Tracking my efforts to beat Myalgic Encephalomyelitis (ME), aka CFIDS, aka CFS

Tracking my efforts to beat Myalgic Encephalomyelitis (ME), aka CFIDS, aka CFS

Friday, March 17, 2017

Personal Update

My last update was in January, right after I'd learned that I have an active Epstein Bar Virus (EBV) infection (positive IgM antibodies) again.  My doctor put me back on a prescription of Valacylovir to deal with the infection.  It's difficult to say whether I am still experiencing the symptoms of EBV or not because my baseline health isn't so great anyway.  I am scheduled to have another blood test on Wednesday, so I should know if I still have an active EBV infection by early April when the results come back.

The bigger story with me is the my shortness of breath (SOB) symptom has finally abated somewhat.  ("Shortness of breath" can be a little bit of a misnomer with ME patients.  When you say you have SOB to a doctor, sometimes they think you're referring to hyperventilation.  It's nothing like that.  If anything, the breathing feels shallow and slow, and no matter how deep of a breath you take, it doesn't seem to satisfy the feeling of air hunger.)

SOB was always a symptom of mine ever since I came down with ME in 2011.  But something seemed to happen in about September of 2015.  I don't know what caused it, but suddenly SOB became a dominant symptom.  I had it every day and, on some days, the hunger for air became so intense that it would become difficult to concentrate on other things.

It started to return to "normal" again in about October of 2016--and by "normal" I mean, I still have the symptoms intermittently, but they are not as intense as they were during the year from September 2015 to October 2016.  And the post-nasal drip that almost always accompanied the SOB flares isn't really there any more.

As always, it's difficult to determine what caused this improvement because I changed a number of treatments all around the same time.  I went back on Equilibrant and another immune modulating supplemental called ImmunoStim, after being off of both for about a year and a half.  This is my best guess for what caused the SOB to improve again.

Another possibility is that I stopped taking probiotics in late summer, 2016.  Then in the Fall, I found a hypoallergenic brand of probiotics which avoids strains of probiotics that are known to trigger histamines.  I started taking that brand instead.

Another possibility is that my diet for a while had grown to include a very significant proportion of nuts, particularly cashews: Cashew butter, cashew milk, raw cashews, Lรคra bars (which are cashew based.)  Then I read about lectins and how cashews are high in lectins.  I'm not necessarily convinced that lectins are problematic in the human diet, and I've never read about any connections between lectins and SOB, but I decided to eliminate cashews for a while.  I did this also in the Fall of 2016, so it's difficult to determine which of these factors helped improve my SOB.

I also started taking Vitamin D3 (5000-10,000 IU's per day) for a while in the Fall of 2016, but now I'm back off of the Vitamin D3 and the SOB is still improved, so I don't think it was that.  I also went back on Valacyclovir in January, but the SOB had already started to improve by then.

I wish I was one of those people who had the patience to methodically experiment with only one variable at a time, but I  can't seem to do it.  So I may never know with certainty what was contributing to the worsening SOB, but I think most likely it was either the lack of immune modulators, the probiotics, or the cashews.

Thursday, January 12, 2017

I have active EBV infection....again?

I received a phone call from my doctor's office today.  Results of a recent blood test show that I am positive for Epstein Barr Virus (EBV) IgM antibodies.  This shouldn't be possible since I have already had EBV in the past.

EBV is a common viral infection which almost 95% of the population has had but, for unknown reasons, it becomes chronic in a tiny portion of the population.  Over the years, research into ME has at various times focused on EBV only to lose interest and move on to other subjects.  It may be that EBV infections are part of the cause for some ME patients and not for others.

IgM antibodies are the first antibodies to respond to an infection.  They give way to IgG antibodies after a few days or weeks. If the person is ever exposed to the same virus again, the body would not produce IgM antibodies the second time.

Right now, I'm looking at my lab results from the year 2005.  They show as positive for an EBV infection, both IgM and IgG.  I was experiencing mononucleosis symptoms at the time, so these results from 2005 may indicate my first exposure to EBV.

I was tested for EBV again right after I came down with ME in 2011 (before any diagnosis), and the results showed negative for IgM, positive IgG—consistent with past infection.  Nothing surprising there.  It was tested again two times after diagnosis, in 2012 and 2014, but only IgG and IgA were tested.  Both times IgG was of course positive, and IgA was negative.

So this latest test result shouldn't be possible, as far as I know.  I called and moved up to doctor's appointment to Monday because I am puzzled and a little concerned.  It's possible this is merely a lab error, but then again, maybe not.  Maybe its time to go back on an antiviral medication such as Valacyclovir?

Friday, December 30, 2016

Closing out 2016

I'll do a more complete personal update after January 1st when I calculate my daily health averages for 2016 and compare it to past years.

In the meantime, after taking most of 2016 off, I'm back on Equilibrant and ImmunoStim (both are over the counter immune modulators) and I continue to believe they are helpful.  Now, unlike before however, I am pulsing the doses with 5 days on, 2 days off.  Dr. C once suggested that some patients have better success when pulsing so that the body doesn't become too accustomed to immune modulators.

I have a firm belief that Th1/Th2 imbalance is a key part of my immune dysfunction; specifically I'm Th2 dominant.  It's beyond the scope of this post to explain exactly why I've come to this conclusion - it would take a 5,000 word essay - but suffice it to say, I am confident of this.  I do understand that many believe the Th1/Th2 model of the immune system is oversimplified, but at the same time, it can still be specific and valid enough to provide treatment guidance.  (If it's good enough for Dr. C and other well respected ME researchers, it's good enough for me.)

For a long time, I have wondered what would happen if I concentrated on an entire protocol of Th1 shifting diet and supplements.  But I was unaware of any existing protocol and didn't have the time to research and invent one myself.  Then I found this protocol from Self Hacked.

Some of Self Hacked's advice on Th1/Th2 seems to be contradictory, so each step of implementing this will require my own confirmatory internet research.  Often times, a single study can be worthless.  I'd like to focus on diet and supplements that have a well-supported history of being found to be Th1 stimulants or Th2 suppressors; not just a single study.

Astralagus is already in Equilibrant, so for now I'm also introducing licourice and gynostemma, as well as new probiotics that focus on certain strains.  Its too early to tell if this will help.  I will update later...


I also received an interesting comment from an anonymous reader to my last post from late November.  The gist of it was that the commenter had success by focusing on treating autonomic dysfunction and suggested I do the same. Others have suggested that to me, but what I found particularly interesting was the statement that  Dr. Nancy Klimas has apparently stated that she believes autonomic dysfucntion is the key to ME (or words to that effect).  I was unaware of that, as I've been a little out of the loop lately.  I'll be looking more into Klimas' comments about autonomic dysfunction.  I'd love to hear others' take on this.

Monday, November 28, 2016

Latest Doctor Appointment

Last week I visited one of my doctors, Dr. M., who specializes primarily in Lyme disease but also treats other hard-to-treat conditions such as ME.  Our focus for this appointment was treating my hypothyroid symptoms.  We started by reviewing my recent laboratory blood test results testing thyroid hormone levels.  My levels of T3 (the active thyroid hormone) were optimal, while my levels of T4 and TSH (essentially, precursors to T3) were low, out of range.  Dr. M seemed concerned about this and wants to try to bringing my T4 levels within range as well.

I asked why it was necessary to bring T4 into range when T3 (the actual, active thyroid hormone) is optional.  My understanding is that, under normal circumstances, when one is not taking thyroid medication, the body produces TSH, which stimulates the production of T4, which in turn stimulates the production of T3.  (This is a bit oversimplified, as discussed below.)  So I wondered if T3 is optimal through medication, why do we need to bother with the precursors.  Why not "cut out the middle man"?

Dr. M asked me if I was still experiencing hypothyroid symptoms.  I admitted that I did still experience at least one symptom: extremely cold hands and feet.  Not just a little bit cold, but almost shockingly, painfully cold sometimes.  I had never considered this before.  Why, if my T3 levels are optimal, do I still have such cold hands and feet.

Dr. M explained that patients will still experience hypothyroid symptoms unless T4 is also brought into a normal range.  She referred me to a book called: Why Do I Still Have Thyroid Symptoms When My Lab Tests Are Normal? by Datis Kharrazian.  How's that for a specific title?  I'm not sure if I'm going to read the book, but regardless we are lowering my T3 dose and increasing my T4 to see if we can find a better balance that reduces symptoms.


Based on recent emergence and prevalence of histamine-related symptoms, we're beginning to suspect that mast cell activation may be present.  Dr. M states there is a test for mast cell activation, and we agreed that I should submit to this test relatively soon.  I plan to undergo a mast cell activation test in the next 3 or 4 months.  If the test is positive, it will be a significant clue to determining which subset of ME patients I fall into.


Finally, Dr. M suggested I consider an emerging treatment for chronic infections called Low Dose immunotherapy, as pioneered by a Dr. Ty Vincent.  This is apparently a somewhat novel approach and I'm not inclined to play the role of Guinea pig at this time.  I will probably not try this treatment.

Sunday, October 30, 2016

Personal Update

I had a birthday this past month.  The big Four-Oh.  Nobody is ever happy about turning 40 and I am no exception.  Officially now, half of my thirties were lived with ME.  But I think about ME less than I did in my first three years of diagnosis.  It is simply part of life now.  

Starting around the beginning of 2016, I believe, I began to ween myself off of the supplement Equilibrant.  (Equilibrant is an immune-modulating supplement that I have written about on this blog--recommended by one of my ME doctors.)  For about 4+ years, I had taken Equilibrant at the full dosage of 6 tablets per day.  During that time, I saw my condition stabilize and I experienced fewer and shorter "crashes."

Equilibrant is expensive and I wasn't sure if continuing to take it was necessary to maintain my level of functionality.  So by about mid-Summer, I had reduced intake all the way down to nothing.  I was completely off of Equilibrant.  And for the first month or two, I didn't notice any change in my health.  

But then my monthly health rating averages fell significantly.  I also developed shingles during that time--possibly related to stopping taking Equilibrant.  Over the same period of time, I also stopped taking daily vitamin B complex tablets.  My energy waned.  

In late September I decided to resume Equilibrant and B complex.  October has been by far my best health month of 2016.  I feel fairly certain that those supplements are helping and that I should continue to take them indefinitely, with occasional breaks or "holidays."  

I also found that my sleep was worse during the time when I was not taking vitamin B complex.  It occurred to me then that many patients say vitamin B12, which is part of the B complex, helps with sleep.  My sleep did improve after resuming B complex.  

So here I am again, stuck in a "holding pattern," very thankful that my case of ME has remained moderate compared to many patients, but also not as hopeful as I once was that I might recover without a breakthrough in ME treatment options.  

Wednesday, September 21, 2016

Beware of Supplements that May Cause Kidney Inflammation or Damages

Since I first developed ME in 2011, one of my on-again-off-again symptoms has been an aching in the area of the kidneys.  Two separate nephrologists (kidney doctors) tested my kidney function and told me it was normal and that I did not have any kidney stones, and yet these aches would persist.  In recent years, the pain has been mostly absent, but would come back 4 or 5 times per year.  

In the past three weeks, the pain has been back again.  It usually comes with strong, persistent thirst. I wondered if there are any supplements that could help reduce this inflammation.  In the process of searching for supplements that would help, I came across this list of 17 drugs and supplements that, according to the American Society of Nephrology, have been associated with kidney inflammation. One of them, to my surprise, was L-Lysine, which I have been taking at a "maintenance dose" ever since my outbreak of the shingles.

It's probably important for anyone who takes supplements to check this list and make sure they are not potentially damaging their kidneys.  

Friday, September 9, 2016

Antivirals May Treat M.E., But For Different Reasons Than We Thought

If you haven't already, check out this article from the Open Medicine Foundation (OMF).  It starts with a general overview of theories of the role of viruses in ME and various approaches to treating the viral component of ME.  But it's conclusion is perhaps the most interesting.  The article concludes that using antiviral treatments for ME may help improve symptoms in patients, but not because antivirals actually decrease viral titers, but because they improve metabolic function.  Again, this seems unproven and possibly speculative at this point, but it does seem to reconcile the puzzling results of some studies on the use of antivirals in ME treatment.