Just read above article in New Yorker, June 30, 2013. It has some new information, a lot of old misinformation, but at least attempts, through the snide attacks on Lyme activists, to present doctors from both sides. Below are some notes I took while reading it. They are in order of appearance in the article. “B-flats” is my pet name for Bb, Borrelia burgdorferii, the most known organism causing Lyme disease in America. Bb =Bb the musical key of B-flat. Just a bit of silliness to lower my stress when dealing with Lyme disease ignorance.
New Yorker article says, “…there is no evidence that prolonged antibiotic therapy helps patients with Lyme disease…”
Well, there is a lot of evidence related to primates and other mammals, and if you are relying on the NIH studies, there is evidence there, distorted as those studies were by sampling errors and cessation of the studies much too soon to call them studies of prolonged antibiotic therapy. And, the insurance-owned doctors who always say “no evidence” disingenuously ignore the fact that they pretty much control research funds. There’s no research because the funding agencies are funding only the research that these doctors, with an interest in the outcome, approve. Round and round. Don’t fund research that would prove it and you can always say, as the insurance companies want you to, that there’s no scientific proof prolonged treatment works. And any graduate student can tell you, if you don’t get funding, there ain’t gonna be no research. Well, aside from me and my ethnographic research. I funded it and that’s why I’m so poor.
Re: RIFE machines “little empirical evidence exists to demonstrate that it works.” Hmmm. Wonder why there’s so little “empirical evidence.” Anybody get funded to study this?
Mentions IDSA guidelines, no mention of ILADS guidelines. Well, no mention of ILADS until way, way into the article. For a balanced presentation, he should have brought them into it in the same paragraph that he brought up IDSA. If you don’t know, IDSA is the Infectious Diseases Society of America, the mainstream doctors with a major stake in keeping Lyme disease “easily diagnosed and treatable,” both because some of them are consultants for insurance companies and research agencies–they get paid to present a certain view–and because they wrote articles at the very beginning of the Lyme epidemic that would now be shown to be incorrect were any research into the opposite view done. They have reputations to maintain and don’t give a rat’s ass for true science, which would demand an open mind and no vested interests.
“. . .in most cases, the tick bite causes a skin rash, called erythema migrans.” Lord, not that again. No, in most cases it does not. 50% of people later diagnosed with Lyme remember neither a tick bite nor a rash. Some say more, some say less. But “most” makes you think its a whole lot, when “most” can be only 51%, leaving the other 49% twisting in the wind. The article later says up to a quarter of patients never get a rash. This may be based on new studies I am not aware of, but even so, 25% of patients who never get a rash is a whole lot, given what the consequences of that are. He should have said, “in some cases” and put in a sentence about the ongoing research into this number.
“(The rash) which is easily identified by its bulls’eye. . .” No, its not easily identified by its bull’s eye. That’s an outdated bit of dogma that should have been dumped long, long ago. The bull’s eye rash can vary a lot with co-infections or its position on the body. Recent publications have said if you had stripes with your rash, it indicates a co-infection with Bartonella. It can be triangular or oval. It can be 2” in diameter or cover your whole back. The only thing easily identifiable about the rash is that it expands outward over time from the tick bite. One of mine, for instance, was in my groin. On my front upper thigh it extended, rapidly because I was already infected, in a perfect half-circle that met curved sides on the back of my thigh. If flattened out, it would have made a semi-circle. That part cleared into a half-bull’s eye with the tick bite in the middle of the straight part.
On my abdomen, it was diagonal, evenly spaced stripes. I can’t remember if they cleared at the same time the semi-circle did. The whole thing went from just above my knee to my bra line. My doctor dismissed me as having Lyme disease because the rash was not “round enough” was “too big” and appeared too early. He ignored my flu-like symptoms which bordered on delirium, perhaps a sign of babesiosis. To humor me, he gave me ten days of erethromycin, which is the wrong antibiotic for too short a time. He misdiagnosed me because he was way, way too influenced by the protocols, established by the mainstream institutions, which rely on the statements of doctors working for the insurance companies. They want a perfectly round bull’s eye rash with no variations, before they will diagnose Lyme disease. Had I been diagnosed correctly at that time, perhaps I would not now be using a wheelchair.
The article says 20% of Lyme patients don’t get better after treatment and that is called Post-Treatment Lyme Disease Syndrome. That’s what doctors following IDSA call it. ILADS calls it chronic Lyme disease. He should have said that immediately after bringing up Post-Treatment Lyme Disease Syndrome. ILADS points out that IDSA has absolutely no evidence to support PLDS whereas there is evidence to support persistent Lyme Disease. (I have a whole notebook of such studies and tomes of such studies have been presented to investigative bodies by Lyme activist organizations. The problem is that a higher standard of evidence is being required for Lyme disease than has been required for other diseases in the past, in part due to the reasons I presented above.)
The article mentions new co-infections I never heard of–at last, some new information. These two are B. miyamotoi, a genetic relative of B. burgdorferii, the bacteria that has been studied and assumed to cause Lyme disease and Powassan virus, about which I know nothing at this point.
Fully two pages into the article we finally get a clue that there is another viewpoint and the author quotes Brian Fallon, a staunch longtime defender of chronic Lymies, and it, finally, mentions ILADS.
The author states that most doctors reject the term “chronic Lyme,” in part because many people who say they have it are not infected with Borrelia. I’m trying not to “go postal” here. He makes absolutely no mention of the gigantic testing problem. Most people are given a Lyme-titer by non-Lyme specialist doctors. It is up to 40% unreliable, giving false pos and false neg. The longer you have had Lyme disease when you get the test, the LESS likely it is that you will test pos. That is why I advise people to skip that test entirely and go to Igenex and get one or both of their panels before believing that they are not infected with Bb. When anyone says anyone is not infected with Borrelia, I want to know what test they had. Are they not infected or did you just not find it because the tests suck?
A really infuriating portion of this article is the one that insinuates strongly that Lyme activists are fanatics who “have not done their homework.” I’d say Lyme activists have done a hell of a lot more homework than the mainstream anti-Lyme activists who lazily or cynically just accept the status quo because its easier to do that. Way easier. Lyme doctors are actively persecuted by anti-Lyme activists, in the past, now, and including the loss of their licenses. The author quotes Gulick (I thought his name was Gluck, don’t know who’s in error) at Cornell calling chronic Lyme patients “true believers.” I’ve heard him do that before. I think he’s a “true believer,” in Lymie true believers. But, I digress.
Here’s something new, or new to me. Researchers can sometimes find different strains of Borrelia in the same tick. I have read that different strains manifest in different ways, causing that much more diagnostic confusion. So now there’s another reason why Lyme disease presents so differently individual to individual. This is in addition to the possibility, a strong one, of multiple co-infections.
The article states that it takes ticks “36 hours to transmit bacteria.” Oh no, it doesn’t. There is enormous variation in the literature on this. I have read many studies by mainstream researchers, trying to get a fix on this. The studies range from zero transmission time to 72 hours. But, get this, there are studies indicating a difference between the East and West Coast on transmission time. Studies have shown that one third of California Lyme ticks carry Bb in their saliva glands, as opposed to their gut. The tick infects you by regurgitation from its gut, which takes time. But, if the tick on you is one of those one-third and it has Bb in it, the logical assumption is that transmission time is immediate. What would stop it?
Not only that, but if you damage the tick while removing it, for instance by scratching it off in your sleep because you are one of the people who is allergic to tick saliva, transmission time is also immediate. That’s why you slap some rubbing alcohol on the bite immediately after removing the tick, to try to kill any B-flats that escaped into your bloodstream while you did that.
Finally, much too late in the article to claim a balanced presentation, the author does mention false negs and pos on tests. We assume he means Lyme-titers here. He says that the PCR test, one of the ones in Igenex’s initial panel, is easily contaminated and produces lots of false positive results. That is true, which is why you want to get a panel of different kinds of tests from an excellent lab that specializes in Lyme disease. Lower chances of contamination. Higher chance of finding B-flats if they are there. He compares the Lyme testing situation to tuberculosis testing in India, where many people test pos and many never develop symptoms but are given highly toxic drugs. Now they have a machine that does it better. One doctor speaking to the testing problem says we need a machine like that for Lyme. Well, gee, any research funding for that? I’m guessing, not.
According to the article, public health officials stress that if doctors see a bull’s eye rash, they should assume Lyme disease. That’s nice, and that’s what has been in the CDC guidelines for reporting for many a year and that was accepted by all doctors for many a year. A “doctor-diagnosed” bull’s eye rash, of course, and I’ve already described my experience with a “doctor-diagnosed” bull’s eye rash. And, I’ve always said, to hell with the doctor-diagnosed part. Its very distinctive and unique. Any fool can compare what’s on her/his body to pictures of Lyme rashes found online. You don’t need no “steeenking” doctor for that. But that’s not what the IDSA guidelines currently say and CDC has been waffling on that. The guidelines put out by IDSA only a few years back removed the bull’s eye rash as a definitive diagnostic for Lyme disease, based on “no scientific evidence whatsoever,” to quote ILADS. CDC removed it from their website as a reporting datum, but individuals at CDC told Lyme activists privately its still a diagnostic and ILADS still includes it in their guidelines.
I’m going a step further. This refers back to my doctor saying my rash appeared “too early” for it to be a Lyme rash. There are indications in the Lyme literature and I have had it confirmed by a Lyme-literate doctor based on his cases, that if you get a bull’s eye rash and/or flu-like symptoms very soon after the tick first attaches, like maybe even hours, it is an indication that you already had Lyme disease. I first saw this reference in Polly Murray’s early book on Lyme disease The Widening Circle (she’s often referred to as the “mother” of Lyme disease because she and another woman were the first to alert public health authorities of a strange medical problem in Lyme CN). She observed that Lymies bitten by subsequent ticks got early symptoms rapidly. Her statement confused me because it said “tick,” not Lyme-tick, bearing Bb. Now there are statements in the literature that it doesn’t even have to be a Lyme-bearing tick. Any tick bite will do it because the B-flats already in the body are reacting to any tick saliva.
That happened to me. My big rash appeared within 20 hours of the tick bite and my doctor therefore dismissed it as “appearing too early.” I now know I had been bitten many times before and some of those had produced bull’s eye rashes and flu-like symptoms. I just ignored it because I didn’t know any better and then later, because I’d had two false negs on Lyme-titers when Lyme-titers got invented. (No worries, many pos tests later, better tests.) Reconstructing my medical history in the light of new knowledge, I now remember that strange rash that expanded out from under my armpit and turned into a circle not long after I held my neighbor’s goose under my bare arm, the goose that was part of a shipment of birds recently in from the East coast a year or two before Lyme disease was named after Lyme CN. And, I have myself seen and photographed a round rash around a bite of some kind (sometimes you can’t see the tick because its a transparent nymph or larva) that appeared on a friend of mine who has had symptoms consistent with Lyme for years. Hers appeared only hours after she took a walk in tick brush, along with fever and mental fuzziness.
The article mentions recent studies, by Fallon and Yale researchers, that “raise the possibility” that Bb persists after treatment. It says especially in areas near cartilage, the B-flats cause swelling. Hello, nice to get a little vindication on that one. I’m not nuts, my ankles and knees have been swollen for 20 years and get worse if I get off my Lyme regimen. I’d say the recent studies don’t raise the possibility of persistence. That possibility has been documented for years, for anyone researching the literature with an open mind. I’d say it confirms the possibility.
The studies include one by Dr. Fallon, who saw metabolic brain abnormalities in documented LD patients who still had symptoms after treatment, as compared to the brains of healthy controls. UC Davis researchers found Bb in macaques who were given LD, then treated with standard treatment. Researchers then put clean ticks on them, ticks they had raised themselves and knew for sure had had no contact with LD. They left them on a while, removed them and found Bb spirochetes in the ticks. Similar research is now in progress for humans.The die-hards will dismiss these because the first did not involve actual B-flats and the second is an indication for primates, not humans specifically. Hey, I studied primatology. I’m an anthropologist. I’d say chances are excellent that what works for or against macaques is very likely going to work for or against humans. But I hope that human study gets out soon and kudos to those heroes now allowing ticks to be put on them.
Here’s a quote from an anti-Lyme disease doctor who has taken much flak from Lyme activists over the years. Dr, Gary Wormser says in this article, “if there were [evidence of persistence] I’d say ‘so what.’ You would have to show me that the spirochetes continue to produce disease and you would have to show me that they would respond to ABx.” Its an overly long quote, much longer than anything Fallon says. Wormser claims undiagnosed but sick people go from doctor to doctor until they find one that will say they have LD. Then those people are happy because somebody has finally taken an interest in them.
He thus implies that we’re all hypochondriacs or in some other way mental cases looking for attention. No suggestion is made that we might be well-trained PhD scientists, entirely comfortable reading dense badly-written medical articles, who thoroughly researched the literature with an unbiased eye and concluded that the best evidence supports the idea that we have Lyme disease and that most doctors are operating on much less information about this disease than we are, therefore we need to search for a doctor who at least knows as much as we do, hopefully more. I’ll say I was happy when I finally found one!! Not because I was seeking attention, but because I was seeking treatment for my nightmarish illness.
Another quote from Wormser, “If you said you had renal failure and need dialysis, the doctor would do a test. If it turned out neg, nobody would do it.” Well, yeah, but longterm oral antibiotics are not nearly comparable to dialysis as a dangerous procedure. IV, maybe, but I still don’t think so. And I’m guessing the test for renal failure is a lot more definitive than the most used test for Lyme disease. In the absence of a good test, but with a strongly suggestive case history, would not a truly conscientious doctor still do the best she/he could for the patient?
Wormer’s school cites 4 double-blind, placebo-controlled NIH (National Institutes for Health, major science funder) trials over last 15 yrs. Each one involving alleged prolonged ABx, testing whether they help to eliminate symptoms. In the two largest, there was no improvement. I have to ask, are these the same ones that as a first step, eliminated all known LD patients from the study on alleged ethical grounds (now, they get ethical, when it will skew the results in the direction they desire) and only went 3 months, which is not nearly long enough? It took me a year or more of oral antibiotics and Flagyl before I began to improve.
Two others were equivocal. None concluded that risks of extended IV ABx outweighed the theoretical benefits of longterm IV ABx. Here is a good example of the bait-and-switch game used so frequently by doctors like Wormser. There is no mention of the lack of danger of longterm oral antibiotics. IVs are risky and can cause severe infections, no argument there. But the question I’d like to have answered is do the risks of longterm oral antibiotics, perhaps in combinations, outweigh the documented benefits of longterm oral antibiotics? Many ILADS doctors say they do and treat patients on that basis.
And here’s another question, does the benefit of longterm antibiotics outweigh the risks of what’s going to happen to Lymies in the longrun if you don’t treat them at all or not enough? Some research, looking at the brains of people post-mortem, indicates that untreated Lyme disease can eventually cause or turn into MS, ALS, Alzheimer’s or Parkinson’s. A friend of mine, longterm Lymie, was just diagnosed with Parkinson’s and I know of two ALS deaths of friends of mine who are very likely to have had Lyme disease. Much likelier than to have had ALS, which is pretty rare. They were tramping around in the same tick-brush I was and ALS, which has a genetic component, was never in their families. I know because I had this conversation with their spouses before they died.
The article mentions Dr. Richard Horowitz, who is what Lymies call a “Lyme-literate” doctor. He has seen 12, 000 patients with tick-borne ailments. He avoids ABx altogether and focuses on co-infections, which he treats with “different regimens.” He uses dietary restrictions and supplements to detoxify the body and starve bacteria and argues that conventional medicine is too focused on just Bb. Half of his patients present with babesiosis. This, he says, is treated in an “entirely different way from Lyme. Together, they cause far more harm than either one does alone.”
Whoa, some validation there. I have no Lyme doctor and had to stop seeing mine after 2.5 years because I just couldn’t make that 600 mile trip anymore. So, I stopped the ABx and went to a holistic regimen including dietary restrictions and supplements and exercise and a whole lot more, including some prescription meds for symptoms. We can’t all get to see Dr. Horowitz, so I don’t know what to do about all the co-infections I believe I have or have had, but I have found his writings very useful in developing my holistic regimen and its nice to know my efforts are supported by someone in the mainstream medical world.
The article mentions a federal advisory committee working on ways to improve Lyme diagnostics. Huh? Who are they, where are they? Whoosh. That one went by real fast. But, I venture to hope that that committee is balanced–unlike the one IDSA used to develop its inaccurate and misleading guidelines and then the one it chose later, after the state of Connecticut held hearings and insisted they write new guidelines with a new panel they were then allowed to select– What??!! Reject their guidelines, require new ones, require a new panel, then allow them to select it? Slice of bias, anyone?
The author admonishes Lyme activists to reject “those who foster dark conspiracies.” He says he talked to “several Lyme activists” who told him Times reporters had been restricted from writing about the Lyme controversy and then he talks about the Plum Island theory. This is one that has been circulating for years. Plum Island, where germ warfare is researched, is very close to Lyme CN, where Lyme disease first was documented. The question is did the government let something escape from Plum Island accidentally or on purpose to test it? Something being worked on as a biological weapon? I don’t have the expertise to speak to that, but I don’t think those who do are “fostering dark conspiracies” and I do think all aspects of this are wide open, since Lyme research is obviously so skewed.
It is true that the U. S. Army has a huge amount of information on Lyme disease. One theory on that is that, because Bb is transmitted in the Persian Gulf area by sand fleas and Gulf War and current soldiers are trained in the desert, get bitten a lot and get Lyme disease, it behooves the U. S. Army to sponsor and collect Lyme research. It has been suggested that Gulf War Syndrome is, in fact, Lyme disease. I believe the government could do it, would do it and has done it. I believe articles I have read and documentaries that have claimed the federal government/military has released germs into the public to test their efficacy as weapons and has otherwise used unknowing civilians as guinea pigs. Developmentally disabled children were fed radioactive food by the government to see what would happen. Tuskeegee. There’s more.
I don’t know if they did do it in the case of Lyme disease, but if they did, it surely is another reason why it is so hard to get anyone’s attention on this or to get research funding into real research on Lyme disease. It would explain the stonewalling and use of ridicule to debunk Lyme activists. In the past, I did have a question for the Plum Island theory people, though. Why would the government choose a disease that can take so long to incubate as a germ warfare weapon? Wouldn’t they want something that moves faster?
That question was recently answered for me by a History Channel program about Plum Island. There was an incident shortly before Lyme disease entered the public consciousness in which saboteurs had infiltrated the Plum Island facility as workers and then stolen a random sample of vials containing diseases. When caught, they confessed dumping the contents on the mainland. They did not know which ones they dumped. Lyme disease could well have been one of those–not kept to turn into a weapon, but kept for other scientific purposes, such as research on prevention and cure, given that soldiers were getting it. That was enough to explain that part of the Plum Island problem for me, but I make no claims as to the accuracy of Plum Island conspiracy theory–I don’t have the energy to research that–I’m just telling you my thinking on the subject.
Now comes another example of the bait-and-switch on longterm ABx risks vs. benefits of same. There is now pending a New York bill that would require insurance companies to reimburse longterm ABx “even though no study has proved them effective and IV antibiotics can cause serious, sometimes fatal complications.” Yeah. Again. Maybe IV antibiotics do, but longterm oral antibiotics don’t, or nearly as much. As Lymies point out all the time, longterm oral antibiotics are used sometimes for years to treat acne. How serious can the effects be? See how neatly he switched from oral ABx to IV ABx to talk about complications? Apples and oranges, but, hey, whatever works.
Another so-called dark conspiracy the author presents is the theory that the NIH made a pact with drug companies to ignore Lyme Disease. He is very dismissive of that suggestion, but presents no research into it. I’ve heard the theory. I can believe it. They would do it, they could do it, it would explain a lot, but I don’t know if they did do it. However, from a sociological viewpoint, I’d say there is every reason to think that happened on some level. Maybe not a pact, maybe just a wink and a nudge between a few powerful people in a private room. Happens all the time, does it not?
The article wraps up with an attack on Lyme activists, comparing them to AIDS activists unfavorably. He says they did their homework and we didn’t. Infuriating. You could only say that if you were yourself completely ignorant of the quality of the research done for years by Lyme activists and ILADS. What evidence is he presenting that Lyme activists are any less informed on their issue than AIDS activists were? The “several” Lyme activists he spoke to who were allegedly engaged in “dark conspiracies?” What a slander! I have to tell you, I’m not a medical doctor, but I’ve read hundreds of articles by doctors on all sides of the issue and I have the credentials to say that by and large the most intelligent and scientifically valid ones are the ones written by Lyme-literate doctors. And also they are the ones most based on actual observation and treatment of real live Lyme patients, not bacteria behaving badly in a Petri dish!! The nerve!
Lastly, a bit of a footnote indicating the sloppiness of much that is written on Lyme disease. At the end of the article is a sidebar on prevention. In this sidebar it is stated that a tick CAN take 36 hours to transmit Lyme disease. In his article, he says it DOES take 36 hours. See what I mean? Big diff.