% taking Propionyl-L-Carnitine improved but only 37% taking both treatments improved. The study noted that Acetyl-L-Carnitine mainly reduced mental fatigue while Propionyl-L-Carnitine was more likely to lower general fatigue. Studies have found ME/CFS patients low in cellular acylcarnitine levels. Deficiency of acylcarnitine can produce symptoms similar to ME/CFS. A study also found that as acylcarnitine levels improved in ME/CFS patients, symptoms improved.


L-Carnitine should be avoided by those ME/CFS patients with low thyroid. If side effects do occur, they may be of a gastrointestinal nature. L-Carnitine should be taken with food and recommended dosages range from 1000mg to 2000mg per day. Patients often start off with a lower dose before increasing the dosage if no side effects occur.



L-Serine(– L-Serine is an amino acid that former ME/CFS specialist Dr. Buttfield believes should help 60% of CFS patients significantly. Dr. Vallings found that 5/6 ME/CFS patients benefited from L-Serine supplementation. A study found that ME/CFS patients had “significantly reduced” levels of L-Serine in their urine when compared to healthy controls. The study continued on to note that those ME/CFS patients with low urinary L-Serine levels had mainly neurological symptoms and high levels of pain.


L-Serine side effects are fairly rare but may consist of sleep disturbance or gastrointestinal symptoms. Dr. Buttfield’s protocol consisted of beginning patients on 500mg of L-Serine in the morning and increasing this dosage to 2 grams per day.



Magnesium– The majority of ME/CFS specialists incorporate either oral magnesium or magnesium injections into their treatment protocol. Dr. Cheney believes magnesium can benefit ME/CFS patients due to; enhancing energy, improving sleep and lowering muscle pain. He advocates oral magnesium glycinate due to its ability to cross the blood-brain barrier and also be absorbed into cells. Other ME/CFS specialists prefer magnesium citrate due to its possible higher levels of bodily absorption.


Another facet of Dr. Cheney’s advocacy of magnesium glycinate is that this treatment is less likely to cause gastrointestinal symptoms. Other forms of magnesium are more likely to cause diarrhea. Magnesium should be taken with food and dosages should begin at low levels before increasing to the 200mg-400mg range.



NADH– This treatment is a form of coenzyme 1. A study found that 31% of ME/CFS patients improved while taking NADH in comparison to 8% of the control group improving. 18 out of 25 (72%) of ME/CFS patients enrolled in the longer follow up version of this study noted improvements. There is some evidence that it may take up to 6 months before certain ME/CFS patients respond to this treatment.


Side effects tend to be rare but mild overstimulation is possible. NADH should be taken on an empty stomach, before breakfast. Recommended dosages range from 5mg up to 20mg per day.



Naphazoline HCL(– Dr. Goldstein, who was an ME/CFS specialist, always tried Naphazoline HCL 0.1% eye drops as an initial treatment when a patient stepped into his office. He claimed that 20% of patients benefited from this treatment and in those patient who benefited, the benefits were remarkable and immediate. He theorised that those patients in the cohort of having severe anxiety were the most likely to respond. In some countries such as Australia, Naphazoline HCL is available over-the-counter.


The delivery process of this treatment involves placing a drop in each eye. Due to the nature of Naphazoline HCL, any benefits will be felt almost instantaneously. One of the most common side effects is local irritation. The occurrence of more serious side effects from this treatment is unlikely but may include; dizziness, headache or nausea. The dosage of the Naphazoline HCL eye drops used should be 0.1% and not 0.01%.



NeuroProtek(– NeuroProtek contains a number of eclectic supplements; luteolin, quercetin and rutin in tandem with the antioxidant, olive kernel oil. Anecdotally, many ME/CFS patients have reported a reduction in cognitive impairment as a result of taking NeuroProtek. A drawback is that often the cognitive impairment returns when the patient ceases taking the treatment. Neuroprotek may be able to normalise mast cell function.


Side effects of NeuroProtek are rare however caution is advised if the patient is concurrently taking drugs that are metabolised by the liver as NeuroProtek may alter the blood levels of these substances. The dosage of NeuroProtek is dependent on the patient’s weight, with a daily dose being 2 capsules taken per 20kg (44lbs) of body weight. The maximum dose, regardless of body weight is 8 capsules per day. Capsules should be taken with food and the dosage spread out across the day.



Nicotine Gum(– Former ME/CFS specialist, Dr. Goldstein wrote fondly of Nicotine Gum as a treatment for ME/CFS. He noted that patients experienced an improvement in energy, cognition and mood as a result of this treatment although did caution that some patients may get worse. It potentially benefits ME/CFS patients due to inhibiting brain inflammation. Several patients have noted an improvement in cognition and increase in energy as a result of this treatment.


Nicotine Gum can be detrimental to those with Crohn’s disease. Dr. Goldstein stipulates that occasional patients will have a worsening of ME/CFS symptoms as a result of taking this treatment. If a patient does improve on this treatment, benefit will be noted soon after taking the gum. One ME/CFS patient took a week before experience more energy. Nicotine may increase blood pressure which may be detrimental if an ME/CFS patient has high blood pressure. Longer term use of nicotine is also conducive to health problems such as addiction, periodontal problems and hair loss. If this treatment is trialled, a low starting dose is imperative.



Oxymatrine( (Equilibrant(– Equilibrant is Dr Chia’s own formulation of Oxymatrine that also contains; Astragalus, Olive Leaf, Liquorice and Shiitake Mushroom. Oxymatrine, derived from the Sophora plant, is thought to be effective against enteroviruses. Dr. Chia has trialled Oxymatrine on 500 ME/CFS patients and has found approximately 52% of his patients improve as a result of taking this treatment.


Common side effects of Oxymatrine can include headache, fatigue or an increase in ME/CFS symptoms. Oxymatrine should be avoided by those with autoimmune tendencies or seizure disorders. A low starting dose of Oxymatrine is essential for ME/CFS patients and the dosage should only be titrated upwards after a week. The maximum dosage of this treatment is in the realm of 200mg taken in the morning and 200mg taken in the afternoon. Dr. Chia’s Equilibrant doesn’t list the amount of Oxymatrine in the product however the recommended initial dosages of this product is 1 tablet per day for 1-2 weeks. This is followed by a gradual increase of dose, with patients taking up to a maximum of 6 tablets per day.



Piracetam(– Piracetam is a supplement that specifically targets enhancing cognition. It may also benefit ME/CFS patients due to increasing blood circulation. A study that gave fatigued patients (not necessarily those with ME/CFS) Piracetam and Cinnarizine (an antihistamine) found that patients’ physical fatigue significantly reduced. There exist several similar products to Piracetam that may also benefit ME/CFS patients and these are classed as nootropics.


In non-ME/CFS studies, Piracetam has rarely caused side effects. One study ascertained that 12% of subjects experienced sleep disturbances while taking this treatment. If a headache does occur while a patient is taking Piracetam, Choline may be a beneficial tandem treatment. Anecdotally some ME/CFS patients have stated that they can only tolerate a small dose of Piracetam\- in the 100mg range. Other patients even find this dose too stimulating. Starting at the normally recommended dosage is not recommended for those with ME/CFS. The dosage of Piracetam used for other indications can be up to 20 grams per day. ME/CFS patients generally require much smaller dosages in the 0.8-4.8 gram range. This dosage is spread out across the day and taken at three different occasions at 8 hour intervals. Different countries have various classifications on Piracetam pertaining to its over-the-counter or prescription status.



Post-Exertional Malaise Treatments(– This debilitating and central symptom of ME/CFS is often overlooked by doctors. There exists a range of treatment worth trying that I’ve written about in the attached link that benefit patients to varying degrees once in a ‘crashed’ state. These include; Hydralyte iceblocks, liquorice, D-Ribose, electrolyte solutions, leg elevation, massage, meditation, warm baths or cold baths.



ProBoost(– Also known as thymic protein A, a study found 16 out of 23 ME/CFS patients experienced a normalisation of immune function as a result of taking this treatment. There was a corresponding improvement in the clinical ME/CFS symptoms of patients in this study. Another study examined the use of thymic protein A in 6 ME/CFS patients with high EBV titre levels. Patients experienced an increase in energy and required less sleep to function. There exist several reports online of patients greatly benefiting from ProBoost. Many ME/CFS patients who feel run down or on the precipice of a virus take ProBoost.


Side effects as a result of taking ProBoost are rare with occasional patients reporting mild, flu like symptoms when they start this treatment. The dosage used varies depending on whether the patient is taking it as a maintenance dosage\- 1 packet a day or are fighting off an acute infection\- 3 packets per day. Dr. Teitelbaum recommends that ME/CFS patients take one packet of ProBoost, 3 times a day.



Propax with NT Factor(– This product contains a number of treatments all in the one formulation. Many of these lone treatments are individually used by ME/CFS patients including; quercetin, L-Glutathione, NAC, grape seed extract, various B supplement and NT factor. A study that was ominously run by the company that produces this product found that those with the symptom of severe fatigue (not necessarily ME/CFS) experienced a reduction in fatigue by on average 40%. Another study found Propax with NT Factor reduced the fatigue experienced by cancer patients. Propax with NT Factor is potentially a form of ‘lipid replacement therapy’. This entails repairing damage to a patient’s mitochondrial membranes. A study examined lipid replacement therapy’s efficacy on ‘moderately fatigued patients.’ As subjects mitochondrial function improved while taking lipid replacement therapy, their fatigue proportionally reduced.


Propax with NT Factor is considered to be a safe product with gastrointestinal symptoms rare but possible. It is recommended that the packet be consumed 2-3 times a day. The tablets in the formulation can be taken with or without food and the soft gel capsule that contains omega-3, EPA and DHA should be taken with food.



Ranitidine(– Ranitidine is a treatment that former ME/CFS specialist Dr. Goldstein found benefited those with infectious mononucleosis. He then began using this treatment on ME/CFS patients with some success. If Ranitidine is not available over the counter in a country, often the alternative Cimetidine is. Dr. Goldstein has found that about 90% of mononucleosis cases respond to Cimetidine. When an ME/CFS patient does respond to one of these drugs, Dr. Goldstein notes that the recovery is remarkable. Approximately 20% of Dr. Goldstein’s ME/CFS patients respond to this type of drug.


Stimulation and headaches are two of the most common side effects of Ranitidine treatment. Dr. Goldstein recommends that 150mg of Ranitidine be taken twice a day. The alternative, Cimetidine, should be taken at 300-400mg. Dr. Goldstein has written that it may take from one hour to one week before a patient notices whether this treatment is working for them.



Selenium (high dose)(– Numerous patients online have noted great benefit from this treatment. The symptoms that have generally improved in these patients are cognitive ability and energy. High dose Selenium may benefit ME/CFS patients due to its antiviral and strong antioxidant properties.


Taking high dose Selenium for more than several months is not recommended as it may increase the chance of toxicity, although Selenium toxicity generally occurs at higher doses (the 2400-3000mcg range). Overdosing on Selenium can cause numerous symptoms. The recommended dosage of the high dose Selenium protocol is between 400-800mcg a day. Some ME/CFS patients have noted side effects if they increase the dosage past 400mcg. The Selenium should be taken on an empty stomach to increase absorption. Yeast-free selenomethionine is thought to be the best form of Selenium to take although other forms may benefit certain patients more effectively.



Sleep Aids(– In this link I present various ME/CFS experts’ opinions on sleep aids including many over-the-counter formulations.



Sulforaphane(– This compound may benefit ME/CFS patients due to shifting the immune system from Th2 dominant to Th1 dominant. Sulforaphane is also an antioxidant, neuroprotective, defensive against oxidative stress and may improve mitochondrial function. It has been studied in autism and benefited those who took it through a mechanism the authors suspected may be due to inducing a “fever effect.”


In the aforementioned autism study, those taking Sulforaphane experienced a tiny increase in their liver enzymes. There is quite some conjecture about the amount of Sulforaphane the body absorbs. This is partly due to the possible discrepancy between the specific forms of Sulforaphane ingested. It is therefore difficult to pinpoint a commonly used dosage.



Thiamine (high dose)(– Anecdotally, some ME/CFS patients have reported benefits from taking high doses of thiamine (vitamin B1). A small study of Fibromyalgia patients found all 3 patients benefiting from high dose thiamine treatment. Thiamine deficiency (which can be caused by a defective enzyme system) can produce similar symptoms to ME/CFS. A study found that fatigue associated with ulcerative colitis and Crohn’s disease can be caused by a thiamine deficiency and that high doses of thiamine resolved this fatigue. Despite this, across multiple studies examining various disease state, patients have normal blood thiamine levels yet improve significantly when taking high dose thiamine. A study has speculated that this may be due to low cellular thiamine transportation or enzymatic problems.


The three Fibromyalgia patients studied experienced no side effects as a result of high dose thiamine. Patients with other disease states taking high dose thiamine have reported insomnia and tachycardia. In the Fibromyalgia\- high dose thiamine study, patients started at 600mg of thiamine a day and gradually increased this dose. Abrupt improvement was seen when patients reached 1800mg a day. Anecdotally, ME/CFS patients that have responded to high dose thiamine seem to have an optimal dose that varies from patient to patient. The challenge is to find this optimal dose without exceeding it and experiencing any side effects. If a patient doesn’t respond to thiamine, they may benefit from Benfotiamine or Allithiamine, which may be better absorbed.



Vagus Nerve Stimulation(– Dr. VanElzakker has theorised that the vagus nerve being infected could explain many of the features of ME/CFS. The vagus nerve has been implicated in several other illnesses such as epilepsy, with stimulation of the nerve proving beneficial. A study implanted Fibromyalgia patients with a vagus nerve stimulation device with the authors concluding that it was a “useful adjunct treatment.” A less invasive measure to stimulate the vagus nerve involves attaching a TENS machine’s electrode pads to the tragus part of the ear.



Vitamin D– Vitamin D deficiency can often be a secondary problem that arises when ME/CFS patients are unable to get proper supplementation from sunlight. A retroactive study of 221 ME/CFS patients found that Vitamin D levels were “moderately to severely suboptimal in CFS patients.” Numerous patients online have benefited to some degree from Vitamin D supplementation. Dr. Lapp recommends Vitamin D3 to almost all of his ME/CFS patients.


Vitamin D side effects are rare at normal doses yet high Vitamin D may cause weakness, headaches or gastrointestinal symptoms. Some patients gain Vitamin D from sunlight or through daily lower level supplementation in the 1000-2000IU range that is available over-the-counter. To definitively raise Vitamin D levels, a single or once a month for several months prescription dose may be required. This may on occasions be as high as 100,000IU. Blood tests can monitor Vitamin D levels yet there is some conjecture about what levels are considered suboptimal. Studies have suggested that those with any form of chronic illness should try and maintain higher vitamin D levels than the healthy population.



## About These Lists


The key purpose behind creating the above lists was to show patients who have lost hope that there are treatment ideas for this illness. Another purpose of these lists was to compile much of the information that was spread haphazardly across this blog in a centralised and easy to access location.


As I continue to write about other ME/CFS treatments on my blog, I will add them to this treatment page. There are many more treatments that I didn’t include in the above lists but ME/CFS patients may benefit from. The following are just some treatments that may help ME/CFS patients based on either study results or their use by some ME/CFS specialists; various probiotics, Glutathione, N-Acetyl Cysteine, methylation cycle treatments, MAF 314, IV saline solution, Gamma Globulin injections/IV, Lidocaine IV, Valtrex, Valcyte, Ergoloid, Levofolinic Acid, Nifedipine, Galantamine, Ampligen and Rituximab.


There seems to be a degree of disease heterogeneity( across the entire collection of ME/CFS studies and indeed often within single ME/CFS studies. Some studies require that just the overly broad Oxford Criteria be met for patient inclusion. In contrast, other studies are narrower and demand more severely affected patients sharing more common symptomology. Many ME/CFS studies aren’t adequately funded and hence; don’t have a high number of participants, lack a placebo group and aren’t considered high quality. If these idealistic studies existed, I would have written more about these and the corresponding treatments but unfortunately they don’t.


It is for the above reasons that I often place a greater emphasis on what an ME/CFS specialist (who has stringently diagnosed ME/CFS) has found the clinical response rate of a treatment to be e.g. 30% of responders. This is why I have attempted to include as many clinical observations and comments from ME/CFS specialists as possible in the above lists.


Finally, I should emphasise that patients should always consult with their physicians prior to taking any treatment. I am not a doctor and nothing on this blog should be construed as medical advice. It is imperative that patients and their physicians are aware of possible side effects, including those not listed before starting any treatment. Patients should also be aware of possible interactions between any treatment they commence and their current medications. Some treatments listed are recommended for short term use only while other treatments may require up to 6 months of usage before effects may be noticed. ME/CFS patients are renowned for having a higher sensitivity to treatments than patients with other diseases. In many cases it is wise to begin treatments at a lower dose to mitigate the chance of more severe side effects.





A Typical Neurosomatic New Patient Treatment Protocol


*Agents tried sequentially Onset of Action Duration of action*


1. Naphazoline HCL 0.1% gtt ┬OU 2 - 3 seconds 3 - 6 hours


2. Nitroglycerin 0.04 mg sublingual 2 - 3 minutes 3 - 6 hours


3. Nimodipine 30 mg po 20 - 40 minutes 4 - 8 hours


4. Gabapentin 100-800 mg po 30 minutes 8 hours


5. Baclofen 10 mg 30 minutes 8 hours


6. Oxytocin 5-10 U IM or BID




Syntocinon 1-2 puffs TID 15 minutes - 72 hrs 12 - 24 hours


7. Pyridostigmine 30 - 60 mg po 30 minutes 4 - 6 hours


8. Hydralazine 10 - 25 mg po 30 - 45 minutes 6 - 12 hours


9. Mexiletine 150 mg po 30 - 45 minutes 6 - 8 hours


10. Tacrine 10 mg 30 minutes 4 - 6 hours


11. Risperidone 0.25 - 0.5 mg 45 - 60 minutes 8 - 12 hours


12. Pindolol 5 mg BID 15 minutes - 7 days 12 hours


13. Lamotrigine 25 - 50 mg QD 30 - 45 minutes 24 hours


14. Sumatriptan 3 - 6 mg SQ 15 - 30 minutes 16 hours


15. Ranitidine 150 mg BID 1 hour - 1 week 12 - 24 hours


16. Doxepin HCL elixir 2 - 20 mg HS 1 hour variable


17. Sertraline 25 - 50 mg QAM




Paroxetine 10 - 20 mg QAM 1 hour - 8 weeks 1 - 2 days


18. Bupropion 100 mg TID 30 minutes - 8 weeks 8 - 24 hours


19. Nefazodone 100 - 300 mg BID 2 - 8 weeks 24 hours


20. Venlafaxine 37.5 - 75 mg BID 1 - 4 weeks 24 hours


21. Glycine powder 0.4 Gm/Kg/day in juice




Cycloserine 15 - 20 mg QD 1 hour 24 hours


22. Felbamate 400 mg 30 minutes 6 - 8 hours


23. Lidocaine 200-300 mg


A-Z Treatments (Comments are by Dr. Goldstein)


*Acetazolamide* (*Diamox*): This drug is a carbonic anhydrase (CA) inhibitor which is routinely used as a cerebral vasodilator in nuclear medicine. Patients will occasionally have a reduction in symptomatology with acetazolamide. Acetazolamide 250 mg eliminated the pain of a 41-year-old female patient with post-traumatic fibromyalgia, helped her feel very relaxed, and markedly reduced her other symptoms.


*Acetyl-L-Carnitine*: In theory, a good drug. It should work as an acetyl group donor to increase acetylcholine, and the carnitine has already been shown to be effective in a double-blind experiment by the Drs. Plioplys. Acetyl-L-carnitine also increases the levels of nerve growth factor (which are four times normal in the spinal fluid of FMS patients) and increases other transmitters like adenosine and ATP. In practice, a semi-dud.


*Adderall*: An amphetamine combination that a few patients find more energizing than plain dexedrine. Only about a third of CFS patients have a good response to stimulants, which act by squeezing dopamine (DA) and norepiniphrine (NE) out of neurons and glia. If these transmitters are much too low already, giving stimulants will further lower the signal-to-noise ratio and increase symptoms.


*Amantadine*: A weak NMDA antagonist. Helpful for a few patients. Doses higher than the PDR recommends may be more effective, but there is an increased risk of adverse drug reactions when exceeding this dose. Israelis have given 100 mg IV with good results in neurogenic pain. IV amantadine is not available in the USA. Amantadine, ketamine, dextromethorphan, and a new MNDA antagonist, memantine, can be used in trigger point injections as well as gel applications for local pain.


*Ambien*: The best sleeping pill. Does not cause dependence except in unusual circumstances.


*Aricept*: A cholinesterase inhibitor marketed for Alzheimer's disease. Has the advantage of once-a-day dosing and no requirement for liver function test. Does not work as well as Cognex, perhaps because it is not a potassium channel blocker. Cognex has several effects on neurotransmitters relevant to CFS/FMS.


*Ascorbic Acid* (*Vitamin C*): Recent research into the role of ascorbic acid in the brain (which has the highest concentrations of this substance in the entire body) has shown that this agent may be beneficial in certain patients with CFS. Ascorbate has been found to be neuroprotective, particularly by inhibiting the redox site of the NMDA receptor and diminishing calcium influx. Trials of high-dose oral ascorbic acid have been generally disappointing. Administration of ascorbic acid is done via IV doses of 25 to 50 grams diluted in half-normal saline of Ringer's lactate over a period of about 90 minutes. Adding magnesium sulfate is recommended because ascorbic acid can cause magnesium shifts from extracellular to intracellular compartments. It is beneficial to add 500 mg of calcium gluconate since ascorbic acid is a calcium chelator and could possibly lower serum calcium. Responders to IV ascorbic acid generally feel considerably better in most respects the day after treatment.



*Baclofen*: A greatly under used medication. A GABA-B agonist with few ADRs, it has an immediate onset of action and is still in my top 10.


*Vitamin B12*: Besides being vital to transmethylation (which helps to synthesize NE), B12 2g. orally in AM decreases inappropriate daytime melatonin secretion, thereby aiding in the treatment of the delayed sleep-wake cycle many CFS patients experience. Very large doses (10 g) may aid transmethylation.


*BuSpar*: The ideal anxiolytic in all respects except efficacy. Best used as an SSRI augmentation agent, especially combined with Visen (not generic Pindolol). Augmentation strategies, of which there are many, do not work nearly as well in CFS as they do in major depression disorder.


*Clonidine*: Another greatly underused drug. Can be good for central pain, ADD, anxiety. Helps all symptoms in some patients. Eliminates nightmares. Safe and cheap. Comes in a patch that lasts all day. Better than Zanaflex, another alpha-2 agonist. Tolerance and depression have not been much of a problem. Adverse drug reactions to clonidine can be reversed by yohimbine, an alpha-2 antagonist. Guanfacine (Tenex) is a less sedating alpha-2 antagonist with a 24-hour duration of action.


*Dexedrine*: An effective stimulant. Makes some patients calm also. May synergize with Ultram. Desoxyn may be better but has neurotoxicity. Many patients like Adderall more.


*Depakote*: In the CFS population its only value is in migraine prophylaxis, for which it is excellent.


*Dilantin*: Useless in every CFS patient I have treated with it.


*DHEA*: Theoretically excellent, it is a neurosteroid which is a GABA antagonist, not necessarily a good thing for some patients. Pregnenolone should be the best neurosteroid (low in PMS).


*Felbamate*(*Felbatol)*: Not used much because of requirement for hematologic and liver function test monitoring. Should be tried in every treatment-resistant patient. May work when nothing else does, especially for intractable headaches. It may cause headaches, however. There's no free lunch.


*Gabapentin* (*Neurontin*): Gabapentin, an antiepileptic drug with a novel mechanism of action, has become one of my five favorite medications (the others are oxytocin, nimopidine, baclofen, and intravenous lidocaine) to treat neurosomatic disorders.



*Gabitril*: The only GABA reuptake inhibitor (like Prozac is a serotonin reuptake inhibitor). Very effective and very safe if you follow PDR dosing suggestions. Increase the dose too rapidly and the patient may get delirious or manic. Effects are reversible with flumazenil if necessary.


*Gingko Biloba*: Useful only for sexual dysfunction induced by serotonin reuptake inhibitors (SRIs). Inhibits platelet aggregation. Rare reports of brain hemorrhage. This adverse reaction raises the risk/benefit ratio.


*Ginseng Saponins*: Works a little like nitroglycerin, which converts to nitric oxide. Increases energy slightly.


*Gotu Kola*: A mild stimulant with no apparent adverse reactions.


*Honey Bee Venom*: As with any "natural product," bee venom has a multitude of ingredients. Patients should be skin tested for bee venom allergy first. Major constituents from my point of view are phospholipase A2 (PLA2), which makes arachidonic acid, the precursor to eicosanoids (prostaglandins, leukotrienes, etc.), dopamine and NE. When it works, the patient often feels like he has been injected with rocket fuel. Effects last about one to two weeks. Has made three patients worse, two of whom were father and daughter. Patients should have an Epi-Pen (if available) and an antihistamine with them at all times. Plaquenil antagonizes PLA2. Arachidonic acid combines with effianolamine in the brain to make anandamide, an endogenous cannabinoid (like marijuana).


*H2 Receptor Antagonists*: The first treatments I developed for CFS were cimetidine and ranitidine. I based this therapy on my successful experience treating acute infectious mononucleosis with cimetidine. When a CFS patient responds to an H2 antagonist (I use ranitidine), the onset of action is similar to that seen in acute infectious mononucleosis, i.e. one or two days at a dose of 150 mg b.i.d. Usually all symptoms are ameliorated. Some patients are unable to take any does of ranitidine because it makes them “hyper.”



*Hydergine*: The most underused effective medication in the PDR. Extremely safe. A dopamine and acetylcholine agonist. There is nothing else like it. Other dopamine agonists seem to be restricted in action to the nigrostriatal dopaminergic tract, which is not important in CFS symptoms. Not the case with Hydergine, which is quite helpful for alertness, especially in those sedated by Baclofen. As with most medications listed, it can sometimes help all symptoms.


*Oxytocin*: Oxytocin has a wide range of behavioral effects. Oxytocin neurons project to many areas of the limbic system, as well as to the frontal cortex. Oxytocin is involved in maternal behavior, female and male sexual behavior, feeding, social behavior, and memory. It also has effects on cardiovascular, autonomic, and thermoregulatory processes. Approximately one-fifth of my patients have a good response to IM oxytocin after failing to respond to numerous oral agents. Cognitive clarity is the most responsive symptom, with fibromyalgia and pain being second.


*Kava-Kava*: One of the two best "natural products" for CFS. May take up to eight weeks to have an effect. No adverse drug reactions.


*Ketamine*: The best single agent for CFS/FMS and all other neurosomatic disorders. Known best as an NMDA receptor antagonist (the NMDA receptor is one of the several receptors for the excitatory amino acid glutamate), it increases dopamine in the limbic system, a very important objective in CFS. I administer it by slow intravenous infusion or in PLO gel for transdermal (through the skin) absorption. The intravenous route is more effective, but transdermal application can be done daily, and if effective, can obviate peaks and valleys and need for IVs. I have seen no cases of Ketamine abuse among my patients. Ketamine is one component of my "resurrection cocktail," for patients who have been bedridden for more than a year and whom I may only see once. The others are IV ascorbate, IV lidocaine, IV thyrotropin\- releasing hormone (which raises all biogenic amines plus acetylcholine), Nimotop, and Neurontin (still the most effective oral agent but is being pushed by Tasmar). I am doing trials with Ketamine eyedrops.


*Klonopin*: The benzodiazepine to use if you are going to use one. Affects neurosteroid biosynthesis.


*Kutapressin*: I don't know how this drug works, but some patients have immediate symptomatic improvement after 2 ml IM. I don't usually prescribe it otherwise since there are so many immediate-acting options. It does increase bradykinin, and adverse drug reactions may be treated with drugs like Vasotec (ACE inhibitors).


*Lamictal*: One of the new anti-epileptic drugs. All of them increase GABA, and most of them are N-methyl-d-aspartate (NMDA) antagonists. Works immediately. The main adverse drug reaction is a rash, which can be minimized by gradual dosage escalations. Affects all symptoms. 50-100 mg of Larnictal and 800-1200 mg of Neurontin have rendered euthymic in 30 minutes every patient with acute manic excitement I have treated. Zyprexa and Rilutek could be added to this cocktail if necessary. Lamictal is also an antidepressant and may also work over four weeks or so.


*IV lidocaine*: In addition to its actions mentioned in *Betrayal by the Brain*, it also acts as an NMDA antagonist. It is the second best treatment. I have given it about a thousand times without a serious adverse drug reaction. Patients have come with great difficulty from other states or countries with the common lament of "If you can't help me I'm going to kill myself' (I hear this about twice a week). At least two patients, achieving complete symptomatic relief with IV lidocaine, returned home and could not find a physician or nursing service to administer it. Since they could not move to southern California, they were again bedridden and had to crawl to the bathroom. Not able to live this way any longer, they committed suicide, a worse outcome than the lidocaine toxicity, which never happens. Many physicians will not prescribe any of the medications I use, even if they help their patients a lot. Some medium-sized cities have not one physician who will care for CFS patients. I must treat them from afar, a hazardous practice medicolegally.


*Marinol*: Marinol-deta-9-tetrahydrocannobinol is a medication I use rarely, because of the medicolegal implications. Among other things, it is a dopamine agonist in the limbic system (at the nucleus accumbens, a key structure in CFS), but an indirect one. It is also a calcium channel blocker. A few patients get total symptomatic relief with Marinol when one hundred other medications have failed. One such patient is applying for disability only because she cannot afford it. It is one of the last and best options for treating the diffuse pain of FMS, and is good for atypical facial pain. In five years it should be used routinely in many situations.


*Methadone*: Another drug I don't use very often, and for the same reason, although California has passed a law that physicians cannot be prosecuted for using opioids responsibly to treat chronic pain. Thus, it is less risky for me. Physicians in some states are afraid to prescribe it. It is the opioid of choice. Besides being an agonist at the mu opioid receptor, it is an NMDA receptor antagonist (like Ketamine), and blocks the serotonin transporter (like SRIs). I described its use as an antidepressant about 15 years ago in the medical literature. It is very cheap, does not produce much opioid euphoria, and often ameliorates all neurosomatic symptoms.


*Nicotine Patch or Gum*: I have been prescribing nicotine in these forms for a long time. Nicotine is analgesic, probably by virtue of its stimulating secretion of dopamine and norepinephrine. It binds to the nicotinic cholinergic receptor and can also have profound effects on mood, energy, and cognition. An occasional patient will have worsening of symptoms with nicotine.


*Papaverine SA*: Marketed many years ago as a vasodilator, this medication will probably be discontinued shortly. It is the only drug available that inhibits adenylate cyclase, thereby increasing cyclic AMP, which you may recall from biology class as being pretty important. There is an experimental antidepressant, rolipram, which has a similar mode of action. It preferentially affects energy, alertness, and cognition, and has very few adverse drug reactions. It is a top-10 drug (cheap, too).


*Pentazocine* (*Talwin*):Occasionally, an extremely treatment-resistant individual has felt much better after taking pentazocine plus naloxone (Talwin-Nx).


*Spironolactone (Aldactone)*: Spironolactone (a mineralocorticoid receptor antagonist) has been used for several years to treat premenstrual syndrome. My experience with spironolactone is that it helps only occasionally, but the effect is rapid (30 minutes or so), and thus can be assessed while the patient is in the office.


*St. John's Wort*(*Hypericum*): The other good "natural" remedy for CFS.


*Tasmar* (*Tolcapone*): Neither an exotic location on the Silk Road nor a Mafia-run turnpike in Chicago, Tasmar is a unique agent. It inhibits the enzyme catechol-ortho-methyltransferase (COMT), one of the two enzymes (monomine oxidase is the other) that metabolizes dopamine and norepinephrine. Tasmar degrades them in the synaptic cleft. I have been waiting for this drug for years. It is marketed for Parkinson's disease, and most physicians have not heard of it yet. It can work as monotherapy, either acutely or after four weeks or so. It may be more effective (immediately) when combined with a dopamine agonist such as Requip (quinpirole) or a reversible inhibitor of monoamine oxidase (RIMA) such as meclobemide, which due to the wisdom of the FDA is available in every other industrialized country in the world but the USA. The package insert advises against combining it with irreversible MAOIs such as Nardil and Pamate, so I have not done so. This combination would leave reuptake as the only mechanism to terminate the post-synaptic effect of catecholamines, although rats do quite well on the two drugs. An accountant, unable to work for three years, is back to work now on meclobemide and Tasmar. Adding Sinemet may enhance the action of Tasmar, since it is metabolized to dopamine. Sinemet may be given instead of Requip or Mirapex, or concomitantly. Requip and Mirapex are useful in that they are D3 agonists also. The D3 receptor is located primarily in the limbic system. Since COMT is a methyl group acceptor, it may work better by combining it with S-adenosylmethionine (SAMe), a methyl group donor with no adverse drug reactions, effective in FMS and depression. SAMe is available in many other countries, and certain buyer's clubs will supply you with it. Tasmar inactivates COMT, allowing SAMe to transfer methyl groups to precursors so that more norepinephrine can he formed. This process is termed "transmethylation" and is too complicated to discuss further in this column. Interested readers may consult the work of John R. Sinythies and R.J. Baldessarini and go from there.


*Topamax*: Another new AED, Topamax has a little more affinity for the ANWA glutamate receptor, as well as the NMDA receptor. It has very few adverse drug reactions, and when it works, is quite energizing. Agonists at the third major class of glutamate receptor, the "metabotropic," of which there are of course various subtypes, are being developed as anxiolytics.


*Viagra*: I don't have enough money to buy stock in anything, but buying Pfizer a few months ago would have been almost as good as buying Microsoft in 1985. This drug works by inhibiting type 5 phosphodiesterase, one of the six known enzymes to degrade cyclic GMP (as important as cyclic AMP, but maybe not covered in biology class). Type 5 is supposed to be specific for the corpus cavemosurn of the penis and probably the clitoris as well. It is not all that specific, though, at least in my patients, who frequently experience flushing and headache. When Viagra works in CFS/FMS, patients experience a reduction in all symptoms. One patient whom I have been treating for 10 years had not responded to one medication until she took Viagra, whereupon she felt almost normal. Nitroglycerin and hydralazine, which stimulate cyclic GMP by different mechanisms, had not helped her.


*Zyprexa*: One of the new "atypical neuroleptics," with Risperdal and Seroquel, Zyprexa can he used as a sleeping aid, antidepressant, anxiolytic, and of special relevance to my practice, is probably the most effective treatment for borderline personality disorder. You can look up the symptoms in the DSM-IV, personality disorder.




“Treatment Protocol for Physicians.” *The National Forum:*


*Dr. Goldstein's summary of his protocol for physicians.*


Goldstein, Jay A.*Betrayal by the Brain: The Neurologic Basis of Chronic Fatigue Syndrome, Fibromyalgia Syndrome, and Related Neural Network Disorders.*Binghamton, New York: Haworth Medical Press, 1996.


*This book is filled with valuable information about how the CFS/ME brain works, and how medications affect it, but you will need a background in biochemistry to make full use of it.*


“The Neuropharmacology of Chronic Fatigue Syndrome.” Jay Goldstein: **(


*In this article, Dr. Goldstein provides an in-depth discussion of diagnosis, tests, associated* *disorders, and neurological findings in CFS/ME patients. From these, Dr. Goldstein draws the conclusion that other than limbic encephalopathy there is no other no other mechanism that could create the constellation symptoms found in CFS/ME.*













Anticonvulsants: Neurontin (g

abapentin), Gabitril (tiagabine) Lyrica (pregabalin)

Antidepressant Drugs: doxepin, amitriptyline, nortriptyline, desipramine, imipramine, trimipramine, clomipramine,

fluoxetine, sertraline, paroxetine, citalopram, excitalopram, bupropion, phenalzine, tranylcypromine,

trazadone, venlafaxine, duloxetine, mirtazapine

Antifungal Agents: Nystatin, Diflucan, Nizoral, Sporanox

Antihistamines: Benadryl (diphenhydramine), Claritin (loratadine), Allegra (fexofenadine), Zyrtec (cetirizine), Chlor\-

Trimeton (chlorpheniramine maleate), Atarax and Vistaril (hydroxyzine), Dramamine (meclizine), DiVertigo

Antiviral Agents: acyclovir, famcyclovir, amantadine, valacyclovir, valganciclovir


Benzodiazepines: clonazepam, diazepam, alprazolam

Beta Blockers: propanolol (Inderol), atenolol (Tenormin), labetalol (Normodyne), nebivolol (Bystolic)

Calcium Channel Blockers: Nicardipine, Nimodipine, Nifedipine, Verapamil

Central Nervous System Stimulants: Ritalin, Dexedrine, Lonamin, Provigil, Strattera

Cytotec (misoprostol)

Diamox (acetazolamide)

Epogen (Procrit)

Flexeril (cyclobenzaprine)

Florinef (fludrocortisone)

Gamma Globulin



H2 Blockers: Tagamet (cimetidine) and Zantac (ranitidine)

Hormones: Growth Hormone, Testosterone, Thyroid Hormones, Hydrocortisone

Hypnotics: Ambien, Lunesta, Rozerem, Xyrem

Kutapressin (see: Nexavir)


Naltrexone (LDN)

Nexavir (formerly Kutapressin)



Pain Relievers: Aspirin, NSAIDs, Tylenol, Aleve, Ultram, Narcotics



Pyridostigmine (Mestinon)

Questran (cholestyramine)


Transfer Factor



Introduction: Useful Resources


Alpha Ketoglutarate (AKG)

Alpha Lipoic Acid

Amino Acids: Carnitine, Glutamine, Lysine, Taurine


Betaine HCl

Bioflavonoids: Grape seed extract, Pycnogenol, Quercetin

Butyric Acid (Butyrate)


CoQ10 (ubiquinone, ubiquinol)


Digestive Enzymes

DHEA (dehydroepiandrosterone)

Essential Fatty Acids: Fish Oil, Flaxseed Oil, Evening Primrose Oil, Borage Seed Oil

FOS (fructooligosaccharides)

GABA (gamma aminobutyric acid)


Glucosamine Sulfate


Herbs: Aloe vera, Astragalus, Chamomile, Echinacea, Garlic, Ginger, Gingko, Ginseng, Goldenseal, Gotu kola, Kava,

Licorice, Lomatium, Milk Thistle, St. John's Wort, Uva ursi, Valerian




Malic Acid


Minerals: Calcium, Magnesium, Selenium, Colloidal Silver, Zinc


Mushroom extracts: LEM (shiitake), Maitake, Cordyceps

NAC (N-acetylcysteine )




Royal Jelly


SAMe (S-Adenosyl methionine)


Vitamin A, Beta-Carotene, Vitamin B12, Vitamin B6, Vitamin B Complex, Vitamin C, Vitamin D, Vitamin E and


Whey Products: Colostrom, Undenatured Whey, Probioplex






Aroma Therapy

Bach Remedies

Bed Rest


Chelation Therapy


CBT (Cognitive Behavioral Therapy)

Exercise; GET (Graded Exercise Therapy)




Massage:Craniosacral Massage, Lymphatic Drainage, Myofascial Release, Perrin Technique, Reflexology, Shiatsu

Meditation; Amygdala Retraining Program


TENS (transcutaneous electrical nerve stimulation)

Visualization and Imagery





Introduction– Pacing Yourself









(for CFS/ME but includes FM)














Asian Ginseng












Butrans Patch®






























































Gammar-P I.V.®






























Licorice Root













Magnesium Malate




























































Rhodiola Rosea















sodium oxybate



St. John's Wort




tiapreferic acid





Tranxene SD®

















Vitamin B-12





















oman P, Carrillo-Trabalón F, Sánchez-Labraca N, Cañadas F, Estévez AF, Cardona D. Are probiotic treatments useful on fibromyalgia syndrome or chronic fatigue syndrome patients? A systematic review. Benef Microbes. 2018 Jun 15;9(4):603-611. PMID: 29695180


This study systematically reviewed the reported effect of probiotic treatments in patients diagnosed with FMS or CFS. The administration of Lactobacillus casei strain Shirota in CFS patients, over the course of 8 weeks, reduced anxiety scores. Additionally, the treatment with Bifidobacterium infantis 35624 in CFS patients, during the same period, reduced inflammatory biomarkers. The evidence about the usefulness of probiotics in CFS and FMS patients remains limited.




Scheibenbogen C, Loebel M, Freitag H, Krueger A, Bauer S, Antelmann M, Doehner W, Scherbakov N, Heidecke H, Reinke P, Volk HD, Grabowski P. Immunoadsorption to remove ß2 adrenergic receptor antibodies in Chronic Fatigue Syndrome CFS/ME. PLoS One. 2018 Mar 15;13(3):e0193672. PMID: 29543914


Ten patients with post-infectious CFS/ME and elevated ß2 autoantibodies were treated with immunoadsorption with an IgG-binding column for 5 days. The researchers concluded that immunoadsorption can remove autoantibodies against ß2 adrenergic receptor and lead to clinical improvement. B cell phenotyping provides evidence for an effect of IA on memory B cell development.




Corbitt M, Campagnolo N, Staines D, Marshall-Gradisnik S. A Systematic Review of Probiotic Interventions for Gastrointestinal Symptoms and Irritable Bowel Syndrome in Chronic Fatigue Syndrome/Myalgic Encephalomyelitis (CFS/ME). Probiotics Antimicrob Proteins. 2018 Sep;10(3):466-477. PMID: 29464501


The aim of this study was to conduct a systematic literature review of gastrointestinal and irritable bowel symptoms in CFS/ME, along with any evidence for probiotics as treatment. The authors concluded that there is currently insufficient evidence for the use of probiotics in CFS/ME patients, despite probiotic interventions being useful in IBS.




Wallis A, Ball M, Butt H, Lewis DP, McKechnie S, Paull P, Jaa-Kwee A, Bruck D. Open-label pilot for treatment targeting gut dysbiosis in myalgic encephalomyelitis/chronic fatigue syndrome: neuropsychological symptoms and sex comparisons. J Transl Med. 2018 Feb 6;16(1):24. PMID: 29409505


Participants in this study included 44 adult ME/CFS patients (27 females) from one specialist medical clinic with Streptococcus viable counts above 3.00 × 10^5 cfu/g (wet weight of faeces). The 4-week treatment protocol included alternate weeks of Erythromycin twice daily and probiotic (D-lactate free multistrain probiotic, 5 × 1010cfu twice daily). Large treatment effects were observed for the intention-to-treat sample with a reduction in Streptococcus viable count and improvement on several clinical outcomes including total symptoms, some sleep (less awakenings, greater efficiency and quality) and cognitive symptoms (attention, processing speed, cognitive flexibility, story memory and verbal fluency). This study’s results support the notion that specific microorganisms interact with some ME/CFS symptoms and offer promise for the therapeutic potential of targeting gut dysbiosis in this population.




Rowe PC, Marden CL, Heinlein S, Edwards CC 2nd. Improvement of severe myalgic encephalomyelitis/chronic fatigue syndrome symptoms following surgical treatment of cervical spinal stenosis. J Transl Med. 2018 Feb 2;16(1):21. PMID: 29391028


The authors describe three consecutive patients with severe ME/CFS whose symptoms improved after recognition and surgical management of their cervical spinal stenosis. The prompt post-surgical restoration of more normal function suggests that cervical spine stenosis contributed to the pathogenesis of refractory ME/CFS and orthostatic symptoms.




Gunn SR, Gunn GG, Mueller FW. Reversal of Refractory Ulcerative Colitis and Severe Chronic Fatigue SyndromeSymptoms Arising from Immune Disturbance in an HLA-DR/DQ Genetically Susceptible Individual with Multiple Biotoxin Exposures. Am J Case Rep. 2016 May 11;17:320-5. PMID: 27165859


A 25-year-old previously healthy male with new-onset refractory ulcerative colitis (RUC) and chronic fatigue syndrome (CFS) tested negative for autoimmune disease biomarkers. However, urine mycotoxin panel testing was positive for trichothecene group and air filter testing from the patient’s water-damaged rental house identified the toxic mold Stachybotrys chartarum. HLA-DR/DQ testing revealed a multisusceptible haplotype for development of chronic inflammation, and serum chronic inflammatory response syndrome (CIRS) biomarker testing was positive for highly elevated TGF-beta and a clinically undetectable level of vasoactive intestinal peptide (VIP). Following elimination of biotoxin exposures, VIP replacement therapy, dental extractions, and implementation of a mind body intervention-relaxation response (MBI-RR) program, the patient’s symptoms resolved. He is off medications, back to work, and resuming normal exercise.




Alegre J, Rosés JM, Javierre C, Ruiz-Baqués A, Segundo MJ, de Sevilla TF. Nicotinamide adenine dinucleotide (NADH) in patients with chronic fatigue syndrome. Rev Clin Esp. 2010 Jun;210(6):284-8. PMID: 20447621


Administration of oral NADH was associated to a decrease in anxiety and maximum heart rate, after a stress test in patients with CFS.




Rao AV, Bested AC, Beaulne TM, Katzman MA, Iorio C, Berardi JM, Logan AC. A randomized, double-blind, placebo-controlled pilot study of a probiotic in emotional symptoms of chronic fatigue syndrome. Gut Pathog. 2009 Mar 19;1(1):6. PMID: 19338686


CFS patients who received 24 billion colony forming units of Lactobacillus casei strain Shirota (LcS) daily for two months had a decrease in anxiety symptoms.




Sullivan A, Nord CE, Evengård B. Effect of supplement with lactic-acid producing bacteria on fatigue and physical activity in patients with chronic fatigue syndrome. Nutr J. 2009 Jan 26;8:4. PMID: 19171024


Severely ill CFS patients were given the probiotics Lactobacillus paracasei ssp. paracasei F19, Lactobacillus acidophilus NCFB 1748 and Bifidobacterium lactis Bb12. The study reported neurocognitive functioning improvements, but no changes in fatigue or physical activity.




Teitelbaum JE, Johnson C, St Cyr J. The use of D-ribose in chronic fatigue syndrome and fibromyalgia: a pilot study. J Altern Complement Med. 2006 Nov;12(9):857-62. PMID: 17109576


D-ribose was effective at improving CFS patients’ energy, sleep, mental clarity, pain intensity and overall feelings of well-being.




Kodama M, Kodama T. The clinical course of interstitial pneumonia alias chronic fatigue syndrome under the control of megadose vitamin C infusion system with dehydroepiandrosterone-cortisol annex. Int J Mol Med. 2005 Jan;15(1):109-16. PMID: 15583836


A combination of high-dose intravenous Vitamin C and DHEA was effective at treating both CFS and interstitial pneumonia.




Vermeulen RC, Scholte HR. Exploratory open label, randomized study of acetyl\- and propionylcarnitine in chronic fatigue syndrome. Psychosom Med. 2004 MarApr;66(2):276-82. PMID: 15039515


The authors compared 2 g/d acetyl-L-carnitine, 2 g/d propionyl-L-carnitine, and its combination in 3 groups of 30 CFS patients during 24 weeks. Acetylcarnitine and propionylcarnitine showed beneficial effect on fatigue and attention concentration. Less improvement was found by the combined treatment. Acetylcarnitine had main effect on mental fatigue and propionylcarnitine on general fatigue.




Santaella ML, Font I, Disdier OM. Comparison of oral nicotinamide adenine dinucleotide (NADH) versus conventional therapy for chronic fatigue syndrome. P R Health Sci J. 2004 Jun;23(2):89-93. PMID: 15377055


NADH was effective in CFS for three months, but the positive results faded after that.




Puri BK, Holmes J, Hamilton G. Eicosapentaenoic acid-rich essential fatty acid supplementation in chronic fatigue syndrome associated with symptom remission and structural brain changes. Int J Clin Pract. 2004 Mar;58(3):297-9. PMID: 15117099


Supplementation of an essential fatty acid rid in eicosapentaenoic acid (EPA) was followed by marked improvement in clinical condition after six weeks. Accurate quantification of the lateral ventricular volumes in the baseline and 16-week follow-up registered images of high-resolution magnetic resonance imaging structural scans showed that the treatment was accompanied by a marked reduction in the lateral ventricular volume during this period.




Puri BK. The use of eicosapentaenoic acid in the treatment of chronic fatigue syndrome. Prostaglandins Leukot Essent Fatty Acids. 2004 Apr;70(4):399-401. PMID: 15041033


A series of patients with chronic fatigue syndrome were treated solely with a higheicosapentaenoic acid-containing essential fatty acid supplement. All showed improvement in their symptomatology within eight to 12 weeks.




Cleare AJ, O’Keane V, Miell JP. Levels of DHEA and DHEAS and responses to CRH stimulation and hydrocortisone treatment in chronic fatigue syndrome. Psychoneuroendocrinology. 2004 Jul;29(6):724-32. PMID: 15110921


DHEA levels are raised in CFS and correlate with the degree of self-reported disability. Hydrocortisone therapy leads to a reduction in these levels towards normal, and an increased DHEA response to CRH, most marked in those who show a clinical response to this therapy.




Cleare AJ, Miell J, Heap E, Sookdeo S, Young L, Malhi GS, O’Keane V. Hypothalamopituitary-adrenal axis dysfunction in chronic fatigue syndrome, and the effects of low-dose hydrocortisone therapy. J Clin Endocrinol Metab. 2001 Aug;86(8):3545-54. PMID: 11502777


The authors treat 32 patients with low-dose hydrocortisone and conclude that the improvement in fatigue seen in some patients with CFS during treatment is accompanied by a reversal of the blunted cortisol responses to human CRH.




Forsyth LM, Preuss HG, MacDowell AL, Chiazze L Jr, Birkmayer GD, Bellanti JA. Therapeutic effects of oral NADH on the symptoms of patients with chronic fatigue syndrome. Ann Allergy Asthma Immunol. 1999 Feb;82(2):185-91. PMID: 10071523


31% of a group of CFS patients responded favorably to NADH, compared to 8% to a placebo.




Warren G, McKendrick M, Peet M. The role of essential fatty acids in chronic fatigue syndrome. A case-controlled study of red-cell membrane essential fatty acids (EFA) and a placebo-controlled treatment study with high dose of EFA. Acta Neurol Scand. 1999 Feb;99(2):112-6. PMID: 10071170


Treatment with an essential fatty acid product (Efamol Marine) did not result in benefits compared to a placebo for CFS patients.




Dykman KD, Tone C, Ford C, Dykman RA. The effects of nutritional supplements on the symptoms of fibromyalgia and chronic fatigue syndrome. Integr Physiol Behav Sci. 1998 Jan-Mar;33(1):61-71. PMID: 9594356


Nutritional supplements resulted in a reduction in initial symptom severity, with continued improvement in the period between initial assessment and the follow-up, in a group of CFS sufferers.




See DM, Cimoch P, Chou S, Chang J, Tilles J. The in vitro immunomodulatory effects of glyconutrients on peripheral blood mononuclear cells of patients with chronic fatigue syndrome. Integr Physiol Behav Sci. 1998 Jul-Sep;33(3):280-7. PMID: 9829439


Addition of glyconutrient homogenate to PBMC from patients with CFS stimulated with phytohemagglutinin significantly increased the expression of each glycoprotein. The glyconutrient preparation significantly enhanced NK cell activity versus human herpes virus 6 (HHV-6)\-infected H9 cells in an 8 h 51Cr release assay compared to placebo for PBMC from patients with CFS (p< .01). Finally, apoptosis was significantly higher in patients with CFS. The percentage of apoptotic cells was significantly decreased in PBMC from patients with CFS that had been incubated for 48 h with glyconutrients.




Plioplys AV, Plioplys S. Amantadine and L-carnitine treatment of Chronic Fatigue Syndrome. Neuropsychobiology. 1997;35(1):16-23. PMID: 9018019


In a group of 30 CFS patients, l-carnitine demonstrated significant improvements within 4-8 weeks. Amantadine, used to treat fatigue in MS, was poorly tolerated by CFS patients.




De Vinci C, Levine PH, Pizza G, Fudenberg HH, Orens P, Pearson G, Viza D. Lessons from a pilot study of transfer factor in chronic fatigue syndrome. Biotherapy. 1996;9(1\- 3):87-90. PMID: 8993764


Of the 20 patients in the placebo-controlled trial of transfer factor, improvement was observed in 12 patients, generally within 3-6 weeks of beginning treatment.




Ablashi DV, Levine PH, De Vinci C, Whitman JE Jr, Pizza G, Viza D. Use of anti HHV-6 transfer factor for the treatment of two patients with chronic fatigue syndrome (CFS). Two case reports. Biotherapy. 1996;9(1-3):81-6. PMID: 8993763


Specific Human Herpes virus-6 (HHV-6) transfer factor (TF) preparation, administered to two chronic fatigue syndrome patients, inhibited the HHV-6 infection. Prior to treatment, both patients exhibited an activated HHV-6 infection. TF treatment significantly improved the clinical manifestations of CFS in one patient who resumed normal duties within weeks, whereas no clinical improvement was observed in the second patient.




Cox IM, Campbell MJ, Dowson D. Red blood cell magnesium and chronic fatigue syndrome. Lancet. 1991 Mar 30;337(8744):757-60. PMID: 1672392


A clinical trial showed that magnesium supplementation may be helpful in CFS.




Behan PO, Behan WM, Horrobin D. Effect of high doses of essential fatty acids on the postviral fatigue syndrome. Acta Neurol Scand. 1990 Sep;82(3):209-16. PMID: 2270749


High doses of essential fatty acids containing linolenic, gamma-linolenic, eicosapentaenoic and docosahexaenoic acidswere helpful in CFS.


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neurotropic cfs - Google Search(


neurorehabilitation drug cfs - Google Search(


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Frontiers | The Influence of Neuron-Extrinsic Factors and Aging on Injury Progression and Axonal Repair in the Central Nervous System | Cell and Developmental Biology(


Neurotrophic factors, cellular bridges and gene therapy for spinal cord injury(


Neurotrophic drugs cfs - Google Search(


Postulated vasoactive neuropeptide immunopathology affecting the blood-brain/blood-spinal barrier in certain neuropsychiatric fatigue-related conditions: A role for phosphodiesterase inhibitors in treatment? - PubMed(


Postulated Vasoactive Neuropeptide Autoimmunity in Fatigue-Related Conditions: A Brief Review and Hypothesis(


Frontiers | Acute Corticotropin-Releasing Factor Receptor Type 2 Agonism Results in Sustained Symptom Improvement in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome | Frontiers in Systems Neuroscience(


nutraceutical neurotrophin - Google Search(


Fibromyalgia Causes And Treatment With Guaifenesin, Amitriptyline, Kratom, Flexeril, And Others. -(


A systematic review of nutraceutical interventions for mitochondrial dysfunctions in myalgic encephalomyelitis/chronic fatigue syndrome | Journal of Translational Medicine | Full Text(


nutraceutical neurotro cfs - Google Search(


nutraceutical neurotro cfs - Google Search(


Microglial Inhibiting Drugs, Supplements and Botanicals to Combat Neuroinflammation - Health Rising(


Myalgic Encephalomyelitis/Chronic Fatigue Syndrome—Metabolic Disease or Disturbed Homeostasis due to Focal Inflammation in the Hypothalamus? - ME-CFS-JPET-9-2018.pdf(chrome-extension://oemmndcbldboiebfnladdacbdfmadadm/https:/


neuropeptide Y - Clincosm(


General Treatment | Phoenix Rising ME/CFS Forums(


Peptidergic Drugs for Treatment of Traumatic Brain Injury(


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New folder


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Nootropics for chronic fatigue Syndrome - Google Search(


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Bacopa monnieri Supplement — Health Benefits, Dosage, Side Effects |


Piracetam + Choline - Google Search(


Supplements for Chronic Fatigue Syndrome?(


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cell membrane glycerolphospholipids cfs - Google Search(


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L-Alpha glyceryl phosphorylcholine "cfs" - Google Search(


14 Nootropics, aka Brain Enhancers, for Your Memory and More(


The Best Nootropics for Energy and Motivation | FOCL(


Thesis - Personalized nootropic formulas to activate every kind of brain.(


NADH – Nootropics Expert(


Biomarker for chronic fatigue syndrome identified : Nootropics(


purinergic antagonists - Google Search(


Treatment of chronic fatigue syndrome with 5-HT3 receptor antagonists - preliminary results: Scandinavian Journal of Rheumatology: Vol 29, No 113(


Anyone had any success dealing with chronic fatigue syndrome? : Nootropics(


Sulbutiamine as a Treatment for Chronic Fatigue Syndrome » Corpina(


Phenylpiracetam - Google Search(


Piracetam - Google Search(


Nimodipine CFS - Google Search(


Drugs and Supplements For Chronic Fatigue Syndrome (ME/CFS) and/or Fibromyalgia - Health Rising(


nimodipine use in me, jan 2014.pdf(chrome-extension://oemmndcbldboiebfnladdacbdfmadadm/https:/,%20jan%202014.pdf)


List of ME/CFS Recovery and Improvement Stories | Phoenix Rising ME/CFS Forums(


When antibiotics turn toxic(


purinergic antagonists chronic fatigue syndrome - Google Search(


neurotrophic cfs - Google Search(


neurotropic cfs - Google Search(


post stroke neurotrophic neurorehabilitation medicine textbook - Google Search(


neurorehabilitation drug cfs - Google Search(


peptide modulation. Some neurons, given neurotrophic factors show regrowth/repair cfs - Google Search(


Neurotrophic Peptide - an overview | ScienceDirect Topics(


Neurotrophic Factors - an overview | ScienceDirect Topics(


Frontiers | Therapeutic Potential of Neurotrophins for Repair After Brain Injury: A Helping Hand From Biomaterials | Neuroscience(


Frontiers | The Influence of Neuron-Extrinsic Factors and Aging on Injury Progression and Axonal Repair in the Central Nervous System | Cell and Developmental Biology(


Neurotrophic factors, cellular bridges and gene therapy for spinal cord injury(


Neurotrophin medication - Google Search(


Neurotrophic drugs cfs - Google Search(


"Neurotrophic" drugs cfs treatment - Google Search(


cfs treatment neuropeptide - Google Search(


Postulated vasoactive neuropeptide immunopathology affecting the blood-brain/blood-spinal barrier in certain neuropsychiatric fatigue-related conditions: A role for phosphodiesterase inhibitors in treatment? - PubMed(


Postulated Vasoactive Neuropeptide Autoimmunity in Fatigue-Related Conditions: A Brief Review and Hypothesis(


Frontiers | Acute Corticotropin-Releasing Factor Receptor Type 2 Agonism Results in Sustained Symptom Improvement in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome | Frontiers in Systems Neuroscience(


A Novel Nutriceutical Treatment of Myalgic Encephalitis/Chronic Fatigue Syndrome (ME/CFS): “What it is and what it is not” - a-novel-nutriceutical-treatment-of-myalgic-encephalitischronic-fatigue-syndrome-mecfs-what-it-is-and-what-it-is-not-2165-8048-10002452.pdf(chrome-extension://oemmndcbldboiebfnladdacbdfmadadm/https:/


nutraceutical cfs - Google Search(


nutraceutical neurotrophin - Google Search(


nutraceutical neurotrophic cfs - Google Search(


Fibromyalgia Causes And Treatment With Guaifenesin, Amitriptyline, Kratom, Flexeril, And Others. -(


A systematic review of nutraceutical interventions for mitochondrial dysfunctions in myalgic encephalomyelitis/chronic fatigue syndrome | Journal of Translational Medicine | Full Text(


nutraceutical neurotro cfs - Google Search(


nutraceutical neurotro cfs - Google Search(


Mitochondrial Modifying Nutrients in Treating Chronic Fatigue Syndrome: A 16-week Open-Label Pilot Study | Request PDF(


You searched for CHRONIc fatigue - ICNR(


Is a Hidden Infection Causing Your Chronic Fatigue?(


Chronic Fatigue - Kelatox(


Phoenix Rising ME/CFS Forums



This is a thread for ME/CFS recovery or improvement stories, detailing patient accounts of treatments which have led to full recovery or substantial improvements in their overall ME/CFS symptoms, as well as treatments which have substantially improved specific ME/CFS symptoms (like fatigue, PEM, brain fog, sound sensitivity, etc).


The degree of improvement a patient achieved (where known) is given in terms of the number of levels they moved up on the ME/CFS scale of: very severe, severe, moderate, mild, remission. For example, if the patient was initially severe, and then moved up to mild as a result of a treatment, that is a 2-level gain.


If anyone knows of any other recovery or improvement stories that could be included in this thread, please post. That way we can build up a repository of interesting treatments.




ME/CFS Recovery and Improvement Stories


Valcyte (Valganciclovir) — Antiviral Drug for Herpesviruses


Valcyte is a potent antiviral drug effective against a wide spectrum of herpesviruses, including EBV, HHV-6, cytomegalovirus, varicella-zoster and herpes simplex. Typical dose for ME/CFS is 900 mg daily. Studies which have examined the efficacy of Valcyte for ME/CFS are detailed in this post.


• ME/CFS patient (OnlyInDreams) — with active cytomegalovirus infection made a 2-level gain, moving from moderate ME/CFS to remission, as a result of taking Valcyte 900 mg daily; but if he stops the Valcyte, he finds the ME/CFS soon returns.


• ME/CFS patient (Mariesak) — went into a partial remission lasting 8 years, after a 9 month course of Valcyte (her health gains remained even after she stopped the Valcyte).


• ME/CFS patient (Mariesak's daughter) — completed a 12 month course of Valcyte and also went into remission, and has remained in remission for over a decade.


• ME/CFS patient (JenB) — found Valcyte had a "profound effect".


• ME/CFS patient (TracyD) — improved on low-dose Valcyte 450 mg once daily.


• ME/CFS patient (SOC) — made a 1-level gain on Valcyte, moving from severe to moderate.


• ME/CFS patient (SOC's daughter) — made a 1½-level gain, going from nearly housebound (moderate ME/CFS) to full remission after 18 months on Valcyte for active HHV-6.


• ME/CFS patient (Peter42) — with mild ME/CFS made a 1-level gain and became almost free of ME/CFS symptoms after taking Valcyte for a year. Then 2 years after he stopped taking Valcyte, his ME/CFS returned.


• ME/CFS patient (ArgyrosfeniX) — made a 1-level gain moving from moderate to mild ME/CFS after two years of Valcyte at 900 mg once daily.


• ME/CFS patient (Dan_USAAZ) — with severe HHV-6-associated ME/CFS improved on Valcyte 900 mg daily, perhaps achieving a ½-level gain.


• ME/CFS patient (jstefl) — achieved a 1-level gain moving from severe ME/CFS to moderate after 450 mg dose of Valcyte twice a day for 10 months. This improvement occurred in 2008, and has lasted more than a decade.


• ME/CFS patient (RUkiddingME) — with severe ME/CFS and bedbound most of the time was able to resume driving and shopping again after a year on Valcyte (1-level gain).



Valtrex (Valaciclovir) — Antiviral Drug


Valtrex is an antiviral effective against Epstein-Barr virus. Some ME/CFS doctors prescribe this drug to ME/CFS patients who have an active EBV infection. For EBV ME/CFS treatment, Dr Lerner used a dose of 1000 mg four times daily. Studies which have examined the efficacy of Valtrex for EBV-associated ME/CFS are detailed in this post.


• ME/CFS patient (Leah) — with severe ME/CFS achieved near recovery (2½-level gain) from a course of Valtrex prescribed by Dr Martin Lerner. She is now able to work and socialize, but cannot exercise vigorously.


• ME/CFS patient (Heather) — fully recovered after a year or so of taking Valtrex prescribed by Dr Martin Lerner.


• ME/CFS patient (Janet, see comments section) — with severe ME/CFS achieved 2-level gain, moving up to mild ME/CFS after taking Valtrex for many years.



Valtrex (Valaciclovir) Plus Valcyte (Valganciclovir) Together


• ME/CFS patient (Jacyln) — with severe EBV ME/CFS achieved 2-level gain, moving up to mild ME/CFS after taking a course of Valcyte 450 mg twice daily plus Valtrex 1500 mg four times daily prescribed by Dr Martin Lerner.


• ME/CFS patient (Marilynne, see comments section) — with severe ME/CFS achieved 2-level gain, moving up to mild ME/CFS after taking a course of Valcyte 450 mg twice daily plus Valtrex 1500 mg four times daily prescribed by Dr Martin Lerner.


• ME/CFS patient (Renee) — with moderate to mild ME/CFS associated with active EBV and cytomegalovirus recovered to a near-normal life (1-level gain) after a course of Valtrex and Valcyte prescribed by Dr Martin Lerner. Leads near normal life but cannot exercise vigorously.



Tenofovir (Viread) — Antiviral Drug


Tenofovir is an antiviral drug normally used for hepatitis B virus or HIV. When used to treat ME/CFS, Dr John Chia reports it works for almost 1 in 3 ME/CFS patients. Refs: 1 2 Some ME/CFS patients find tenofovir hard to tolerate initially, but this issue can be avoided by starting at low doses of 30 mg daily, and working up to the full dose of 300 mg daily.


• This ME/CFS patient (Keela Too) — experienced a 1-level gain moving from approximately severe ME/CFS to moderate after taking a course of tenofovir for 12 months. The gains in her health have remained permanently so far.


• ME/CFS patient — with active coxsackievirus B4 infection noticed substantial improvements from tenofovir after just 4 months at 150 mg daily (he took combination pill containing tenofovir + lamivudine). He said: "I almost have my life back. My endurance has increased beyond belief, and PEM is a thing of the past". Even after he stopped tenofovir at the 4 month point, his gains remained. He also found that tenofovir resulted in a suspected nail psoriasis (autoimmune condition) he had for 5 years to suddenly heal.



Antiretrovirals (Tenofovir, Raltegravir, AZT)


These HIV antivirals are immunomodulatory, and can inhibit human endogenous retroviruses (HERVs). Ref: 1 HERV-K activity has been linked to moderate (but not severe) ME/CFS. Ref: 1


• ME/CFS patients (Dr Jamie Deckoff-Jones and her daughter Ali) — both had improvements in their ME/CFS after taking tenofovir 300 mg once daily plus raltegravir 400 mg twice daily.


• ME/CFS patient (Dr Michael Snyderman) — had success in treating his ME/CFS with AZT, raltegravir and tenofovir.



Ampligen (Rintatolimod)


Ampligen is an interferon inducer which stimulates the immune system to fight viral infections. Ampligen has been shown efficacious for ME/CFS in a phase III clinical trial. Ampligen is licensed as an ME/CFS treatment in Argentina, but not in the US or Europe, so is difficult to obtain, and not normally covered by insurance. Ampligen is expensive, costing around $15,000 a year (excluding the medical costs of the infusions). Ampligen is administered by intravenous infusion twice a week.


• ME/CFS patient (Kelvin Lord) — after a year on Ampligen infusions went from severe ME/CFS ("I was barely able to get out of bed") to mild (2-level gain) ME/CFS. He said "Ampligen makes you feel like you have the flu twice a week. The reality is when you are on it, it is pretty much hell. Hell with hope". See his Ampligen blogs here.


• ME/CFS patient (niall) — improved "by 30%" after a course of Ampligen.


• ME/CFS patient (LaurelW) — was on Ampligen for 7 years, improved from severe to moderate (1-level gain), and maintained their gains in health even after stopping Ampligen.


Some other Ampligen stories here.



Oxymatrine (Equilibrant) — Immunomodulator


Oxymatrine is an immunomodulatory herbal extract which ramps up the antiviral Th1 immune response. Dr John Chia uses oxymatrine to treat enterovirus ME/CFS.


• ME/CFS patient (Diwi9) — with enterovirus ME/CFS achieved a substantial improvement from oxymatrine (in the form of Dr Chia's Equilibrant).


• ME/CFS patient (tdog333) — did well taking 6 pills of oxymatrine daily.


• ME/CFS patient (.jm.) — with mild enterovirus ME/CFS went into remission (1-level gain) as a result of taking oxymatrine.



GcMAF — Immunomodulator


GcMAF is an immunomodulatory protein which stimulates macrophages to fight pathogens in the body. GcMAF can be taken orally, by transdermal cream, or via injection. Some sources for GcMAF in this post.


• ME/CFS patient (carlystar13) — obtained a 3-level gain, going from severe ME/CFS to full remission, after a year of taking Goleic GcMAF.


• ME/CFS patient (CindyWillis) — almost completely recovered taking from 40 to 80 ng of GcMAF over a month and a half.



Low-Dose Oral Interferon Alpha


Interferon alpha is a potent immunomodulator that activates the intracellular immune response. You can buy interferon alpha suppositories or nasal sprays cheaply from Russian online pharmacies (see this post), and these may be adapted for oral use.


• ME/CFS patient (Linda) — fully recovered using low doses of interferon alpha taken orally (rather than the usual subcutaneous injection route). She took 250 IU of interferon alpha orally four times a day. Brain fog began to improve after a few weeks, and her ME/CFS pain symptom cleared up after two months. Possibly this oral route interferon targets enterovirus infections in the stomach tissues?



High-Dose Selenium


The high-dose selenium protocol used here is detailed in this post.


• ME/CFS patient (Hip) — achieved a ½-level gain moving from the bottom end of moderate to the top within only 10 days as a result of high-dose selenium (taking selenomethionine 400 mcg once daily on an empty stomach).



Inosine + DMAE = Home-Made Imunovir


According to a ME/CFS patient blog article (now deleted), mixing inosine and DMAE together creates what is equivalent to the antiviral drug Imunovir (isoprinosine). To create home-made Imunovir, as this post details, you simply take equal weights of these two supplements (eg, DMAE 500 mg plus inosine 500 mg). The two supplements will combine in the stomach to make the molecular complex that is Imunovir.


Note however that many ME/CFS patients cannot tolerate Imunovir, and some report getting permanently worse from it: see this thread and this thread.


• ME/CFS patient (Doug) — with major mold exposure-induced illness was more-or-less cured by inosine 2000 mg daily plus DMAE 700 mg, as well as other supplements. See also here. Doug tried inosine on its own for some months, but it was not until he added DMAE to the inosine that he obtained a large increase in health.



Low-Dose Abilify (Aripiprazole)


The Open Medicine Foundation are currently running a clinical trial to determine whether low doses of the drug Abilify (aripiprazole) can benefit ME/CFS. Trial results are not yet available, but several ME/CFS patients have found Abilify in doses of around 0.1 to 2.5 mg daily rapidly leads to major improvements in their ME/CFS symptoms.


• ME/CFS patient (Martin aka paused||M.E.) — moved from very severe to moderate (2-level gain) after two months on Abilify 4 mg daily (plus LDN and Celebrex).


• ME/CFS patient (Jaybee00) — moved from moderate to mild (1-level gain) after 6 weeks on Abilify 2 mg daily. He noticed improvements began to manifest after a week or so.


• ME/CFS patient (Butydoc) — moved from severe to moderate (1-level gain) within a matter of weeks on 0.2 mg of Abilify daily.


• ME/CFS patient (Jessie 107) — improved on 2.5 mg Abilify daily. She said she did not notice much improvement until she reached the 2 mg daily dose level.


• ME/CFS patient (erist) — back in 2012 took 0.5 mg to 1 mg Abilify daily, and found more energy, more appetite, much easier time getting up in the morning, but also restless agitation.



Low-Dose Naltrexone (LDN)


The drug naltrexone at a low dose of 3 to 4.5 mg daily before bed, can have positive effects for ME/CFS as well as autoimmune and neurodegenerative diseases. Dr John Chia finds LDN helps only 10% to 20% of ME/CFS patients, but for those it helps, it does so significantly. Refs: 1 2


• ME/CFS patient (Maija Haavisto) — found LDN had immediate benefits, improving fatigue and muscle weakness, making PEM episodes rarer and milder, and almost eliminating her chronic fever and chronic urticaria symptoms (see "My Own Perspective" section in the link).



Nimodipine (Nimotop)


Nimodipine is a calcium channel blocker which increases blood flow to the brain. Dr David Mason Brown says nimodipine helps 20% of ME/CFS patients quickly, and another 20% over six months. The Mason Brown protocol begins with a nimodipine dose of 7.5 mg per day. The dose is slowly increased by 7.5 mg each week, up to a maximum dose of 120 mg daily. Nimodipine has many drug interactions.


• ME/CFS patient — with severe ME/CFS became very mild (2-level gain) on 90 mg of nimodipine daily (30 mg taken three times daily). This patient has maintained his improvement in health for 7 years without relapse. However, every time he reduces his nimodipine dose, his ME/CFS gets worse again. He finds the minimum dose that produces some benefits is 45 mg daily; but it is not until he increases the dose to 90 mg daily does he get the full benefits



Rapamycin (Sirolimus, Rapamune)


Rapamycin is a drug which calms the immune response, and is usually used to prevent organ transplant rejection, and to treat some autoimmune diseases. It is also used by the anti-aging community, as it extends lifespan in animal tests.


• Several ME/CFS patients — observed improvements on rapamycin.



Tagamet (Cimetidine)


Tagamet is an H2 antihistamine that has immunomodulatory properties: it boosts NK cell activity, and reduces T-regs (doing the latter may not be a good idea in autoimmunity or in those with organ transplants).


Tagamet is a known testicular toxicant, but vitamin B12 helps mitigate this damage. Ref: 1. Tagamet has a lot of interactions with other drugs, so you may like to consult a drug interactions checker to check if it interacts with any drugs you are taking.


• ME/CFS patient ( — took Tagamet 200 mg every other day, and was able to go back to work.



Ketogenic Diet


A ketogenic diet is a very low-carb and high-fat diet. On a ketogenic diet, the brain is fueled by ketones rather than the usual glucose. Ketogenic diets are known to increase the number of mitochondria in brain cells. These diets are traditionally prescribed for patients with seizures.


• ME/CFS patient (leokitten) — with severe bedbound ME/CFS improved substantially with a ketogenic diet, so that he is no longer bedbound or housebound (2-level gain). But later he said he found it hard to sustain the diet long-term, and found the diet did not prevent crashes when he tried to live a regular life, so currently he is back to bedbound.



Helminth Therapy


Helminths are microscopic parasitic worms which live in the intestines. They modulate the immune function in the gut, which can have benefit in some diseases, especially autoimmune illnesses.


• ME/CFS patient (Gyre) — achieved a 2-level gain, moving from severe ME/CFS to mild as a result of helminth therapy, using the worm Necator americanus.


• ME/CFS patient (Henrik) — went from moderate to mild (1-level gain) using helminthic therapy with Necator americanus.


Several more ME/CFS recovery and improvement stories from Necator americanus detailed here.



Kambo (Medicine From an Amazonian Frog)


Kambo is a substance secreted by the Amazonian giant leaf frog, containing a range of bioactive principles, including sauvagine, a hormone related to the experimental ME/CFS drug CT38 (the Cortene Peptide).


• ME/CFS patient (Jox) — went from severe to near remission (2½-level gain) by taking the Amazonian medicine kambo once a week.



Fecal Microbiota Transplantation (FMT)


FMT involves transplanting fecal material from a healthy donor into a patient's intestines.


• Chronic Lyme patient (Kasia Vermaire) — with severe illness experienced a 3-level gain and made a full recovery after FMT treatment at the Taymount Clinic. Blog article here.



Low-Level Laser Therapy / LED Light Therapy


Also known as photobiomodulation, this therapy uses red or infrared light emitted by a laser or LED lamp, applied to the area of interest, such as the head and brain. Light of these wavelengths is known to stimulate mitochondrial complex IV.


• ME/CFS patient (ScottTriGuy) — housebound with moderate ME/CFS quickly recovered enough health to return to work (1-level gain) as a result low-level laser therapy (LLLT) applied to his head.


• ME/CFS patient (Johannes) — move from severe ME/CFS to moderate ME/CFS (1-level gain) using red and infrared light therapy on on his entire head and body daily (10 minutes on the front of the body and 10 minutes on the back). Light power used is 90 mW/cm2. Ref: 1



C60 Supplement


C60 (buckminsterfullerene) is a molecule comprising 60 carbon atoms that are arranged into a spherical shape. C60 targets the mitochondria where it acts as a non-perishable resuable antioxidant. 1


• ME/CFS patient — with moderate ME/CFS makes at least a 1-level gain and goes back to work as a result of taking a C60 supplement.



Bob Beck Microbe Electrifier


• ME/CFS patient (intheknow) — with moderate ME/CFS recovered after 90 hours of treatment with a Bob Beck Microbe Electrifier connected across his wrists (2-level gain).



Nitrate Drugs


Nitrate drugs increase levels of nitric oxide in the body. These drugs are vasodilators typically given to relieve angina pains.


• ME/CFS patient (zzz) — experienced a 3-level gain going from severe ME/CFS to full remission in a matter of weeks after taking a single 10 mg dose of isosorbide dinitrate (a nitrate drug). That remission lasted for 8 years, but then relapse occurred after a minor surgery.



Statin Drug Atorvastatin


• ME/CFS patient (Hopefulone) — with moderate ME/CFS greatly improved after starting atorvastatin 80 mg daily.



Mitochondrial Cocktail


• ME/CFS patient (MrTwoToedSloth) — with moderate-to-severe ME/CFS went up to mild after taking a mitochondrial cocktail comprising Q10 300 mg, acetyl-L-carnitine, Na-D-alpha lipoic acid, nicotinamide riboside and a vitamin B complex for 3 months (1½-level gain).



Dr Kenny De Meirleir Protocol


• ME/CFS patient (sam.d) — with severe ME/CFS and who was not even able to speak, experienced a 1-level gain on a protocol prescribed by KDM. He became moderate, and able to do volunteer work from home. The KDM protocol included: Gammanorm (immunoglobulin IgG), breathing oxygen for 5 hours daily, vitamin B12 injections, and several other treatments.



Peptides LL-37 + BPC-157


LL-37 is a broad-spectrum antimicrobial peptide naturally made in the body. Anecdotally, supplemental LL-37 helps fix gut issues. BPC-157 is a peptide naturally found in the stomach which may promote healing and tissue regeneration.


• ME/CFS patient (beatsmyth) — with severe ME/CFS experienced a 2-level gain, moving up to mild ME/CFS, after taking a combination of two peptides LL-37 and BPC-157 for three months. He took 125 mcg of LL-37 daily for 6 weeks, then took a 2 week break, and then took LL-37 for another 6 weeks. This treatment also fixed his IBS.



ATP Injections


• ME/CFS patient (Keshav) — rapidly improved in a matter of days from ATP injections.



Daosin (Diamine Oxidase) Supplement


Daosin is a supplement providing diamine oxidase, an enzyme produced in the body to break down excess histamine.


• ME/CFS patient (xlynx) — with severe bedbound ME/CFS and a diamine oxidase deficiency greatly improved by taking the supplement Daosin.



High-Dose Sublingual Biotin


High-dose biotin (100 mg three times daily) has been used experimentally to treat multiple sclerosis. Ref: here.


• ME/CFS patient (BiotinJunkie) — found taking 10 mg of biotin sublingually several times daily worked well for his symptoms.


• One individual with autism (LouiseLouise) — found high-dose biotin 100 mg twice daily dramatically improved her autism.



Surgical Treatment of a Jawbone Cavitation Infection


Jawbone infections (osteomyelitis) can develop inside hollow pockets within the jawbone called cavitations. Cavitations may be left in the jawbone after a tooth extraction. Jawbone cavitation infections induce the inflammatory chemokine RANTES, as well as FGF-2, which are both linked to systemic disease.


A simple test for a jawbone infection is applying pressure with a finger on the gums to the jawbone beneath; if any area feels painful, this indicates a possible jawbone infection (though this method will not always detect jawbone infection). More reliable tests are MRI STIR scans and Cavitat scans. More info here.


• ME/CFS patient (Ian) — recovered from ME/CFS after surgically treating an infection within a jawbone cavitation.


• ME/CFS patient (ERROL_FARNHAMSURREY) — with mild ME/CFS made substantial improvements after treating a jawbone cavitation infection.


• ME/CFS patient (Dukey) — with moderate (housebound) ME/CFS got better after surgery to remove a jawbone cavitation infection (cavitational osteonecrosis).



Treating Nasopharynx Inflammation (in Vaccine-Triggered ME/CFS)


This thread details a published study in which patients with vaccine-triggered ME/CFS (or an ME/CFS-like illness) are cured or improved by treating their nasopharynx inflammation at the back of their nasal cavity with the topical anti-inflammatory zinc chloride.


• ME/CFS patient (DrFaust) — cured his ME/CFS using topical zinc chloride to treat his nasopharyngitis (nasopharynx inflammation).



Surgery for Craniocervical Instability


Craniocervical instability (CCI) is a looseness or laxity of the joint connecting the top of the spine with the skull. The Phoenix Rising CCI forum is here.


• ME/CFS patient (jeff_w) — was cured of his severe ME/CFS by surgery to fix his craniocervical instability (3-level gain).


• ME/CFS patient (JenB) — was cured of her ME/CFS by surgery to fix craniocervical instability, atlantoaxial instability and tethered cord.


• ME/CFS patient (Danielle) — with severe ME/CFS went into full remission (3-level gain) after C1-C2 fusion surgery for atlantoaxial instability, and surgery for occult tethered cord syndrome.


• ME/CFS patient (Karen) — had a major improvement after CCI fusion surgery.



Jawbone Realignment


The following two jawbone realignments were performed by Dr Amir, a dentist based in London:


• Patient with ME/CFS-like illness (Uzma Qureshi) — recovered after jaw realignment using dental appliances.


• Patient with ME/CFS-like illness (Hannah) — recovered after jaw realignment using dental appliances.



Tricyclic Antidepressants


Tricyclic antidepressants (TCAs) like amitriptyline increase the amount of serotonin and norepinephrine in the brain, and block the action of acetylcholine.


• Patient with ME/CFS or ME/CFS-like illness (RuralRick) — finds high doses of tricyclic antidepressants (TCAs) put his ME/CFS into remission.



Mild Hyperbaric Oxygen Therapy (mHBOT)


Mild hyperbaric oxygen therapy (mHBOT) is performed in a soft hyperbaric oxygen chamber that patients usually buy and keep in their home. Whereas regular hyperbaric oxygen therapy (HBOT) uses pressures up to 2 or 3 atmospheres, mHBOT pressures only go up to around 1.3 or 1.5 atmospheres.


• ME/CFS patient or possibly a post-viral fatigue patient (Jesse2233) — had a moderate ME/CFS illness that started with a viral infection, and lasted about 18 months before it went into remission. He had high antibody levels of 1:640 to coxsackie virus B4 on the ARUP lab tests.1 He went into remission (2-level gain) while doing mild hyperbaric oxygen therapy sessions daily in a home soft hyperbaric chamber, and credits his remission to mHBOT. (Although if it he had post-viral fatigue rather than ME/CFS, it may have resolved on its own anyway). He estimates he did over 200 hours of mHBOT.


• ME/CFS patient (used_to_race) — with mild-to-moderate ME/CFS associated with active EBV went into remission (1½-level gain) after two years of mild hyperbaric oxygen (mHBOT) sessions daily at 45 to 90 minutes each session. He also took hydroxychloroquine 400 mg daily during this time, so is not sure which led to his remission.



Pridgen Protocol (Famvir + Celecoxib)


The Pridgen protocol was devised by Dr William Pridgen as a means to treat the herpes simplex virus infections he believes may underpin fibromyalgia. This protocol is being experimentally used to treat ME/CFS as well. The protocol is based on the antiviral drug Famvir (famciclovir), to which the COX inhibitor celecoxib is added, as COX inhibitors are shown to have antiviral effects against herpes simplex.


• ME/CFS patient — improved substantially on the Pridgen protocol (normally Famvir 250 mg twice daily and celecoxib 200 mg twice daily) along with an antidepressant.



Consuming IgY Immunoglobulins From Chicken Eggs


• ME/CFS patient (Maj-Britt) — a Swedish women cured her Chlamydia pneumoniae-associated ME/CFS with a simple home treatment consisting of orally consuming IgY antibodies from a chicken egg yolk. She injected the chicken with her blood, so the chicken started making antibodies against the infections in her blood. Those chicken antibodies are naturally produced in large quantities in the eggs the chicken lays.





Yoga is thought to up-regulate the parasympathetic nervous system. The newly-discovered link between ME/CFS and spinal/cranial conditions like craniocervical instability perhaps throws a light on why yoga might help some ME/CFS patients, given that many yoga asanas stretch and tone the spine and neck.


• ME/CFS patient (Sally) — with moderate ME/CFS recovered through yoga (2-level gain), according to a newspaper article.


• Patient with ME/CFS-like illness (Dan) — with symptoms like slurred speech and wild myoclonic jerks sending his limbs flying, went into near remission after doing lots of yoga.



Moving to Hot, Humid and Sunny Costa Rica


• ME/CFS patient (Paul) — with moderate-to-severe ME/CFS went into near remission (2-level gain) after 4 days of arriving in Costa Rica. On going back to his home in Canada, his ME/CFS quickly reappeared. But returning Costa Rica for a second time placed him back into remission, again after around 4 days of arriving. And previously, when Paul had a lingering post-viral fatigue after an infection, it was observed this was fully cured during a visit to Thailand (which is on the same latitude as Costa Rica, and with a similar hot and humid climate). Paul moved to Costa Rica permanently, in order to keep his ME/CFS in remission.



Active Prism Lenses To Treat Proprioception Dysfunction


Proprioception is a bodily sense deriving from receptors in our muscles which (without any visual clues) informs the brain of the current position of your limbs. People with poor proprioception find it hard to know where their limbs are, unless they look visually. One study observed a rapid recovery from severe ME/CFS after treating proprioception dysfunction with active prism lenses.


• ME/CFS patient (Donsboig) — moved from severe to moderate (2-level gain) using active prism lenses to treat his proprioception dysfunction.




Improving PEM


Post-exertional malaise (PEM) is the temporary worsening of ME/CFS symptoms which occurs after physical or mental exertion.


A useful thread detailing many treatments for PEM is found here. The PEM busters in that thread include: corticosteroids, Mestinon, cannabis, D-ribose, BCAA, Q10 and sodium bicarbonate.




• ME/CFS patient (Hamsterman) — normally bedbound with severe ME/CFS found a one-off dose of 20 mg of prednisolone taken 30 minutes before a major exertion completely prevents PEM. He found taking prednisolone just before exercise allowed him to do a full workout at the gym without getting any PEM repercussion whatsoever. But he cautions that these doses of prednisolone should not be used daily, only occasionally, as the immunosuppressive effects of daily prednisolone will likely allow underlying viral infections to proliferate.





• Several ME/CFS patients — report cannabis is a good PEM shielder and PEM reliever: they find if cannabis is taken just when the first signs of PEM appear, at the first PEM "danger signals", then it will prevent the PEM from fully manifesting.



Mestinon (Pyridostigmine)


• ME/CFS patient (Mel9) — found Mestinon greatly reduced her PEM. Taking 30 mg of Mestinon once every four hours allows her to have a relatively active day (4 km walks).


• ME/CFS patient — with this illness for 28 years found Mestinon 180 mg per day eliminated her PEM, allowing her to do 3 mile runs and go to the gym without any PEM repercussion.




Improving Energy


MitoQ Supplement


MitoQ is a mitochondrially-targeted form of Q10. There is a lot of published research on MitoQ.


• ME/CFS patient (cigana) — finds that MitoQ significantly decreases his fatigue levels. He speculates his genetic A16V (rs4880) +/+ mutation, which results in lower levels of the mitochondrial antioxidant Mn-SOD, may explain why he gets substantial benefit from MitoQ. So those with an A16V +/+ mutation might consider trying MitoQ. However, later he concluded that this energy boost only appeared when he took GcMAF at the same time as MitoQ.



Dichloroacetate (DCA)


Dichloroacetate in ME/CFS studies was found to stimulate mitochondrial energy metabolism, and improve fatigue, brain fog and pain in about one-third of patients (but the study found those with comorbid autoimmune conditions are less likely to respond to DCA). Refs: 1 2 See these tips for avoiding the possible neuropathy side effects of DCA.


• ME/CFS patient (XenForo) experienced "a lot more energy" from DCA.



Cellfood (Deuterium Sulfate)


The active ingredient in Cellfood is deuterium sulfate, a form of sulfuric acid based on the hydrogen isotope deuterium (formula D2SO4). Deuterium sulfate is claimed to have an enzymatic action which improves tissue oxygenation and reduces oxidative stress.


• ME/CFS patient (Mary) — found the supplement Cellfood 10 drops three times daily increased her energy.




Improving Brain Fog


Vitamin B12 Injections / Transdermal B12 Oils


• ME/CFS patient (Hip) — found the B12 transdermal oils formulated by Dr Greg Russell-Jones in Australia help improve brain fog.





• ME/CFS patient (Hip) — found piracetam 800 mg daily helps improve brain fog.




Improving Sound or Light Sensitivity


Very Low-Dose Amisulpride


• ME/CFS patient (Hip) — finds the dopamine system stabilizer drug amisulpride in very low-doses reduces sound sensitivity (hyperacusis), and has several other beneficial effects on ME/CFS symptoms.




Improving Emotional/Stress Sensitivity


Hydrogen-Rich Water


Hydrogen-rich water is made by dissolving hydrogen gas into water under pressure. HRW known to stimulate the release of the hormone ghrelin, which in turn stimulates the hypothalamus. The H2 molecule within HRW is also an antioxidant.


• ME/CFS patient (Hip) — found hydrogen-rich water noticeably reduces the emotional sensitivity / stress sensitivity symptom of ME/CFS.




Improving Gut Health, IBS and SIBO


Chloramine Avoidance


Chloramine is a disinfectant added to the drinking water in some regions. Chloramine can be irritant to the mucous membranes. Note that chloramine is not the same as chlorine, and carbon water filters do not remove chloramine.


• ME/CFS patient (Hip)— substantially improved his IBS-D by removing chloramines from his tap drinking water, which is done by adding a pinch of ascorbic acid (vitamin C) powder to the water, as this reacts with and neutralizes the chloramine.




Improving the "Wired but Tired" Hyperarousal


Useful thread: Five ways to reduce your ME/CFS "wired but tired" hyperaroused brain state




Treating Anxiety




• ME/CFS patient (Hip) — was able to eliminate his moderate-to-severe generalized anxiety disorder with a set of supplements including N-acetyl-glucosamine (NAG). Many other ME/CFS patients with anxiety who tried these supplements also observed a major reduction in anxiety levels, so this is a tried and tested treatment.





Prebiotics are food which feed friendly bacteria in the gut, but which bad bacteria cannot eat.


• ME/CFS patient (Hip) — found prebiotics such as inulin and FOS greatly reduced anxiety levels and improved mood.




Treating Depression




• ME/CFS patient (Hip) — finds Spanish saffron 100 mg quite helpful for depression. Antidepressant effects kick in within an hour or so of taking it. One systematic review found saffron to be as effective as standard pharmaceutical drugs. But watch out for fake saffron.




Treating Headaches or Migraines




Trimetazidine is a drug which improves myocardial glucose utilization.


• ME/CFS patient (Hip) — finds a single dose of trimetazidine 40 mg eliminates his normally 3-day long headaches within 12 hours, and if taken at the initial signs of headache, prevent the headache from manifesting in the first place.




Improving Sleep




• ME/CFS patient (Iquitos) — finds taking 15 drops of cannabidiol (CBD) oil allow him to sleep much better.





• ME/CFS patient (Hip) — finds taking melatonin 2 hours before planning to go to bed helps get him to sleep, and helps prevent the sleep cycle inversion of ME/CFS (where you are awake very late at night, and sleeping during day), and stops his non-24 (where you keep going to bed later and later as the days progress).


• ME/CFS patient (Hip) — finds when you are go to bed but find you are still awake an hour or so later, and cannot get to sleep, getting out of bed and performing 80 squats in rapid succession (which takes about 80 seconds) in order to exhaust the leg muscles and generate some lactate, is a remarkably effective way (almost infallible) of getting to sleep. After performing the squats and going back to be, he finds he then goes to sleep within 5 minutes.


• ME/CFS patient (SpiralOut) — finds when using Luminette glasses for several hours daily, which provide the equivalent of 10,000 lux of light to the eyes, it completely fixes his non-24 sleep issues (non-24 is where each day you go to bed later than the day before, because your circadian rhythm does not match the normal daily 24 hour cycle).




Relieving Pain


Low-Dose Naltrexone (LDN)


• ME/CFS patient (Wishful) — finds LDN works very well to relieve his ME/CFS body aches, which he thinks may be neuropathic pain.




Improving the "Molasses" Heavy Limbs Feeling


Far Infrared Heat


• ME/CFS patient (Hip) — finds far infrared heat on his back for several hours a day reduces the heavy limb feeling of ME/CFS, perhaps by its anti-inflammatory effects on the spine (as he speculates spinal ganglion inflammation might cause the heavy limb feeling).



From: Reviving the Broken Marionette: Treatments for CFS/ME and Fibromyalgia

Phenytoin is believed to act by modulating glutamatergic transmission. It has been in clinical use as an anticonvulsant for over 50 years, but it is also an antiarrhythmic similar to lidocaine and mexiletine. It has analgesic, anxiolytic and mood stabilizing properties. Jay Goldstein has used it to treat CFS/ME and fibromyalgia in a low dose of 100 mg a day.62 He reports synergistic effects from combining it with gabapentin.


Phenytoin may also help tinnitus.63


Phenytoin is generally thought to have adverse effects on cognition, but this may only apply to the large doses used to treat epilepsy. Smaller doses have even been shown to positively influence cognition.64 In one study phenytoin was found to cause a significant increase in right brain volume in patients with PTSD.65


The most common side effects include tiredness, nausea, ataxia (impaired coordination), nystagmus, dizziness and tremor. Phenytoin may reduce the blood levels of folic acid, biotin, calcium, vitamins B1 and B12, vitamin D, vitamin K and carnitine, but folate also decreases blood levels of the drug. Phenytoin can also interact with a number of different medications, including many antibiotics, anticoagulants, azoles, opiates, benzodiazepines, other anticonvulsants and oral contraceptives.


Phenytoin is available virtually everywhere and it is very inexpensive. It can be used topically as an analgesic, but this form is not commercially available and must be compounded

What is meldonium and why was it banned


Meldonium is used to treat ischaemia: A lack of blood flow to parts of the body, particularly in cases of angina, chronic heart failure, cardiomyopathy and other cardiovascular disorders.The drug also helps to adjust the body's use of energy and can boost stamina and endurance. It increases blood flow, which improves exercise capacity in athletes and increased blood flow means more oxygen to muscle tissue


Please also see links page

Psilopcybin and neuroplasticity is a topic I will review and update the site with

Lithium side effects can include fatigue. In some patients it has shown to combat fatigue. There are two types of medicinal Lithium Lithium is prescription and Lithium is otc. It may help CFS (page 3), TBIcf alttherapy (59) and OCD (68), supplements (8

therapeutic treatment of long covid as applied to chronic fatigue syndrome