Friday, July 1, 2011

19 Admin Update: Holiday break & Request For Topics

I've been pounding the keys pretty heavily in the past couple days on commentary, and after taking a break for a few days, I would like to get back to discussing more of the science of Lyme disease.

I have some topics in the pipeline I can write about, but I'm putting out a request for feedback here:

What Lyme disease and other tickborne infection topics would you like to know more about?

Please leave your topics in comments - your top three choices if you have them, but one is okay, too.



  1. CO,

    Despite the single-dose of doxycycline being highlighted in the 2006 update of the IDSA guidelines, that approach doesn't make sense to me given studies that imply a short course of antibiotics might be enough to turn off the immune response without adequately addressing the infection. This is old news, I realize but information that now seems to be refuted:

    N Engl J Med. 1988 Dec 1;319(22):1441-6.
    Seronegative Lyme disease. Dissociation of specific T- and B-lymphocyte responses to Borrelia burgdorferi.
    Dattwyler RJ, Volkman DJ, Luft BJ, Halperin JJ, Thomas J, Golightly MG.
    SourceDepartment of Medicine, State University of New York, School of Medicine, Stony Brook 11794-8161.

    The diagnosis of Lyme disease often depends on the measurement of serum antibodies to Borrelia burgdorferi, the spirochete that causes this disorder. Although prompt treatment with antibiotics may abrogate the antibody response to the infection, symptoms persist in some patients. We studied 17 patients who had presented with acute Lyme disease and received prompt treatment with oral antibiotics, but in whom chronic Lyme disease subsequently developed. Although these patients had clinically active disease, none had diagnostic levels of antibodies to B. burgdorferi on either a standard enzyme-linked immunosorbent assay or immunofluorescence assay. On Western blot analysis, the level of immunoglobulin reactivity against B. burgdorferi in serum from these patients was no greater than that in serum from normal controls. The patients had a vigorous T-cell proliferative response to whole B. burgdorferi, with a mean ( +/- SEM) stimulation index of 17.8 +/- 3.3, similar to that (15.8 +/- 3.2) in 18 patients with chronic Lyme disease who had detectable antibodies. The T-cell response of both groups was greater than that of a control group of healthy subjects (3.1 +/- 0.5; P less than 0.001). We conclude that the presence of chronic Lyme disease cannot be excluded by the absence of antibodies against B. burgdorferi and that a specific T-cell blastogenic response to B. burgdorferi is evidence of infection in seronegative patients with clinical indications of chronic Lyme disease.

    Comment in
    N Engl J Med. 1989 May 11;320(19):1279-80.
    PMID: 3054554 [PubMed - indexed for MEDLINE]

    I find a recent Case Study disturbing for a number of reasons -- not the least of which is the implication that if 7 days of antibiotic treatment is not enough to treat the infection, but more than enough to make someone seronegative, what about anything else less than the IDSA's upper limit of 28 days? Does the prophylactic single-dose cause more harm than good?

    Here's the longer version with more details:

    Rita A

    (more thoughts to follow)

  2. CO,

    Again, an older study ... but how can anyone deny the fact that symptoms persist in a high percentage of patients previously treated for Lyme disease? In this case, patients received 2 weeks of IV antibiotics, but close to 40% either relapsed or didn't improve to begin with when followed up 6 months after treatment:

    N Engl J Med. 1990 Nov 22;323(21):1438-44.

    Chronic neurologic manifestations of Lyme disease.

    Logigian EL, Kaplan RF, Steere AC.
    SourceDepartment of Neurology, Tufts University School of Medicine, Boston, MA 02111.

    BACKGROUND AND METHODS:Lyme disease, caused by the tick-borne spirochete Borrelia burgdorferi, is associated with a wide variety of neurologic manifestations. To define further the chronic neurologic abnormalities of Lyme disease, we studied 27 patients (age range, 25 to 72 years) with previous signs of Lyme disease, current evidence of immunity to B. burgdorferi, and chronic neurologic symptoms with no other identifiable cause. Eight of the patients had been followed prospectively for 8 to 12 years after the onset of infection.

    RESULTS:Of the 27 patients, 24 (89 percent) had a mild encephalopathy that began 1 month to 14 years after the onset of the disease and was characterized by memory loss, mood changes, or sleep disturbance. Of the 24 patients, 14 had memory impairment on neuropsychological tests, and 18 had increased cerebrospinal fluid protein levels, evidence of intrathecal production of antibody to B. burgdorferi, or both. Nineteen of the 27 patients (70 percent) had polyneuropathy with radicular pain or distal paresthesias; all but two of these patients also had encephalopathy. In 16 patients electrophysiologic testing showed an axonal polyneuropathy. One patient had leukoencephalitis with asymmetric spastic diplegia, periventricular white-matter lesions, and intrathecal production of antibody to B. burgdorferi. Among the 27 patients, associated symptoms included fatigue (74 percent), headache (48 percent), arthritis (37 percent), and hearing loss (15 percent). At the time of examination, chronic neurologic abnormalities had been present from 3 months to 14 years, usually with little progression. Six months after a two-week course of intravenous ceftriaxone (2 g daily), 17 patients (63 percent) had improvement, 6 (22 percent) had improvement but then relapsed, and 4 (15 percent) had no change in their condition.

    CONCLUSIONS:Months to years after the initial infection with B. burgdorferi, patients with Lyme disease may have chronic encephalopathy, polyneuropathy, or less commonly, leukoencephalitis. These chronic neurologic abnormalities usually improve with antibiotic therapy.

    Comment in
    N Engl J Med. 1991 Apr 18;324(16):1137.
    PMID: 2172819 [PubMed - indexed for MEDLINE]

    "Chronic" wasn't a taboo word in the 1980's and although ~ 60% might qualify as "usually" when it comes to improvement, where does that leave the other close to 40% of people who are left with chronic neurologic symptoms. It doesn't appear that these people were offered any alternative treatments -- and that hasn't changed.

    Rita A

    (one more comment to follow)

  3. CO,

    Last but not least, here's another "old" study that confirms a high percentage of Lyme disease patients with persistent symptoms have basically been ignored, and even abandoned, by mainstream medicine:

    J Rheumatol. 1994 Mar;21(3):454-61.

    Lyme disease: an infectious and postinfectious syndrome.

    Asch ES, Bujak DI, Weiss M, Peterson MG, Weinstein A.
    SourceDepartment of Medicine, New York Medical College, Valhalla 10595.

    OBJECTIVE:To determine chronic morbidity and the variables that influence recovery in patients who had been treated for Lyme disease.

    METHODS:Retrospective evaluation of 215 patients from Westchester County, NY, who fulfilled Centers for Disease Control case definition for Lyme disease, were anti-Borrelia antibody positive and were diagnosed and treated at least one year before our examination.

    RESULTS:Erythema migrans had occurred in 70% of patients, neurological involvement in 29%, objective cardiac problems in 6%, arthralgia in 78% and arthritis in 41%. Patients were seen at a mean of 3.2 years after initial treatment. A history of relapse with major organ involvement had occurred in 28% and a history of reinfection in 18%. Anti-Borrelia antibodies, initially present in all patients, were still positive in 32%. At followup, 82 (38%) patients were asymptomatic and clinically active Lyme disease was found in 19 (9%). Persistent symptoms of arthralgia, arthritis, cardiac or neurologic involvement with or without fatigue were present in 114 (53%) patients. Persistent symptoms correlated with a history of major organ involvement or relapse but not the continued presence of anti-Borrelial antibodies. Thirty-five of the 114 (31%) patients with persistent symptoms had predominantly arthralgia and fatigue. Antibiotic treatment within 4 weeks of disease onset was more likely to result in complete recovery. Children did not significantly differ from adults in disease manifestations or in the frequency of relapse, reinfection or complete recovery.

    CONCLUSION:Despite recognition and treatment, Lyme disease is associated with significant infectious and postinfectious sequelae.

    PMID: 8006888 [PubMed - indexed for MEDLINE]

    The current position by IDSA and others that Lyme disease is easily diagnosed and treated -- regardless of the stage -- goes against an entire body of research and the experiences of many, many people. Instead of spending their energy trying to block the broadcast of "Under Our Skin", it's a shame that some IDSA and ALDF members don't try to figure out how to help people suffering long-term consequences of Lyme disease instead of doing all they can to ridicule and belittle them.

    Rita A

  4. Hi Rita A,

    It's late at night and a holiday weekend here, but I decided to check comments and can respond briefly before I head to bed.

    I was wondering if you intended to post these comments on my post about the 2006 Lyme disease guidelines, or if you meant to put it here under my request for topics? Either way, I'm up for discussing these each in more detail at some point, just not late at night.

    Re the single dose prophylaxis for Lyme disease: I am with Volkman on this, and he has protested against the IDSA vociferously about this guideline. I would refer to this letter Dr. Volkman sent to the IDSA, and scroll down until you reach the section on prophylaxis.

    If he is correct in stating that they were so convinced their sera would be positive after using prophylaxis on mice that they discarded it without even testing it, that falls into the realm of arrogance and incomplete science for me. That's a source of data, and they threw it away.

    As for the child with the damaged ankle who had 7 days of antibiotics and no fever and other symptoms of Lyme disease after a tick bite (and was seronegative), I think this is an example of why Lyme disease is so difficult for doctors to deal with. But yes - 7 days of antibiotics was not enough, and led to more advanced problems.

    Why he only received 7 days of antibiotics is not something I understand - that's fewer days than the IDSA guidelines recommends.

  5. Re the Logigian/Steere Chronic Lyme study:

    This is the study I think Dr. Cameron mentioned in passing in the chat recap I posted on Friday.

    I've read the abstract before; I need to read the full text. One piece of information I am missing that I already want is from the background and methods, and that is which (if any) of these patients had been treated for Lyme disease before. We know they've had symptoms for years, and they show immune response to Bb, chronic neurological symptoms with no other cause found, and so on... but there is no mention of whether or not any of them had antibiotics before this study.

    The study was published in 1990. It states that it followed these patients for 8-12 years. Doing the math, it means some of these patients were studied before 1982, when Borrelia burgdorferi, the causative agent for Lyme disease, was discovered. Could studying these patients began during the time when Steere was insistent that Lyme disease was caused by a virus, and thus no antibiotics were given then? I don't recall what year Dr. Edlow wrote that Steere decided to follow the treatment plan of his neighbors down the road in Groton and began giving his patients penicillin too.

    I would have to say that there is a possibility the study subjects never received antibiotic treatment before these two weeks of IV abx, but I don't know - I don't have the full text to see what information I'm missing. But it would be hard to know how to treat people if you weren't sure what was causing their illness to begin with.

    You said, "but how can anyone deny the fact that symptoms persist in a high percentage of patients previously treated for Lyme disease?"

    I don't think anyone denies that there are chronic symptoms in patients who have been treated for Lyme disease. But the cause of those symptoms differs based on whether you're asking the IDSA Lyme guidelines panel about it or you are asking ILADS about it - and also if you talk to microbiologists about it, who break down into their own camps as well.

    All of them pretty much agree there can be serious chronic symptoms after a treated Lyme disease infection. But some say it is a persisting infection, while others say it is some distinctly different disorder or problem (immune dysregulation, autoimmune disorder, other infectious disease not identified and treated, etc.).

    I think that one of the really telling things to look into in terms of the guidelines are these items:

    1) How was the treatment for late stage Lyme disease determined, specifically, and how does that compare to early stage?

    2) How do they determine the rate of neurological infection in all patients? Who has neuroborreliosis, how soon, and how can they make that determination - how does any doctor make that determination?

    3) If less than 10% of early stage, acutely infected patients have treatment failures, do you decide to retreat then - or do you automatically mark those early stage patients off as having an autoimmune disorder?

    There is a point here where the science has to be more supportive of the guidelines I see, even without looking at the failure rates. And the failure rates - as you've noticed - are quite high.

    I'm really tired, and I'm probably not giving my response as clear a head as I could - so if you have a third comment I see in the queue for moderation tonight, I'll post it but won't be responding right away. I need to sleep.

  6. Hi CO, I have many questions as usual...
    -Why is it so hard to bust the IDSA? It seems the corruption is blatant. What ever came of the Blumenthal hearings? The IOM dropouts? The HON. CHRISTOPHER H. SMITH speech to The House of Representatives? And all juicy bits scattered in courts all over the world? I just don't get it. The IDSA is the ENRON of the Lyme world. I thought the 'democracy', majority rule, justice and science were real things. Silly girl...
    -I would like to learn more about why chronic inflammatory diseases are deficient in 25-hydroxyvitamin D (25-D) And the role of secosteroids, D as a immunosuppressant. You often write about immune dysregulation. The spirochetes mess up the immune response. Can our own immune system (secosteroids) be activated to eliminate bacteria and viruses?
    -You mentioned proteomics. Fascinating stuff. But what has been discovered relevant to Lyme? Isn't the ELISA and Western Blot using specific protein biomarkers proteomics? Shotgun proteomics and PROTOMAP sounds sexy and promising. More please!

  7. Sorry, CO. I was quickly cutting and pasting those studies after being upset by the case study about the young boy. One would think that doctors in an area known to be endemic for Lyme disease would have treated for a minimum of 10 days and not relied so heavily on current testing methods when the boy developed symptoms that appeared to be triggered by a tick bite.

    It was late/early here too (~4 AM), but I didn't want to forget the studies that seemed to confirm my impression that too little treatment might be worse than no treatment at all when it comes to the diagnosis of LD. I was also reminded that the number of treatment failures (possibly because of under-treatment) is probably much higher than the 5 to 10% estimates that I've read by some authors.

    Some doctors imply that depression is the root cause for post-Lyme disease syndrome, offering a third (and growing) hypothesis about the persistence of "vague" symptoms after "standard" treatment:

    I believe the conclusion: "Patients with chronic Lyme disease differ with regard to gender from those with either B. burgdorferi infection or post-Lyme disease syndrome. This finding suggests that illnesses with a female preponderance, such as fibromyalgia, chronic fatigue syndrome, or depression, may be misdiagnosed as chronic Lyme disease" could easily be reversed to read:

    "Chronic Lyme disease may be misdiagnosed as fibromyalgia, chronic fatigue syndrome, or depression".

    That's just my person opinion based on anecdotal accounts as opposed to case studies or clinical trials, and therein lies part of the problem (as you are well aware).

    There's no shortage of evidence to suggest (if not confirm) the persistence of infection, but I'm not so sure about the autoimmune element (although I don't rule out any possibility). MS is currently classified by many as an autoimmune illness, but is it really? Have any antibodies been consistently elevated in MS patients and where does CCSVI fit in for both MS and some Lyme disease patients? There are just so many questions, and so few answers.

    Thanks for all you do.

    Rita A

  8. CO,

    I don't meant to fill your comments section, but I was just trying to answer my own question about autoimmunity in MS. There are new theories (about antibodies not restricted to MS), but here's an interesting one about EBV:

    "Our findings extend the result of an earlier report and strengthen the association between EBV and multiple sclerosis".

    The Epstein Barr virus is associated with quite a number of illnesses, but isn't necessarily the cause. Then again, infections of any kind likely do have an impact on immunity (auto and otherwise).


  9. To any of the posters here and to any other Lyme patients:

    For what it's worth------ I wouldn't deny or otherwise even remotely suggest that an 'old' study or abstract isn't worthy of attention. (Except of course when newer technology has refuted some of the 'science')

    "New" sometimes simply means someone is publishing before they perish.

    "New" may mean it's not withstood the test of time.

    "Old" is many times (not always, mind you) is still worth while.

    Looking at the few archives of the Journal of Spirochetal and Tick Borne Diseases is still worth while. [JSTD] It used to be archived at the LDF web site but are no longer. Some can be found using the Wayback Machine.

  10. Jess,

    Thank you for your suggestions for future topics. I'm not going to be able to address them now in the space of a comment, so look for them in a future post.

    The IDSA one is the thorniest topic to discuss - there has been much speculation and not enough clear answers. I have plenty of material from other Lyme advocates I can fall back on, but can it be compiled and laid out in different ways to tell different stories, depending on who you ask?

    At baseline, my observation is that somewhere along the line, something went wrong. Whatever people think is true about the persistence of Lyme disease, somewhere along the line patients began to receive less respect and more scorn and disbelief. When did this begin, and how? This is a good question to ask.

    I'll be more likely to be posting about immune dysregulation and proteomics before I get to a post on the IDSA and the questions you ask about Blumenthal.

  11. Rita A,

    No apologies are necessary.

    Regarding the study about the 7 yr old: If I recall correctly, that boy actually did not show early symptoms of Lyme disease after he had been bitten by a tick - at least according to the publication. This was part of why the situation was so tricky; he may have been asymptomatic upon infection and only went on to show late stage sequelae that got attention later.

    This is one of the issues with Lyme disease - it can be asymptomatic at first. It could also be that there was a delay between when the boy got bitten and a flu-like illness later, but I don't recall mention of it. Please let me know if I misread the publication.

    Having treatment failures early in infection would seem to indicate to me the patient needs more treatment and to get evaluated for neuroborreliosis, though the evaluation that is suggested is not the most effective - CSF tests are only going to return 10-30% positive in the first 2 weeks after infection, and that is the best it gets from what I've read (this was mentioned in the recent IOM summary report, and my posts on IOM and neuroborreliosis).

    I suspect that since Borrelia is neurotropic that a number of people move to the early disseminated phase quickly and may have un- or under treated neuroborreliosis, and that leads to some patients developing persistent symptoms. This is Dr. Fallon's take, I believe.

    But I also think that even without neuroborreliosis, there are things we haven't definitely tested in vivo in people which are difficult to test - such as intracellular infection.

    Doing something to address the immune system dysregulation would be a good clinical trial to run, as that too is a contributing factor. I suspect it's a bigger one than all these forms (L-form, spheroblast, etc) patients keep discussing, too, but this is just speculation based on reading I've done to date.


  12. (more for Rita A)

    I don't think depression is the root cause of Lyme disease, unless antibiotics have an antidepressant effect? I think depression can be a secondary effect of being ill - this is the case with many illnesses, though, and not particular to Lyme disease. Regardless, one has to be sure that there isn't an underlying organic cause of depression, like deficiencies, endocrine disorders, hypothyroidism, infections, sleep deprivation, and brain disorders or tumors. Ruling out a biological cause for depression is important in order to make sure patients have the right treatment. It would be great to see a clinical study on this depression in Lyme disease patients: If all your symptoms improve while on antibiotic therapy and these symptoms aren't touched by antidepressants, what is going on there?

    You said,

    "Patients with chronic Lyme disease differ with regard to gender from those with either B. burgdorferi infection or post-Lyme disease syndrome. This finding suggests that illnesses with a female preponderance, such as fibromyalgia, chronic fatigue syndrome, or depression, may be misdiagnosed as chronic Lyme disease" could easily be reversed to read:

    "Chronic Lyme disease may be misdiagnosed as fibromyalgia, chronic fatigue syndrome, or depression".

    Of course it is directly reversible. Absolutely.

    Two things which these researchers should note in their own studies is 1) how women's immune systems and hormones affect their response to infection and 2) what they know about men with chronic persisting symptoms post-treatment, because they do exist (really, they're just not talking about it online the way women tend to).

    According to statistics, men are more likely to contract Lyme disease than women in the first place. Yet there is some difference here in the proportion of men who go on to report persisting symptoms compared to women.

    One can argue that women are more likely to develop autoimmune disorders, and thusly it's likely that post-Lyme is just one more example of this. But they need to stop offering such a pat answer and look at what is happening before any autoimmunity occurs and look at how much homogeneity this group has. If it's not that homogenous, then perhaps this or that defining factor is not the cause of persisting symptoms.

  13. CO,

    Thanks very much for your very thorough analysis and responses. I do believe that chronic illness of any kind can easily produce a secondary (i.e. reactive) depression even if it isn't already a component of the many neuropsychiatric aspects of tick-borne illnesses. I am offended by the pat and dismissive answers/theories so often put forth when it comes to Lyme disease.

    Women -- and especially as we age -- do have increased rates of autoimmune disorders and I believe that's at least partly due to our slightly more complex biology (especially with regard to hormones). Sorry that I don't have a reliable source to quote from at my fingertips, but there are many.

    I agree that men are far less apt to participate on online forums having to do with Lyme disease. Having lived and worked with men (father, brothers, husband, IT colleagues) most of my life, this shouldn't be too surprising. I'm trying to refrain from overgeneralizing and making sexist remarks, however I will say that men have a tendency to downplay their health issues.

    I just read a reference on LymeNet Europe to Flagyl (metronidazole) triggering depression in some people, and I know from the drug insert warnings that Avelox (moxifloxacin, another antibiotic) may also produce or aggravate symptoms of depression for reasons that remain unclear (at least to the general public). There may be multiple and complex contributing factors when it comes to the depression so often seen in people with Lyme disease (as well as MS, PD and many others). To chalk all depressive symptoms up to a primary psychiatric disorder is indeed an attempt to oversimplify and overlook reality.

    From a personal perspective, antibiotic therapy was the only effective treatment for sometimes debilitating neurological and cognitive problems. The "depression" I experienced was chalked up to my unwillingness to accept my disability -- even though the cause could not be pinpointed until I was diagnosed with late-stage Lyme disease last August. It really was amazing how a combination of antibiotics addressed my supposedly "reactive" depression. I had been prescribed a multitude of psychoactive medications that only made things worse over the past decade -- sometimes much, much worse.

    I can say with conviction through my personal experiences that if late-stage Lyme disease doesn't contribute to neuropsychiatric signs and symptoms, the psychiatric community is missing out on the miracle of antibiotics for treating people with atypical and sometimes highly variable psychiatric symptoms.

    I completely agree that far more research into the causes and treatments for post-treatment Lyme disease is more than justified. I've been learning how easily valid and relevant research can be brushed aside if it threatens the status quo, and I'm doing my best not to be discouraged by this.

    Rita A

  14. Rita A,

    There are already a number of studies out there about the relationship between infection and psychological state, and some on the relationship between subclinical encephalitis and Lyme disease to mood. I would always look at all underlying factors that could contribute to a patient's condition and do rule outs.

    Re men: I don't think it's a matter of downplaying health, necessarily. Talk to guys you think are close enough you'll get an answer. If I have to make a generalization, I think it's more a matter of being pragmatic and not wanting to belabor the issue.

    Depending on what Lyme support forum you're talking about, some are more welcoming to men than others. If they're full of too many sparkly rainbows and not enough substance, something else has to make guys stick around at that group. Lurking is more useful in this case.

    You said,

    "To chalk all depressive symptoms up to a primary psychiatric disorder is indeed an attempt to oversimplify and overlook reality."

    Yes. But sadly, this is often what happens, because there is a pill for everything nowadays and antidepressants work for the most severely depressed. For everyone else, though (mild-moderate depression), studies have shown they're no better than placebo. Now what? Is the issue that they don't work for this population - or is it that the source of their depression is another cause and another treatment is needed?

    Too often I hear stories about people getting switched from one antidepressant to another, which may not work when what a person needs is a full work-up to find out what else is wrong.

    You said,

    "I completely agree that far more research into the causes and treatments for post-treatment Lyme disease is more than justified. I've been learning how easily valid and relevant research can be brushed aside if it threatens the status quo, and I'm doing my best not to be discouraged by this."

    One thing which troubles me about the entire situation is that those on the IDSA guidelines panel who are defending the autoimmune model do not seem to be expending much energy on clinical trials to help patients with post-treatment Lyme disease symptoms. If they're so sure their hypothesis is the best one to explain persisting symptoms, why aren't we seeing more studies and trials that put it to the test? Why not some interleukin-mediating treatments? Why not some other trials to test treatments which are non-antibiotic focused?

    While I believe that there is a basis for the persistence model, there are likely to be some post-treatment Lyme disease patients who can no longer tolerate antibiotics or choose not to take them who may want to sign up for such studies.

    Some people may view participating in such trials as a betrayal of the persistence model. I don't see it as either betrayal or support of one model or the other. I see it as one more step in confirming what helps and what doesn't for specific groups of patients.

    The thing one has to be careful about in any clinical trial is that the study is conducted with integrity and the data is handled scrupulously. Because of concerns about this from both sides of the fence, patients are best off having these studies be conducted by independent researchers not on the panel or affiliated with it, and not affiliated with LLMDs. This would be done in order to prevent potential conflicts of interest and bias.

    Who would be best to conduct such studies now becomes the $2 m question... Answer that one and you win a prize.

  15. CO,

    I just keyed in a rather lengthy comment that got lost in cyberspace, but the main message was that I smiled when I read this comment from you:

    "Re men: I don't think it's a matter of downplaying health, necessarily. Talk to guys you think are close enough you'll get an answer. If I have to make a generalization, I think it's more a matter of being pragmatic and not wanting to belabor the issue".

    That matches my personal experiences for the most part as people of both sexes tend to confide in me. Women generally do so at far greater length and with much more detail, and there may be biological reasons for this. Here are a couple of links related to this:

    Two Quotes:

    "That helps to explain in my book, Men are From Mars, why women will come home from work, and often they’ll want to talk about what happened. Men are wondering why. Why bring up the problems? Let’s just forget them".

    "As long as he can do something about the problem, then his stress level stays low. Some men may have higher stress loads because they feel powerless to solve the problems in their life".

    As far as an unbiased research team is concerned, one can only hope that a brilliant group of scientists has been marooned (think Gilligan's Island) in a remote location for the past 3 decades or so and has recently been rescued. On a more serious note, I think it will be difficult to find anyone who hasn't been influenced by the LD controversy. We tend to believe what we are taught by our mentors (whether educators, parents or friends) and rarely question deeply-held beliefs unless personal experience forces us to do so.

    Rita A

  16. Hello CO,

    A subject I would find interesting which doesn't get much attention (but I think should) is the periodicity of some symptoms of Lyme patients and the possible processes that could explain them. Can these cycle be explained by all the various hypothesis (auto-immunity, chronic infection, etc)?

    This particularity of the disease has barely been mentioned in the IDSA guidelines, and we see scant references to this in few publications (we do have this in Burrascano JJ. Lyme disease. In: Rakel RE, ed. Conn’s Current Therapy. - "As antibiotics kill organisms only during their growth phase, therapy is designed to bracket at least one entire 4-week generation cycle", "During treatment, symptoms will wax and wane every 4 weeks, reflecting the growth period of this Borrelia, similar to what is seen in the relapsing fevers", "The very occurrence of ongoing monthly cycles indicates that living organisms are still present and that antibiotics should be continued until these cycles no longer occur").

    What exactly are the facts on these cycles? Is there supporting scientific material to these assertions by Dr. Burrascano?

    I am personally suffering from chronic Lyme disease and have been experiencing very distinctive cycles of approximately one month for some symptoms: insomnia, depersonalization (drunk-like dizziness), pain in various lymph nodes moving from day-top-day, all this lasting for about one week. The remaining three weeks are usually not too bad, with the usual tinnitus, fasciculations, slight arthralgia of the right knee and myalgia of the left arm that come and go. I have been (and still am) taking 100mg doxycycline bid for Rosacea (which I believe in my case is a manifestation of Lyme) for the last few months.

    There is no question in my mind that these symptoms of mine have been triggered by a tick borne disease as despite being negative on various Lyme tests, my history is very clear (tick attachment prior to symptoms - camping in Lyme endemic area - multiple secondary rashes - knee arthritis and multiple neurological symptoms - slow progression with symptoms starting 3 months after tick bite, approx. one new symptom per month). I could go on for many pages with my personal story... The point is, there are clear cycles which I have a hard time believing they could be explained other than by an active infection.

    I have seen some web discussions/papers about these "flare cycles" on this site:
    Maybe these could be a starting point for a discussion on the topic.

    BTW, I really enjoy reading your very well thought-out and informative blog posts.

    TicksSuck from ON, Canada

  17. Hi TicksSuck,

    Thanks for your question about periodicity of symptoms or flare-ups and Lyme disease. It is something I've known about more anecdotally, as women have discussed a flaring of symptoms coincident with the onset of PMS. But there is a correlation between a drop in female hormone levels and immune system reactivity, and it's something Dr. Marylynn Barkley, of UC Davis has studied.

    You might want to check out this transcript from Lymeinfo, but also look up Dr. Barkley's studies independently:

    An excerpt from the above applies directly to our discussion:

    "... there is a period known as the immune response interval that is occurring approximately three days prior to, including the day of menses, and three days thereafter. If you then take the data and look at
    the pattern of estradiol secretion in normal women versus the pattern of night sweat activity in women with Lyme disease, what you see is, indeed, at the time that you see a decline in ovarian hormone production, in terms of estradiol secretion and progesterone secretion, which is the hallmark of the period prior to menses, this is when you see
    intensification of the immune system response."

    However, this only explains some of what may be happening with female Lyme disease patients. And I wonder, does this happen to all women or only some of them?

    By this logic, menopausal women should be faring worse with symptoms throughout the month than fertile women.

    And what about men? Do they experience monthly fluctuations of their own, and if so, are they less pronounced?

    Speculating on this, one would think a female who is menopausal has more intense symptoms spread out over time with marked peaks when the bacteria divides, a female who is fertile experiences fewer symptoms throughout the month but worse ones up to one week a month, and men are more likely to notice peaks in symptoms once a month, too - but perhaps for less than a month's time and less intensely.

    Does reality match up to this speculation? I don't know. I think it's a good suggestion to mark this topic for further investigation and discussion in a post and examine Rakel's sources for information in the process... Knowing more about these 4 week cycles of the organism sans human hormonal changes would be useful.

    Thank you for reading CO blog. Please feel free to pass it on to others you think might enjoy it - or to others who just want to rant alongside me on my commentary posts.

  18. Additional note:

    I recall reading somewhere that testosterone has a moderating influence on symptoms and fewer men develop persisting symptoms of Lyme disease as a whole - I need to confirm that, though, so don't hold me to it.

  19. BTW, I forgot to mention, I am male. There is obviously more than menstrual cycle at play in these cycles, but it seems not everyone experiences this. Thanks for the link on lymeinfo. Those transcripts are very interesting and I hadn't seen them before.



You can use <b>bold</b>, <i>italics</i>, and <a href="url">link</a> for links.

The Camp Other Song Of The Month

Why is this posted? Just for fun!

Get this widget

Lyme Disease




Related Posts Plugin for WordPress, Blogger...