In my previous blog entry, found here, I wrote about the general theory of heparin as a treatment for ME. This blog entry will detail my personal rationale for trying heparin. I will essentially illustrate why I believed this treatment was in theory suitable for me. Following this, I will describe the results of my heparin trial.


APS Antibodies

Several months ago, I had a blood test performed for antiphospholipid syndrome (APS). The results came back as follows:
Cardiolipin IgG Ab= 26     (normal is less than 12)

Beta 2 glycoprotein IgG Ab= 58     (normal is less than 20)
The footnote beneath the test read: “This result is consistent with antiphospholipid syndrome.” Thus begun my dalliance with hypercoagulation and subsequently heparin.
APS is an autoimmune condition. The hypercoagulation aspect of APS is caused by the APS antibodies. A diagnosis of APS generally requires 1 out of 3 positive antibody tests (I had two positive).  It also entails the occurrence of a past thrombotic event (which I haven’t experienced) or in women, pregnancy complications. The actual criteria are far more complicated and nuanced than this. Three papers by Berg et al. that I wrote about in my last blog entry, discuss why some ME patients have these antibodies and how they may indicate hypercoagulation in this patient population.

Raynaud’s Phenomenon

My former and now retired ME Specialist, stated that I had the coldest hands out of his 500 ME patients. My hands and feet have been consistently icy throughout the duration of my illness.
According to the paper ‘Low Level Activation of Coagulation with Coagulopathies in the Etiology of CFS / FM and Chronic Illnesses. An Explanatory Model.Increased SFM in the plasma may increase the plasma viscosity. Increased plasma viscosity decreases blood flow. Decreased blood flow may cause some end organ dysfunction. This may explain the Raynaud’s phenomenon of cold hands and/or cold feet.” Essentially the paper explains that the cold hands and feet of ME patients may be due to hypercoagulation.


My SPECT scan showed hypoperfusion in the brain.
Kato et al. in the 1997 study ‘Hypoperfusion of brain single photon emission computerized tomography in patients with antiphospholipid antibodies’ found SPECT scan hypoperfusion in headache patients with APS antibodies. They concluded that the SPECT scan results may be caused by “microarterial thrombosis, microvenous thrombosis or vascular spasms.”

Sed Rate

Since the onset of my ME, my sedimentation rate (sed rate) has been most commonly 2.
Referring to CFS and hypercoagulation, Researcher David Berg writes, “The normal range for sed rates should start above 3 or 4. Values below this are correlated with high SFM values. As the Soluble Fibrin Monomer (SFM) goes up in the plasma, these molecules form dimers (2 stuck together). This physically blocks the RBCs from settling out of the plasma, thus a low sed rate. The only other clinical condition to demonstrate low values involves paraproteins in the plasma such as in a cancer patient.”

Cold Water Therapy

The only treatment that has provided me with any significant improvement towards my ME symptoms has been immersing myself in cold water. Early on in my illness, this treatment would act like an elixir for several hours before wearing off. Eventually, I failed to respond to cold water therapy.
The following information from Professor Kakkar is from a tertiary source. Professor Kakkar of the Thrombosis Research Unit in Europe found poor blood circulation is CFS patients, this causes a reduction in oxygen supply to the brain and muscles. Professor Kakkar suggests that the production of the normal blood thinning enzyme TPA is reduced, as well as certain blood clotting proteins. Interestingly, Professor Kakkar advocates thermo regulatory hydrotherapy (TRHT), i.e. cold baths as the treatment for this poor circulation. Berg believes heparin is a more effective treatment.

Why Have I Been Treatment-Resistant?

I have tried hundreds of different treatments for my ME. Many of these treatments cause improvement in ME patients however the only treatment to significantly benefit me has been the cold water therapy, which as mentioned above, wore off. It is fairly unusual for an ME patient not to respond to the plethora of treatments I have tried. The hypercoagulation hypothesis is consistent with my non-responding status. CFS specialist Dr. Teitelbaum writes, “Using the blood thinner heparin has been able to help half of those who failed all other treatments.” He continues writing that “I find that about half of my patients with the most severe and refractory symptoms of CFS/FMS get better with this treatment.”

Coagulation issues

Prior to getting my blood drawn, I drink 1 litre of water. Despite this, the blood pathology nurse regularly comments that my blood is not flowing well and asks if I have consumed any water at all. Several patients online that have tested positive to hypercoagulation have also reported problems with their blood being drawn.

Hypercoagulation and Genetics

My 23 and ME genetic data lists venous thromboembolism as my highest-risk health condition relative to average. Based on my genes, my risk is 2.90x the norm. CFS &/or FM patients who have a hereditary deficiency for thrombophilia or hypofibrinolysis may be unable to control thrombin generation properly.” This is according to the Berg et al. paper, ‘Chronic Fatigue Syndrome (CFS) &/or Fibromyalgia (FM) as a Variation of Antiphospholipid Antibody Syndrome (APS): An Explanatory Model and Approach to Laboratory Diagnosis.’



Heparin-CFS Studies

I wrote in more detail about the heparin studies on CFS patients in my last blog entry. However I will now briefly outline the results of these studies. In the first study, 15/16 CFS patients benefited from heparin treatment either moderately or significantly. The second study found that on average, the 60 CFS patients improved by 85% while taking heparin.


Several of the above reasons for trying heparin are spurious and probably examples of my own confirmation bias. I hoped that the above pieces of eclectic evidence supporting heparin benefiting me would slot together like a jigsaw.

My Experience with Heparin

I was somewhat undecided over which type of heparin to inject. Unfractionated heparin was mainly utilised in the CFS studies and Dr. Teitelbaum used this type. It did however have the negative potential of having more side effects. Low molecular weight heparin is considered to be safer, yet due to only being recently introduced into the USA, it is less tried on ME patients. Ultimately, I used the unfractionated heparin.
On the 7th of July, I began the heparin injections, subcutaneously around my stomach. The dosage was 5000 IU, twice a day (a total of 10,000 IU a day). I would inject upon waking and again just before sleep. I also began taking 500mg of bromelain in the morning and 500mg in the afternoon as it helps improve fibrinolysis. David Berg’s protocol incorporates it for certain patients, depending on their blood test results.
After 3 weeks on the heparin, I had failed to notice any positive or negative effects. I therefore began taking piracetam concurrently. Piracetam is a nootropic and a study found that when piracetam is taken with heparin, the effects of both treatments are enhanced. I started at a low dosage of piracetam and gradually titrated this number upwards to a maximum of 4.8 grams (1.6 grams taken three times a day). I first tried piracetam 5 years ago and experienced no real effects. I have written about piracetam for ME here.
After 3 weeks of heparin, I gradually began to increase the dosage upwards to a maximum of 7,500 IU twice a day (15,000 IU total a day). Dr. Teitelbaum has patients maximise their heparin dosage at 8,000 units twice a day (16,000 IU total a day), if their blood work remains normal. I did have regular blood tests while on the heparin.
On the 10th of August, I ceased the heparin injections. After 5 weeks, I had not managed to note one iota of improvement. Alternately, I didn’t experience any side effects either. The patients Dr. Teitelbaum treats with heparin tend to improve within 2 weeks. The Berg et al. study patients drastically improved within 2-4 days of commencing treatment. I was never planning on trialling heparin for an extended period of time and I believe 5 weeks was sufficient to prove that it was not working for me.


APS Blood Test Meaning

I believe the abnormal APS blood tests may provide some clues into my ME etiology. This study by Hokama et al. found cardiolipin antibodies in a high portion of CFS patients. The results varied depending on which cardiolipin antibody was being tested. My cardiolipin IgG levels were 26 (normal is less than 12). 4/40 CFS patients tested in the study had positive IgG levels. The Hokama et al. study found 95% of CFS patients testing positive to cardiolipin IgM antibodies. The authors’ conclusion writes “…suggesting that CFS may be an autoimmune condition.” The paper also states that CFS patients may aim to suppress the cardiolipin antibodies in their blood. The authors continue on to argue that this may be achieved through Rituximab usage because “Rituximab may serve as an effective therapeutic agent for ameliorating the symptoms of CFS.” It is interesting that Rituximab is now emerging as a promising treatment for ME.
My Beta 2 glycoprotein IgG levels of 58 (normal range is less than 20) is most commonly associated with APS. Levels of 20 of greater exceed the 99th percentile. The precise meaning of this test is complicated but it can also be indicative of an autoimmune disease.


Heparin was a treatment that I held lots of hope for. My above abnormal APS blood test results fitted in well with the Berg et al. papers and the hypercoagulation hypothesis. My peripheral justifications for trialling heparin such as my Raynaud’s phenomenon, brain hypoperfusion and low sed rate coupled with my various other idiosyncratic symptoms posited heparin as the perfect treatment for me.


My hopes of improving as a consequence of taking heparin were dashed in a sluggish manner. Day-by-day I failed to improve on the injections until after 5 weeks I thwarted my heparin therapy. Most treatments I trial are directed somewhat at me but more broadly the generic ME patient- whomever he or she is. This was a treatment that seemed tailor-made for my symptoms and blood test results. From a different perspective, heparin is a risky treatment and I am pleased that I didn’t experience any side effects. It is unfortunate that it didn’t work, although I am now quite accustomed to ME treatments not working for me! I am hopeful that my APS blood test results can provide an inkling into the lingering mystery that is my ME.



Heparin for ME

Heparin is an anticoagulant drug that may be useful to some ME patients. It is typically used in the prevention and treatment of both pulmonary embolism and deep vein thrombosis. It has been theorised that ME in some instances may be caused by a hypercoagulable state and thus heparin would treat this. I will; examine the heparin studies on ME patients, present the opinions of ME experts on heparin and detail which patients may benefit from either heparin or an alternative anticoagulation treatment.


The theory

The human body’s coagulation process is complicated. The ME-coagulation theory is doubly complex and a simplified theory describing it is as follows. Patients initially are struck down with an infection such as; HHV-6, EBV, CMV, chlamydia pneumonia, a tick borne disease or another pathogen. Research involving David Berg suggests that numerous infections can instigate the body’s blood clotting system. This may target those people with an acquired or genetic coagulation defect. After the clotting process is activated, the body creates ‘soluble fibrin monomers’ (SFM). These SFM are analogous to sheets that cover the blood vessels. The resultant impairment of blood circulation is then responsible for ME symptoms.


The studies

The first study by Berg et al. was published in 1998 and titled ‘Is CFS/FM due to an Undefined Hypercoagulable State Brought on by Immune Activation of Coagulation? Does Adding Anticoagulant Therapy Improve CFS/FM Patient Symptoms?’ The full paper can be found here. 20 CFS/Fibromyalgia patients were involved in this pilot study however there was no control group. The patients were tested for various coagulation measures. 90% had an abnormal ‘sonoclot rate’, 88% had abnormal ‘SFM’, 48% had abnormal ‘fibrinogen’ and 60% had abnormal ‘platelet activation’.

16 of the patients with positive ‘baseline studies’ were treated with placebo for a week followed by heparin. The heparin was administered subcutaneously twice a day and ranged from 5000 units to 8000 units. After one month, the subjects rated their subjective improvements. All 7 of the fibromyalgia patients improved. 1 patient noted some improvement, 3 had moderate improvement and 3 experienced significant improvement. All 9 of the CFS patients improved. 4 said they had moderate improvement whilst 5 had significant improvement. The paper continues on to state that most of the patients began to feel like their “old selves” within 2-4 days of commencing the heparin treatment.

The second study Berg et al. published was in 1999 and titled Chronic Fatigue Syndrome (CFS) &/or Fibromyalgia (FM) as a Variation of Antiphospholipid Antibody Syndrome (APS): An Explanatory Model and Approach to Laboratory Diagnosis.’ The full paper can be found here.  A blinded ‘prospective’ study is detailed within this paper. It contained 54 CFS/Fibromyalgia patients and 23 controls. Five specific coagulation tests were performed on all subjects and two positive tests were required to be classified as having coagulation problems. 94% of the CFS/Fibromyalgia patients were positive for hypercoagulation, in contrast to just 4% of the controls testing positive.


The Third paper by Berg et al. was titled ‘Low Level Activation of Coagulation with Coagulopathies in the Etiology of CFS / FM and Chronic Illnesses. An Explanatory Model.’ The full paper is behind a paywall but can be accessed here for free. This paper claims that in excess of 3000 patients with chronic illnesses have been tested for coagulation problems and over 80% of these patients have tested positive. The paper also mentions that genetic studies have found a 2-10 fold increase in coagulation protein defects among CFS/fibromyalgia patients and others with a chronic illness. The paper also alludes to ‘unpublished data’ that shows having SFM in the blood may cause very low sedimentation rates (in the 0-4 range).

The paper also refers to a retrospective study involving a cohort of 60 CFS/fibromyalgia patients. The subjects were given 5000 units subcutaneously of heparin, twice a day for an average of 8 months. The average improvement on a scale of 1-10 was 8.5, equivalent to an 85% improvement.


A Negative study has also been published by Kennedy et al. The 2006 study was titled ‘Is chronic fatigue syndrome associated with platelet activation?’ The full study can be found here. The study included 17 ‘CFS’ patients who fulfilled the contentious Fukuda criteria as well as 16 controls. The study found no coagulation abnormalities in the CFS patients studied.


What the ME Specialists Say

Dr. Teitelbaum has written “Using the blood thinner heparin has been able to help half of those who failed all other treatments.” He continues writing that “I find that about half of my patients with the most severe and refractory symptoms of CFS/FMS get better with this treatment.” Dr. Teitelbaum has found that almost every CFS patient he has tested to be positive for hypercoagulation. He does however stipulate that he hasn’t tested healthy controls to compare his results. Dr. Teitelbaum also warns about the dangers of heparin treatment and warns that it is a riskier drug than most of the other drugs he recommends. He tends to use it as a last resort. Dr. Teitelbam is also not 100% convinced in the hypercoagulation hypothesis. He speculates that another feature of heparin may be responsible for the positive effects on CFS patients such as its antiviral properties.

Dr. Cheney mentions heparin in a talk given in the year 2000. He speaks of its ability to shift the immune system from Th2 dominant to Th1. This may potentially benefit ME patients with a Th2 shifted immune system. Dr. Cheney only recommends heparin if the patient tests positive to hypercoagulation. He has found approximately 50% of his patients testing positive.

Dr. Myhill is not an advocate of heparin in ME patients. She has trialled heparin usage in 4 of her patients with no success. She cites the aforementioned negative Kennedy et al. study as evidence against hypercoagulation being a factor in ME.



When it comes to hypercoagulation testing and ME, things can become complicated. It has been suggested by David Berg that any ME patient with cold hands and feet/Raynaud’s phenomenon and a low sedimentation rate be tested for hypercoagulation. Berg, who introduced the concept of specialised coagulation testing has found sedimentation rates “below 4 or 5” indicative of hypercoagulation in ME patients. Sedimentation testing is a standard blood test that is routinely done with most normal blood tests. Most ME patients will probably have this test on file and it is commonly listed as ‘ESR.’

The coagulation tests so far mentioned in the above studies and requested by the ME physicians have been specialised and done by the Hemex laboratory. They were taken over by Esoterix Laboratory Services who now do the coagulation tests and are based in the United States. This is considered the gold standard test in hypercoagulation.

blood coagulation

Antiphospholipid antibody syndrome (APS), also sometimes referred to colloquially as Hughes’ Syndrome is an autoimmune disease that is characterised by blood coagulation. Standard laboratories around the world can test for APS. The studies and papers by Berg et al. above refer to their findings in ME patients as a “Variation of Antiphospholipid Antibody Syndrome.”  The papers continue on to mention that “Antiphospholipid (APL) antibodies have been long associated with a hypercoagulable state, involving both procoagulant activity as well as inhibition of anticoagulant and fibrinolytic activity.” One of the APS antibodies that can be readily tested for is called ‘beta-2-glycoprotein.’ This according to Berg et al. can trigger the chain of clotting. The other subtests and their implication in APS are detailed here.


Heparin Protocols

There exist several theories pertaining to the best methods of taking the heparin once hypercoagulation has been established in an ME patient.

Dr. Teielbaum does not mention what dosage of heparin he starts his patients on however if the patient doesn’t improve and the PTT blood test is still normal, he increases the dose to a maximum of 8000 units twice a day (a total of 16,000 units a day.) The heparin is administered by subcutaneous injection for the first six weeks. He switches them to nose spray heparin or sublingual heparin. Dr. Teitelbaum prophesizes that patients should start to feel better around the 10-14 day mark of treatment. He adds a 6-12 month course of either antibiotics such as doxycycline or antivirals depending on laboratory results. These are taken while the patient is still on heparin. Dr. Teitelbaum has his patients get a platelet count and PTT blood test every 3 days for the first 9 days after commencing heparin therapy and every week thereafter.

David Berg developed a protocol for treating ME patients for hypercoagulation and this can be found here. His system involves heparin being taken for 180 days. Transfer factor is taken from day 30-120 and antibiotics from day 30-90. If a patient has high Lp(a) or PAI-1 levels, he recommends bromelain be taken from day 1 to day 120.

Ken Lassesen has a model of ME that incorporates the hypercoagulation aspect. He has written about this here and here. He writes that the cause of the poor blood flow that is shown in many ME patients SPECT scan results may be due to hypercoagulation. He refers to a study in which the nootropic piracetam was taken concurrently with heparin. The accumulative effects of piracetam plus heparin were more beneficial to blood flow in the brain than the theoretical adding of piracetam and heparin. In other words, the piracetam and heparin complemented each other to combine to a greater efficacy.


Type of Heparin and Dosage

There exists two types of injectable heparin used by ME patients. The first is unfractionated heparin (UFH). Most of the above studies used UFH and Dr. Teitelbaum used this type on his patients. Due to the short half-life of UFH, it requires subcutaneous injection twice a day. The dosage used varies but generally starts at around 4000-5000 units twice a day in a 0.2ml-1ml solution. Berg has stated that patients less than 68kg (150lbs) should start at 4000 units twice a day. In contrast, those over 68kg (150lbs) should begin their dose at 5000 units twice a day. Some specialists increase this up to a maximum of 8000 units twice a day if bloodwork remains normal. It is imperative to monitor UFH usage via blood tests. As mentioned earlier, Dr. Teitelbaum has his patients get a platelet count and PTT blood test every 3 days for the first 9 days of UFH treatment and every week thereafter. Dr. Teitelbaum instructs patients to use an insulin syringe to inject the UFH while others recommend using a tuberculin syringe.

syringe photo

The second type of subcutaneous, injectable heparin is known as low molecular weight heparin (LMWH). This variant is more predictable than UFH and is generally considered to be safer. The studies on ME patients and heparin usage are largely void, primarily due to LMWH more recently being introduced to the United States. Berg recommends patients under 68kg (150lbs) taking 30mg of LMWH in the morning. He encourages those over 68kg (150lbs) to take 30mg of LMWH in the morning and 15mg at night. Patients taking LMWH may require an anti-factor Xa activity blood test if they have other medical conditions such as renal impairment.

Sublingual UFH is another alternative for hypercoagulation. Ken Lassesen has written that this form can be of equitable effectiveness. It requires 2 minutes under the tongue before being spit out. After 6 weeks of UFH subcutaneous injection treatment, Dr. Teitelbaum has patients switch to either sublingual heparin or heparin in the form of a nasal spray.


Side effects

Heparin-induced thrombocytopenia (HIT) is a potential side effect of heparin treatment. There is a lower likelihood of this occurring if the patient takes LMWH. Several studies have examined the risk of HIT with heparin usage and the chances of this occurring varies depending on the disease studied. The chance of LMWH causing HIT is fairly remote however there is a higher chance of UFH causing HIT. HIT causes a low platelet count and is most likely to occur 5-14 days after commencing heparin therapy. Vitamin D and calcium supplementation may reduce the chances of HIT occurring.

If Heparin is used for an extended period, a DEXA bone density scan should be performed. It is also imperative to have kidney and liver function tests prior to commencing heparin treatment. Those who have had a peptic ulcer should not take heparin. I should emphasise that heparin treatment is a riskier treatment than most other ME treatments. It is essential that a doctor monitors the progress of the treatment and is aware of the potential dangers.



The ME-hypercoagulation link, in some cases, can theoretically be treated without heparin and with supplements. Dr. Teitelbaum has written that the anticoagulation supplements his patients have tried have failed to yield any positive results. Despite this, there exists numerous accounts online of ME patients benefiting from anticoagulant supplements. Whether this is due to the supplements effects on coagulation or because of some other mechanism is not known. The supplements should not be taken with heparin due to the risk of excessive bleeding.

Nattokinase is an enzyme that is derived from the fermented soybeans called Nattō. Multiple studies have found it to have various anticoagulant properties.  Numerous anecdotal reports litter the internet of non-ME patients replacing the prescription Warfarin with Nattokinase with degrees of success. Some ME patients have also found Nattokinase to be beneficial. The dosage should not exceed the maximum amount of 4000 fibrin units.


Lumbrokinase is an enzyme that is sourced from a type of earthworm. Some patients take it to break down the fibrin implicated in hypercoagulation. Several ME patients have noted an improvement in symptoms after taking Lumbrokinase. Serrapeptase is a similar enzyme to Lumbrokinase.



The ME-Hypercoagulation connection was a very promising theory until a small study with Fukuda criteria patients found no coagulation problems in CFS patients. The subsequent coagulation research in ME was then discontinued. Regardless of the validity of the hypercoagulation theory in ME, heparin has been an effective treatment for many patients. Those in the Berg studies experienced dramatic improvements and Dr. Teitelbaum’s comment that half of those ME patients with the most severe and difficult to treat symptoms “get better” with heparin provides hope. The double-edged sword with heparin is the potential side effects. This shifts the dynamics of the risk-reward ratio. If an ME patient is severely ill, with cold hands and feet and a low sedimentation rate, it may be worth getting subsequent and specialised coagulation testing done and discussing with their physician about whether heparin treatment is warranted.


Gabapentin is an anticonvulsant drug primarily used to treat epilepsy that may be helpful to some ME patients.

Gabapentin may benefit ME patients due to:

  • Reducing general pain
  • Thwarting neuropathic pain
  • Minimising fatigue
  • Relieving muscle cramps
  • Enhancing sleep quality
  • Stopping restless legs syndrome
  • Improving bladder function
  • Having potential neuroprotective properties
  • Decreasing multiple chemical sensitivity symptoms

It was originally thought that Gabapentin primarily worked due to its effects on the GABA neurotransmitter hence inducing calmness and sleep. It is now thought that Gabapentin’s mechanism of action is due to it being a calcium channel blocker. As a consequence, it may reduce the secretion of certain neurotransmitters that cause pain and stimulate the brain. Anecdotally, many ME patients have gained more energy as a consequence of taking Gabapentin. Unfortunately, in a reasonable portion of these cases, the effects seem to have gradually worn off.
ME specialists and doctors opinions’ on Gabapentin

Dr. Goldstein listed Gabepentin among his five most favoured treatments for those with ME. The others being; Nimodipine, oxytocin, intravenous lidocaine and baclofen. Dr. Goldstein believed that Gabapentin may regulate the neurotransmitter imbalance in the brains of ME and fibromyalgia patients. He recommended a low dose of 100mg-800mg, stating that effects should be noticed in the timeframe between 30 minutes and 8 hours. If tolerated, he would recommend the dose be slowly titrated upwards to a maximum dosage of 5000mg per day (e.g. 3 doses per day totalling 5000mg.) Dr. Goldstein found that a fairly high portion of his patients reported increased energy soon after their first dose with some patients also experiencing Gabapentin’s antidepressant effects.
Dr. Teitelbaum uses Gabapentin on some of his patients for sleep enhancement. He groups Gabapentin with Gabitril and Lyrica, stipulating that despite all three drugs being related, one of the three will often be effective and tolerated by the patient even if the other two are not. Dr. Teitelbaum generally starts patients on either Gabapentin or Gabitril and only prescribes them Lyrica if these drugs are not effective. He has found these three treatments to reduce pain levels, improve restless legs syndrome symptoms and improve the patient’s deep sleep. Dr. Teitelbaum warns that the aforementioned three drugs are not addictive but it is imperative that they be weaned off slowly especially if taken for a long period of time. He starts patients on 100-300mg per night of Gabapentin and gradually increments the dosage to 300-900mg three times per day.
Dr. Cheney categorises Gabapentin into the class of neuroprotective drugs that may help improve ME patients’ sensitivity to stimulation. He started those with ME on 300mg three times per day. He believes some doctors use doses of Gabapentin that are too high. In a 2009 talk, Dr. Cheney seemed to be less of an advocate of Gabapentin.
Dr. Enlander uses Gabapentin on some of this patients. He believes that Gabapentin stops the “abnormal impulses” ME and fibromyalgia patients’ brains experience. As a consequence, the brain’s muscle fibres experience a reduction in fatigue. Dr. Enlander uses doses up to a maximum of 2400mg per day

A 2007 study by Arnold et al. was performed on fibromyalgia patients who took Gabapentin at doses between 1200mg and 2400mg for a period of 12 weeks. Patients experienced significantly improved sleep as well as less pain and less fatigue compared to the placebo group. The most frequent side effects noted were sedation and dizziness.
A 2010 study by Usui et al. found a strong indicator concerning which fibromyalgia patients were likely to respond to Gabapentin. Those patients unlikely to respond to Gabapentin had hyperperfusion in certain parts of the brain as determined by a SPECT scan. Essentially, increased blood flow in the brain was strongly linked with a poor patient response to Gabapentin.
A 2015 study by North et al. examined the effects of an extended release version of Gabapentin on fibromyalgia patients over 15 weeks. Patients noted a reduction in pain, improved quality of life as well as an increase in quality and quantity of sleep. Many improvements were noted after only 4 weeks. Unlike the Arnold et al. study, this study had a smaller sample size and no control group.
Side Effects
Gabapentin is generally considered to be fairly safe and well tolerated. Despite this, some ME patients have anecdotally experienced side effects. A Cochrane Review by Moore et al. in 2011 based on data from chronic neuropathic pain patients concluded that Gabapentin was mostly tolerable however adverse events were frequent. 12% of patients withdrew from studies due to side effects. The most common being; dizziness, somnolence, peripheral oedema and gait disturbance. The Cochrane Review stipulated that serious adverse events were no more common in the Gabapentin group than the placebo group.
It should be emphasized that there is fairly universal agreement that Gabapentin should be started off at a lower dose and gradually increased if tolerated. Also stopping treatment suddenly may be harmful and patients are commonly advised to reduce the dosage slowly. Some doctors recommend Gabapentin only before bedtime with the motive of improving sleep whilst doctors with other objectives recommend that it be taken three times a day.
My Experience with Gabapentin

I began taking Gabapentin late in 2015, hopeful that I would reap several of its benefits. My poor sleep was the primary reason I chose to take Gabapentin. Related to this, I was interested to see whether my restless legs syndrome symptoms would ease. Gabapentin sometimes reduces patients’ overstimulation although I was slightly dubious as to whether this key symptom of mine would recede. I was also hopeful that I would join the anecdotal reports of ME patients who have gained more energy as a result of taking this drug.
I began taking 100mg of Gabapentin before bed and gradually increased this dosage as I failed to notice any side effects. I topped out my dosage at the relatively small maximum of 300mg per night. At this quantity I would sleep fairly deeply throughout the night but wake up still feeling unrefreshed. Curiously, my restless legs syndrome was unaffected by the Gabapentin. I was reluctant to increase the dosage any higher as I felt mildly ‘zonked’ throughout the days. Gabapentin’s effect of knocking me out during the night was a secondary reason to not increase the dosage further.
After 300mg per night of Gabapentin for a period of a month, its ability to keep me asleep during the night started to diminish. I then tapered off the drug with relative ease as its only real positive effect of keeping me asleep for most of the night had begun to wane. Several months later, I tried Gabapentin at an identical dosage and had a parallel experience. After one month, its sleep producing effects had diminished.
Overall, I didn’t notice any of the more common side effects of Gabapentin and its efficacy towards improving my general ME was negligible. Based on the Usui et al. study mentioned earlier, it was more likely that I would be in the responder group. My SPECT scan showed hypoperfusion (reduced bloodflow) in the brain- the opposite to the fibromyalgia patients who failed to respond to Gabapentin.

Gabapentin is a fairly common drug in the ME realm, although more regularly prescribed for fibromyalgia. It has the ability to target multiple, seemingly unrelated ME symptoms and thus patients take it for different reasons. My sleep length improved as a consequence of this drug but my sleep quality failed to be enhanced. Ultimately this single positive effect wore off causing me to stop taking the Gabapentin.




Over the past 12 months, I have tried many treatments that I haven’t written about in previous blog entries. This article will briefly touch on these treatments. Following this, I will detail how my health has played out throughout 2015.


2015 was a year that I trialled many ME treatments. These primary treatments were articulated in more detail in blog entries during the year. The following is a list of treatments I trialled at various stages of 2015 that I haven’t written about previously.



The main motive for me taking astaxanthin was its powerful anti-inflammatory effects. I have been experiencing joint pain during 2015 and I thought of astaxanthin as a safer long-term alternative to NSAIDs. One health questionnaire of 247 sufferers of back pain and rheumatoid arthritis or osteoarthritis found over 80% improving after taking astaxanthin. This supplement also has immunomodulatory effects and many other potential benefits.




I started taking 12mg of astaxanthin in November 2015 and plan to reduce the dose to 4mg within the coming weeks. The joint pain in my fingers, wrists and knees has all improved since I started taking the astaxanthin although I’m unsure if this is coincidental or not.


Benfotiamine and Allithiamine

During 2013, I took high dose thiamine (vitamin B1) and didn’t notice any effects. I wrote about this treatment in more detail here. In 2015, I trialled allithiamine and benfotiamine which are essentially different versions of thiamine. These two versions of thiamine may be better absorbed by the body than standard thiamine. Anecdotally, some patients have reported one of these versions to benefit them whilst standard high dose thiamine has not. I felt a bit sicker while taking 100mg of Allithiamine in combination with a mutli B supplement and I hence stopped this treatment after several days. I took 500mg of benfotiamine for about a month with no effects noted.


Elimination Diet

I have seldom written about diet on my blog for two primary reasons. The first is that food doesn’t seem to affect any of my symptoms. Secondly, I have tried omitting various types of food such as gluten, dairy products etc, at various times throughout my illness but have failed to notice any effects of these food omissions.


Fast forward to mid 2015 and I received an email from a fellow Australian ME patient who had similar symptoms to me and benefited remarkably from trying the elimination diet. I am grateful for their thoughts and must thank them for this. The elimination diet that I tried was devised by the Royal Prince Alfred Hospital with the premise of stopping food intolerances. Salicylates, amines, glutamate, gluten and food additives amongst other substances are avoided in the diet. These omissions ultimately don’t leave much to eat and following the strictest version of the diet was challenging to start with before I gradually adapted. I had a night of refreshing sleep while on the diet which is a once every two year rarity for me but other than that, I didn’t notice any other changes. I am planning to try the diet again in mid 2016 for a longer period of time.


There are various types of elimination diets and Dr. Cheney has written fondly of an elimination diet. He mentions, “Elimination diets, and improving digestion and gut epithelial function can pay huge dividends in this patient population.” Dr Cheney has found over half of his CFS patients studied to have food sensitivities. He believes an elimination diet is the best way to determine a patient’s food intolerances.



The primary motive for me taking IP-6 was its ability to increase Natural Killer (NK) cell activity which is often impaired in ME patients. Dr. Edward Conley reports that he has used IP-6 to improve NK cell function in “dozens of cases” of CFIDS.  He elaborates on one case in which NK cell function improved 200% and the patient went from being unable to work to managing a 32-40 hour job.


I took IP-6 for a month during 2016 and didn’t notice any effects. The dose I was taking was 3.2 grams twice a day on an empty stomach. I didn’t have the ability to perform a natural killer cell function test to monitor its NK cell effects on me.


Naphazoline HCL

Dr Goldstein wrote prolifically about ME/CFS and his treatments always interest me as they seem divergent from many other ME specialists treatments, yet steeped in theoretical/practical evidence. He compiled a list of treatments he trialled often sequentially when a new ME/CFS patient visited him. This list is well worth reading and can be found here. Also listed are his musing on an assortment of other treatments. Naphazoline HCL 0.1% eye drops were the first treatment he tried on patients whom stepped into his office. If the patient benefited from this treatment, they would feel better immediately. Dr. Goldstein theorised that the trigeminal nerve would change the patient’s brain function as a result of these eye drops. It has been claimed that 20% of patients benefited from this treatment and on those patients whom they worked, the drops worked remarkably well.


It is imperative that the drops used are 0.1% not 0.01% drops. In some countries, the 0.1% drops are available over the counter. I tried the Naphazoline eye drops on two occasions during 2015 but didn’t notice any effects.



Dr. Goldstein originally tried Ranitidine on infectious mononucleosis patients in the 1980s and due to the success he experienced began using it on ME patients. Ranitidine (Zantac) along with Cimetidine (Tagamet) are H2 receptor antagonists. Dr. Goldstein recommends the dosing structure of 150mg twice a day for one or two days. When patients do respond to one of these H2 receptor antagonists, Dr. Goldstein writes that the recovery is remarkable. He continues on to state that these drugs may cause overstimulation in ME/CFS patients.




An anecdotal report of a patient significantly improving after taking Ranitidine can be found here. This patient did however experience severe headaches as a consequence of the treatment which is a possible side effect. Ranitidine is available over the counter in many countries, if not, Cimetidine is normally available over the counter instead. I took 150mg of Ranitidine twice a day for three days but didn’t notice any effects.


My Health in 2015


Dust Allergy

The major improvement in my health last year was the reduction in nasal mucus discharge or mucus coughed up. This was my first ME symptom to emerge and for many years I was using two boxes of tissues a day. A few years ago, I had an allergy test and was put on dust allergy drops plus the nasal spray Avamys. This improved my tissue usage to around one box a day. In 2015, my sister moved out of the house and I moved into her room with only the bare essentials cluttering the room. This further reduced my dust allergy and I am currently down to using one box of tissues per week- a far cry from the 14 boxes a week I was using for 6 years!


Joint Pain

During mid 2015, my big toe joints began to experience pain, make cracking sounds and generally feel uncomfortable. My ankle joints also felt a similar sensation. In October, my finger, wrist, knee and neck joints also became painful. I began taking Astaxanthin, which I wrote about at the top of this blog entry. My newly developed finger, wrist, knee and neck pain improved however my toe and ankle pain persisted. I was referred to a rheumatologist who thought I may have osteoarthritis or rheumatoid arthritis however was unsure. He prescribed me painkillers and thought he would have a more clear idea of what’s going on after my symptoms had more time to progress. I see the rheumatologist again in March. Joint pain is often included on criteria lists for ME/CFS so it may simply be secondary to my illness.


joint pain


I wrote a blog entry many years ago about the strange, permanent and dark spots that emerged on my joints when my illness initiated. This blog entry, found here, shows photos of the spots on my toes and fingers. I have over the past 12 months noticed a darkening of the big toe spots as well as the development of spots on the joint located at the base of my big toe. I’m unsure if this is related to the joint pain I’ve been experiencing. Also, further spots have appeared on my index and middle finger joints.



2015 was the year that I struggled with sleep the most. Earlier in my illness, I would sleep right through the night and need an alarm clock to stop me sleeping for extended hours. This situation has inverted over the past handful of years and I now struggle to fall asleep. Also, when I wake during the night I am now often unable to get back to sleep. My Restless Legs Syndrome also prohibits my sleep.


Back Pain

The final significant health change that occurred to me in 2015 was my back pain. In late 2014 I suffered a thoracic back sprain by simply standing up from a sitting position. I have since experienced some quite irksome back problems. During 2015, I saw the physio every two weeks for the entirety of the year and took many painkillers for my back. I have been doing some very basic and modified stretches for my back too. I aggravated my back during August, September and October of 2015 by simply standing up from a sitting position and couldn’t really stand or walk properly on each of these occasions for a week. The rheumatologist whom I saw for my joint pain suspects that my back pain is related.



Overall, my ME health remained rather static in 2015. The peripheral symptoms I have written about above were nothing more than a blip on the radar when compared to how the crux of the ME has affected me. I am thankful that the mucus production symptom is being thwarted and I hope this continues into 2016. At present, the joint pain isn’t significant and I plan on continuing the Astaxanthin which may be easing it. My sleep and sleep treatments are something that I wrote about more extensively in my last blog entry and I have a sense of optimism that 2015 was an outlier as far as my insomnia was concerned. Regarding my back pain, I have found through trial and error that sleeping on the right type of mattress significantly improves this symptom. By finding the optimal mattress in 2016, this may not only ease the back pain but perhaps improve my sleep too. Improving my ME is a more difficult matter, although I have some more ideas up my sleeve for 2016!

“Sleep is that golden chain that ties health and our bodies together.” –Thomas Dekker
M.E. patients are often nocturnal creatures- not by choice but as a consequence of their illness. It is a bitter irony that many of us feel the desperate need for sleep during the daylight hours but as soon as nightfall sets in, so does the insomnia or unrefreshing sleep. This blog entry will examine the myriads of potential sleep treatments that the ME/CFS experts of the world prefer. Following this, I will detail my experiences over the years with both sleep enhancing supplements and prescription drugs.
Sleep Treatments the ME/CFS Specialists Recommend

It is imperative that I mention that some of these specialists’ recommended treatments are sleep initiators while others are sleep prolongers.
Dr. Cheney

Dr Cheney is an advocate of Klonopin and likes using Doxepin Elixir drops in synchronicity with the Klonopin. He states that B12 in the form of hydroxocobalamin injections may help sleep, it taken at night. Magnesium also plays a pivotal part in Dr. Cheney’s sleep repertoire and he prefers it in the form of magnesium glycinate.
Dr. Teitelbaum

Dr. Teitelbaum’s approach towards patients’ sleep is multi-faceted. He emphasises that quality sleep is utterly fundamental so much so that his ‘SHINE’ protocol starts with ‘S’ for sleep. Dr. Teitelbaum thinks patients can get the greatest benefit from sleep aids by taking small amounts of as many different sleep aids as required to a maximum of “5 or 6.” He sells his own OTC sleep formula that contains many of the ingredients that he believes helps CFS patients sleep. The supplements Dr. Teitelbaum is an advocate of include; Suntheanine, Wild Lettuce, Jamaican Dogwood, Hops, Passionflower and Valerian. The medications he writes fondly of for sleep, in the order that he generally prescribes them for CFS patients are; Ambien, Trazodone, Klonopin, Gabapentin, Doxylamine (OTC), Carisoprodol, Doxepin, Cyclobenzaprine, Tizanidine and Zaleplon. He describes some patients needing to try different medications and other patients requiring a different order of trial to the above sequence.
Dr. Klimas

Dr. Klimas states that sleep improvement isn’t as easy as taking a magic pill. She believes that patients who wake up exhausted require a sleep study that takes place in a specialised sleep lab. The sleep study will determine if the sleep problems are caused by a characterised sleep disorder such as sleep apnea. The study will also document sleep patterns including the need for stage 3 and 4 sleep. Dr. Klimas believes treatment can then proceed following the results of the sleep study. When Dr. Klimas does prescribe sleep drugs, she avoids the likes of Ambien and Restoril believing that they don’t promote quality sleep, instead just instigating sleep. Dr. Klimas is mainly an advocate of Elavil and Doxepin. She also likes Flexeril and Klonopin.
Dr. Lapp

Dr. Lapp shares a similar penchant to Dr. Cheney for Klonopin used in tandem with Doxepin, both at a low dosage. He also emphasises that patients needn’t start with prescription drugs for sleep. He thinks milder sleep problems may be quashed by the use of; Valerian, Excedrin PM, Tylenol PM and Melatonin. Trazodone, hypnotic drugs and SSRIs are all sleep treatment possibilities according to Dr. Lapp.
Dr. Myhill

Dr. Myhill writes of numerous, non-tablet techniques to maximise the chances of a first-class sleep. She also uses a mixture of supplements and prescription drugs to improve her patients’ sleep. She is an advocate of; Melatonin, Valerian and Nytol. If these treatments prove to be ineffective, she tries prescription drugs including; Elavil, Surmontil, Sonata and Diazapam.
Dr. Enlander

Dr. Enlander emphasises the nuanced world of sleep problems and warns of caution when treating sleep apnea sufferers with sleep drugs. He often starts with a drug that is in his words “the least provocative” in Diphenhydramine. If this is ineffective, he commonly tries patients on Trazodone. Other sleep treatments that Dr. Enlander utilises include; Ambien, Sonata, Klonopin, Zanaflex or Flexeril.
 sleep tablets
Sleep Aids

Over the past few months I have taken 3 different sleep aids with the goal of improving my sleep.

GABA’s primary action in the brain is to tame the over firing of neurotransmitters. A potential problem with GABA supplementation for sleep is its inability to cross the blood-brain barrier. Due to this pitfall, GABA supplements may work through an alternate mechanism. This is through the GABA supplement’s ability to calm the body and hence reduce insomnia. A sublingual version of GABA may be more effective than the capsule form.

5-HTP is a version of the amino acid tryptophan and was found in two studies to improve Fibromyalgia patient’s symptoms. This study by Puttini et al. involved 50 Fibromyalgia patients taking 5-HTP for 90 days. Improvements were seen in the areas of; fatigue, sleep quality, pain, anxiety and the number of tender points. A ‘good’ or ‘fair’ improvement was seen in about 50% of patients. 30% of patients reported side effects but only one patient dropped out of the study for this reason.
This second study by Caruso et al. was double blinded and placebo controlled. 25 Fibromyalgia patients were given the placebo and the other 25 Fibromyalgia patients took the 5-HTP. The group given the 5-HTP were provided with 100mg three times a day for 30 days. Similarly to the previous study, improvements were seen in tender points, pain, sleep, anxiety and morning stiffness in the group taking 5-HTP. Although the placebo group also improved in sleep and pain measurements. 5-HTP is used by the body to make serotonin which may improve sleep quality. Serotonin syndrome is a risk if other treatments to increase serotonin are taken with 5-HTP such as SSRIs.
Suntheanine (L-theanine)

L-theanine is an amino acid and may improve sleep due to playing a role in increasing brain levels of GABA, serotonin and dopamine. L-theanine is responsible for the taste and calming effect of green tea. Dr. Teitelbaum is an advocate of L-theanine and recommends 50mg to 200mg before bedtime to improve sleep. He also writes that it can be taken several times during the day to improve anxiety. This study found 400mg of L-theanine to improve the sleep of boys with ADHD.
valerian tablets
My Experience with these Sleep Aids

Over the past few months, I trialled each of these sleep aids.

I took 750mg of GABA for a period of a week and didn’t notice any effect on my sleep.

I took 200mg of 5-HTP before bed for a week and similarly failed to notice any effects.

I took a dosage of 300mg of L-theanine before sleep and 150mg upon waking during the night and this improved my sleep marginally. I have been desperate for any improvement in my sleep and hence I continue to take L-theanine every night although only 150mg before bed and 150mg when I wake during the night.
My Long Term Sleep Treatments

Sleep improvement is widely known as being a lynchpin in countless ME protocols. Over the past 10 years, I have woken up every morning feeling more sleepy and groggy than when I went to sleep the night before. There have been several exception to this, which I vividly recall- mornings when I have woken and felt well rested. These instances have occurred after I took; a Myers’ cocktailTTA and on the last occasion Moringa Oleifera. 
The quality sleep these treatments provided me was only transient-lasting one or two nights. It is a curiosity that each of these treatments lacks a direct mechanism of action on sleep and I took them for ulterior purposes. I have also experienced insomnia for the past 4 years of my illness and continue to battle this.
There have been many treatments that I have taken to try and improve my sleep over the years. I have trialled:

  • Elavil (in a low dose form) on several occasions. It perpetually induced next-morning drowsiness.
  • Diazepam which I have rarely used and 1.25mg is sufficient to induce sleep for me. I only take this if necessary and have only consumed it once in the past few months.
  • Low dose naltrexone for the past 5 years and I continue to take this. Its only effect on me seems to be that it has slightly improved my sleep length.
  • Melatonin, long term and I only recently stopped this as it wasn’t having as much of an effect on me. It does however have multiple potential mechanisms of actions on ME symptoms and these studies emphasise its potential benefits.
  • Valerian tablets, which are probably the most effective sleep aid for me and I continue to take them before bed and when I wake up during the night.

Currently my nightly sleep tablet regiment involves; low dose naltrexone, valerian and L-theanine. I also use nasal strips every night for my sleep.
“I want to go to sleep in my time machine and wake up eight hours in the future.” –Jarod Kintz

Dr. Brewer’s Protocol

Dr. Brewer has developed a protocol for treating mycotoxin involvement in ME/CFS. This protocol is dynamic and over the past couple of years has been modified based on patient response. The crux of his protocol involves patients taking either nasal Amphotericin B or a compounded Nystatin that is atomised before being absorbed nasally by the patient. In tandem with one of the aforementioned treatments, patients must take chelating PX which comprises nasal EDTA with a surfactant.
Specialised testing has ascertained that 93% (104/112) of CFS patients studied tested positive to at least one of three mycotoxin. In contrast 0% (0/55) of the healthy controls tested positive. This study can be found here.
Brewer et al. have written this paper probing the relationship between chronic illness and mold/mycotoxins. The paper theorises that the sinuses are the main reservoir of the mycotoxin hence most of the treatments are focused on this portion of the body. The paper continues on to state that indoor, water damaged environments are hot-spots for mycotoxin production. Detailed mechanism of action and case studies are also provided to support the argument of Brewer et al.
The success of Dr. Brewer’s protocol on his patients has also been impressive. A pilot study by him found that 56 of the 151 patients treated could not tolerate the Amphotericin B. 88 out of the remaining 94 patients noticed improvements- That equates in percentage terms to a staggering 93.6% of the ME/CFS patients having a reduction in their symptoms. Approximately a third of these 88 patients achieved remission. Since this study, Dr. Brewer has found the atomised Nystatin to have a better safety profile than the Amphotericin B.
The Patient Advocate has written extensively on Dr. Brewer’s protocol here, here and here. The Phoenix Rising forums also contains an extensive discussion of this protocol here. Within it are many anecdotal reports and experiences of patients whom have attempted this protocol.
ASL/TAG were originally the compounding pharmacies providing the Brewer’s protocol products (after a prescription is presented or mailed) however they recently went out of business. Woodland Hills Pharmacy in California and Albers Pharmacy in Missouri are now compounding the Brewer protocol medications.
My Experience With Dr. Brewer’s Protocol
I enquired with the American pharmacies that provide the substances required to complete Dr. Brewer’s protocol however they informed me that they don’t ship to Australia. I therefore decided to trial a modified Dr. Brewer protocol. This consisted of:

  • A nebuliser used rather than an atomiser.
  • Capsule Nystatin opened and some of the powder mixed with distilled water and later nebulised and inhaled nasally.
  • A BEG nasal spray used that contained EDTA however no surfactant.
  • Nebulised Argyntyn 23, nasally inhaled.

I began different portions of this treatment over a staggered period of time, beginning in March 2015.
The nebulised Argyntyn 23 affected my sleep and hence I only trialled this for a few days. I again started this a few weeks later but similarly, my sleep quality diminished. I tolerated the nebulised Nystatin and continued this treatment for 3 months. I persisted with the BEG nasal spray despite it causing mild yet continuous nose bleeds. Eventually, I determined that the BEG nasal spray was a double-edged sword- My sleep quality deteriorated whilst on it. Every morning I would wake at 4am and struggle to get back to sleep. Curiously, my restless legs syndrome stopped while I took the BEG nasal spray. After 2 months of the BEG nasal spray, I decided to cease the treatment and within days my sleep quality improved and RLS returned.
Overall, I had a very haphazard approach to the Dr. Brewer protocol, largely due to not being able to gain the identical ingredients he used on his patients. His protocol is also intended for long term use and my 2 months of simultaneously taking BEG nasal spray and nebulised Nystatin wasn’t long enough to determine its true effectiveness on me. Over the coming days I will post another blog entry detailing the other ME treatments I have trialled recently.

Ten years of M.E.

Today marks an anniversary for me with this illness. A decade ago to the day, my first symptoms emerged, although they were relatively mild at the time. This is my journey…

I have spent the last ten years of my life living with Myalgic Encephalomyelitis.

Prior to my illness, I would run around the suburbs of Adelaide. My rangy shadow at my feet, wind smacking my face, endorphins pumping through my body and the insatiable appetite for more. I would breathe in and everything would make sense. Running was put simply my raison d’être.

At the cruel age of 17, I began developing physical symptoms that gradually restricted me. My days of unbridled living and having free range roaming Adelaide were no more. I began studying astrophysics at university however my muddled brain started to become as nebulous as the stars I was studying. I switched courses to focus on the less intense universe of philosophy. After six months I became a university dropout.

Specialised testing ascertained that the blood wasn’t flowing freely around my brain and my immune system was impaired. I was thus diagnosed with Myalgic Encephalomyelitis (ME.) This name was all too familiar to me. I was the sixth person on my maternal side to be given a similar diagnosis. I had a list of symptoms that couldn’t be contained to an A4 page and this tally has only extended to the present.

To list my symptoms is monotonous. I consider them all to be various manifestations of one of pain’s faces. Like Plato’s Cave, pain cannot be described to someone void of it- one must suffer to understand this abstract word. My most curious symptom to those unfamiliar with this disease is ‘post-exertional malaise’ which restricts my walking ability to fifty metres and talking ability to short spurts. Like a video game character that is only given a certain amount of power before keeling over- I must ration my experiences.

Any tale of struggle wouldn’t be apt without a dose of wisdom imparted. From patience, to increased empathy, a decade of reflection was going to turn me into more of a philosopher than any university course would.

I started an online blog detailing my travails with ME. I discuss treatments that I’ve attempted, research that has emerged and my own personal journey. This is a branch into the outside world that lets me associate with similarly afflicted patients. In a self-referring twist, my ME only allows me to write occasional blog entries about my health. The very nature of this illness dictates that I read the latest medical studies to try and find a solution to my complex disease. ME is heterogeneous and ranges in seriousness. I have been served an overflowing plateful of severe.

Despite my disability, I am seldom bored and often recall Jean-Paul Sartre’s quote “If you are lonely when you’re alone, you are in bad company.”  I am in constant pain but despite this, I am joyous. My upbeat attitude living with a chronic illness is partly due to the hedonic adaptation of having become accustomed to suffering. I survive in some way due to living at home with a supportive family, having a dedicated doctor and living drenched in positivity.

Each day as the sun sinks, I hear the same echoes of runner’s footsteps outside my home. I look up to only catch a shadow- soon that will be my shadow again.