Thursday, January 26, 2012

5 Two New Hypotheses For Chronic Lyme Disease Symptoms?

There have been a few hypotheses as to why some people experience persisting symptoms after antibiotic treatment for Lyme disease.

The predominant hypothesis supported by most of the Lyme disease patient community is that a chronic and persisting infection is caused by spirochetes sequestered in immune privileged sites - possibly dormant at stages - and difficult to beat without long term high doses of antibiotics. The predominant hypothesis supported by the IDSA Lyme disease guidelines panel appears to be divided between one where patients with persisting symptoms have some condition completely unrelated to Lyme disease - or patients have an autoimmune disorder triggered by Lyme disease.

There have been other hypotheses as to the cause on the table by various parties which are mostly immune-related, such as immune dysregulation and Pam3Cys/OspA immunosuppression. But now there may be two new hypotheses to add to the stack which might apply to some patients with chronic Lyme disease.

(Note that I say "might" and "some" in the previous statement. I have no means for testing these hypotheses, but it is something interesting to speculate about and discuss.)

Hypothesis #1: Chronic Lyme disease could be a metabolic disorder.

In a paper published in December in The Quarterly Review of Biology, one researcher argues that multiple sclerosis (MS) is not an autoimmune disorder as many have thought. She proposes that MS is actually a metabolic disorder.

To quote from Medscape:
"Corthals believes that the primary cause of MS can be traced to transcription factors in cell nuclei that control the uptake, breakdown, and release of lipids (fats and similar compounds) throughout the body. Disruption of these proteins, known as peroxisome proliferator-activated receptors (PPARs), causes a toxic byproduct of "bad" cholesterol called oxidized LDL to form plaques on the affected tissue. The accumulation of plaque in turn triggers an immune response, which ultimately leads to scarring. This is essentially the same mechanism involved in atherosclerosis, in which PPAR failure causes plaque accumulation, immune response, and scarring in coronary arteries."
What if infection with Lyme disease (and possibly coinfections) leads to disruption of PPARs and ultimately, tissue damage? What if at least some portion of patients with chronic Lyme disease are suffering from a metabolic disorder instead of a chronic infection?

What can patients do to treat and prevent this? It appears diet does play some role in developing MS - people with a Vitamin D deficiency and a high fat, high carbohydrate diet were more likely to develop MS than those who did not have a deficiency and such a diet. MS patients have said that taking more Vitamin D and switching to a low fat, low carbohydrate healthy diet has helped with their symptoms.

Other risk factors for developing MS include specific genetic backgrounds, pathogens (infections), and major cellular trauma. The same kind of factors may be relevant for Lyme disease patients who develop chronic symptoms.

Read more for food for thought: 

Angelique Corthals, "Multiple Sclerosis (MS) is not a disease of the immune system," The Quarterly Review of Biology 86:4 (December 2011)

Hypothesis #2: Chronic Lyme disease could be a neurological/neurosensory disorder.

Lymenet Europe has been a wealth of scientific information over the years, and recent postings are no exception.

Recently, a thread on sympathetic neural hyperalgesia edema syndrome was posted, mentioning that its symptoms overlap many of those found in Lyme disease. Conditions and symptoms which relate to this syndrome are pelvic pain, abdominal pain, interstitial cystitis, backache, headache, arthritis, fibromyalgia, and mastalgia. This disorder may also manifest as unexplained weight gain, urticaria, chronic fatigue, and vasomotor symptoms unresponsive to estrogen, and a pseudohypothyroid state, according to the research cited on this thread (DOI: 10.1002/ibd.21269).

The proposed treatment for this condition? Dexedrine. That's right, good old dextroamphetamine sulfate, which is an amphetamine used to treat ADHD in adults and children.

While patients receiving this treatment achieved marked improvement in pain and relief from symptoms, I would be concerned about the long term potential for addiction and for side effects in people with certain preexisting conditions. On the other hand, if it is a drug which helps people with their symptoms and improves their quality of life, I think it might be a good idea for doctors to consider trying it on a case by case basis after giving patients an education about its benefits and drawbacks. Patients need to make a decision after being fully informed about its risks in particular.

Caution would also be warranted for patients who wished to try it alongside other supplements, medications, and antibiotics, given that some antibiotics (such as macrolides), medications, and supplements can affect heart rhythms and blood pressure - doubling up on this effect by using Dexedrine as well could have a serious impact on one's health.

This is one reason why I want more research: to know how often chronic infection plays a role in persisting symptoms and how often other conditions may be responsible for these symptoms - either concurrently or alone. Also, I'd want more specific treatments which are either curative and/or supportive for chronic Lyme disease to be investigated through clinical trials. It would be good to know how different potentially curative and supportive treatments could be helpful and harmful to a large body of patients and not just rely on the anecdotes and case studies of only a few.


  1. This is hilarious, right?

    I looked at the news item for hypothesis #1, about MS being a metabolic disorder and suggested that maybe Lyme disease could be a metabolic disorder.

    Guess what I just found? This bit, on a study which was awarded a grant:

    "A Lyme disease grant has also been awarded to Dr. Tara Moriarty of the University of Toronto, who will investigate the possible role of metabolic syndrome in some cases of unresolved Lyme disease. Metabolic syndrome is a combination of clinical factors that increase the risk of cardiovascular disease and diabetes, and its incidence has grown dramatically over the last few decades.

    Preliminary work in Dr. Moriarty’s lab indicates that when mice are given a high fat diet that induces atherosclerosis, obesity and hyperglycemia, they experience a higher burden of infection when exposed to B. burgdorferi than do mice with normal metabolism. Dr. Moriarty will
    continue this work in an attempt to tease out the specific metabolic factors that increase host susceptibility to disseminated Lyme disease; this may lead to novel treatments for human patients with unresolved illness."

    Whoa. Pretty interesting.

    This came from here:

  2. Here's something else I found today which may be related to this concept of "Lyme disease as metabolic condition" - at least at the edges:

    Gene Scientist Maps Own Type 2 Diabetes Arrival And Departure:

    The gist of it is:

    The researcher tracked changes in his genes over time, including through viral infections. During infection, 2,000 of his genes were highly upregulated and another 2,200 genes were elevated at low levels. Some of these genes are involved with immune processes and phagocytosis.

    Not only that, but Dr. Snyder had higher levels of auto-antibodies and one auto-antibody in particular had targeted an insulin receptor-binding protein.

    After the viral infections, his glucose regulation went awry each time. He had his blood glucose levels tested on the heels of his viral infections, and it turned out he developed type 2 diabetes. With changes to his diet and exercise, though, he was able to reverse the disease.

    So the questions are: Can the presence of infection trigger metabolic disorders for which one is genetically predisposed? Is that what happened in this situation?

  3. Very interesting. When my neurological symptoms initially started I had a period of abnormal glucose results which were brought back through diet and exercise. The doctors couldn't explain it.

  4. Anonymous 08:06 AM,

    That is very interesting. I wonder what is happening? I also think this research on metabolic disorders is related to a more recent post on immunological differences in response between men and women:

    I'm wondering how much infection contributes to hormone imbalances on a deeper level - that dysregulation occurs on a local, organ-based level first, then perhaps there is endocrine disruption in the brain?

  5. I have tracked all of my blood work results over time and several patters emerged. Relative lymphocytosis decreased with time. Borrelia IgM response withered and eventually disappeared. Borrelia IgG got stronger. Creatine Kinase returned to normal range. Fibrogen returned to normal. Electrolytes returned to mean levels (were at the extreme ends). It is safe to say there were several immune/endocrine disruptions at play.


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