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.
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.
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.”
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.”
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.’
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.