So called "evidence based medicine" has done more to harm medicine than anything else I can recall during my 30 year tenure in medicine. Doctors have become technicians, rather than practitioners following in the traditions of healers who have come before.
When I was in college, science as we know it, existed within a framework-a caste system-a pecking order. Mathematics was considered the purest science: provable with irrefutable equations. Physics took second place. It described fundamental properties of the world/universe around us, supported by mathematical equations. Chemistry followed next and then biology. The order of descent was based on how hard, irrefutable and provable the conclusions were. All science is validated by the scientific method: a theory or hypothesis is proved by well designed experiments which can be replicated in a variety of places, times and circumstances.
When I entered medicine in the 1980s, medicine was more than a job or ordinary profession. It was a commitment, a lofty avocation, a calling of sorts. (at least according to my father)--I agree. Medicine was a healing art, in the tradition of the many who had preceded us, predicated on science. It was not a science.
Sometime around 1995 the term "evidence based medicine" insinuated itself, increasingly into the verbiage of the profession. I suspect it was in large part driven by managed care companies, looking to control costs, and then, high powered medical institutions jumped onto the band-wagon, in the belief that medicine was really science, not art: throwing out the baby with the bathwater.
Properly designed controlled medical studies were carefully analyzed by statisticians. Sometimes multiple studies were combined and analyzed-- meta-analysis. Problem. Only a few potential questions were addressed. Most studies were funded, at least partly, by big Pharma, with pre-existing agendas, undoubtedly tied to feathering the pockets of CEOs and stock holders (follow the money). Medical research, by its very nature, is simplistic. In truth, it is impossible to do proper science when it comes to studying something as complicated as people. Newer studies replace and refute older ones on a regular basis. It is impossible to control the variables, many of which are unknown, poorly understood or yet to be discovered. If it takes a room of statisticians, as is frequently the case, to prove a point, it should give one pause.
The single biggest problem: data obtained from a single study is extrapolated widely, to support wide ranging conclusions, based on faulty logic superimposed on bad science.
To makes things worse, evidence, as it were, is now broken down into levels/categories-- again, a pecking order. Most in the profession have accepted this new and improved medicine without giving its precepts a second thought.
First we have placebo controlled, double blinded, randomized studies, the results of which are statistically validated and replicated in subsequent studies.
Then we have non blinded controlled studies, non-controlled studies, head to head studies, published studies, clinical reports published in journals and lastly recommendations of a body of experts--my perennial favorite.
How can opinion be science?
So, let us get back to Lyme, the subject of this blog. The Klemper, Krupp and Fallon studies, are in my mind, weak science at best. They also all have somewhat different study designs and conclusions. The limitations of these studies has been discussed in detail elsewhere. The "experts" put these findings together and give us a final product: evidence based guidelines.
The better science is what physicians seem to dismiss and ignore: test tube science and other forms of "basic" science. Borrelia has been shown to convert from spirochete to cyst forms in the laboratory and back the other way. Spirochetes have been shown to exist as L-forms. Research in immunology support beliefs that infected hosts cannot be sterilized of Lyme. Human and animal models have proved that Lyme persists in the face of massive doses of antibiotics. This sort of science can control the variables. It can be replicated in multiple settings over time. The same cannot be said for clinical studies, the type of science clinical doctors rely upon, which are pooled into meta-analyses, looking for statistically significant conclusions. I could go on, write a book about this subject, with foot notes and citations. Not here.
This post is a about "evidence based medicine." In my opinion, this is a sham, a fraud. Perhaps it works for HMO physicians who are required to see patients in 6 minutes: cookbook medicine. It is not a useful tool for thoughtful, curious physicians, intent on practicing their art to the best of their ability. Patients are all different as are all physicians. Diseases are nuanced and complex.
The practice of medicine is a mosaic of science, judgment, clinical experience and yes-intuition, a clinical nose, the product of years of practice.
So yes, this dumbed down version of medicine has now framed the basis for the national debate about lower cost, higher quality medicine. According to national political "experts", electronic medical records and evidenced based medicine (the mantra), will solve systemic problems with our health care system.
Who decides which evidence we use? Ivory tower physicians. Iconic figures. The Gary Wormsers of the world. Doctors for the most part, are reassured by practice guidelines: complex decisions have already been decided for them. A few other physicians, the outliers, and their demanding-annoying patients, just won't go away. It is no wonder that many readers shudder when the hear the words: evidence based medicine.
Every pre-med student is ultimately asked the question: why do you want to become a doctor. Inevitably, they all give the same, banal answer: I want to help people.
For those of us who want to be included amongst healers who use science, the state of the art as it exists at any particular point in time, as a basis, but only a starting point for the practice of their art: the art of healing; this answer turns out, in the final analysis, to not be so banal after all.
Evidence based medicine? Thumbs down.
Saturday, February 27, 2010
Friday, February 26, 2010
H. pylori
My patient, age 32: "This is the best I have felt in five years. I feel like a whole organism. Rashes on my body, face-circles under my eyes, they have all cleared. My abdominal pain is all gone. My acid reflux is gone. Total body stiffness and pain are gone--after 5 years. Fatigue is gone: I am so energetic. My body has changed. My middle section has reduced in size. The bloating and swelling is gone. My appetite is better: I am know longer hungry all the time. My taste buds work better. My neighbors have so much energy, now I am like them. Thank you."
"Did you have any side effects from the medicine?"
"For the first two weeks I had nightmares--mild headaches, then everything went away."
One month prior to this visit, a test for H. pylori was positive: the IgM ELISA. Most labs only perform the IgG ELISA. I request the IgA, IgM and IgG antibodies for H. pylori (Helicobacter pylori). Any one could be positive. IgA goes along with mucosal disease and IgM indicates active disease.
This patient has a number of chronic medical problems. The test was ordered because of persistent heartburn (GERD). Her treatment: Nexium 40mg 2x daily, Biaxin 500mg 2x daily and Amoxil one gram 2x daily, for 30 days. She has been off therapy for a week and is continuing to improve. I told her if symptoms return maybe we should retreat.
I leave this vignette for you to interpret.
"Did you have any side effects from the medicine?"
"For the first two weeks I had nightmares--mild headaches, then everything went away."
One month prior to this visit, a test for H. pylori was positive: the IgM ELISA. Most labs only perform the IgG ELISA. I request the IgA, IgM and IgG antibodies for H. pylori (Helicobacter pylori). Any one could be positive. IgA goes along with mucosal disease and IgM indicates active disease.
This patient has a number of chronic medical problems. The test was ordered because of persistent heartburn (GERD). Her treatment: Nexium 40mg 2x daily, Biaxin 500mg 2x daily and Amoxil one gram 2x daily, for 30 days. She has been off therapy for a week and is continuing to improve. I told her if symptoms return maybe we should retreat.
I leave this vignette for you to interpret.
Thursday, February 25, 2010
Three patients today: wet mounts, osteomyelitis and ulcerative colitis
This 35 year old female went to the local ER in October 2008. She had a rash, fever to 101 f, and chills. She was sent home without treatment. I saw her in the office a few days later. She had a very large and very red inflammed EM rash on her right chest wall. I decided to be aggressive. I double covered with Amoxil one gram twice daily and Doxy 100mg twice daily for 30 days.
I saw her 4 weeks later; everything had resolved. In June 2009 she complained of new onset fatigue--severe, disabling for several months, brain fog and word retrieval difficulties. Lab testing was then performed. A CD57 count was 28. A standard Lyme Western Blot showed 41 bands. The Babesia WA 1 aby reacted 1:256, the lowest positive titer. A Clongen WB showed multiple bands, including IgM 23 and 41. A wet mount was performed. This showed numerous small round bacteria--presumptive of a Bartonella species and "numerous large elongated extracellular motile organisms(look like a protozoan or tiny round worm)." Contemporaneously, she developed pelvic pain. She was treated with: Amoxicillin, Zithromax, Rifampin and Tindamax. This was followed by a course of Levaquin. She improved nearly 100% within 7 months-- except for pelvic pain. At her request, a repeat wet mount was performed. This time scarce, elongated, curved, extracellular organisms were seen. The Bartonella like organisms were gone. Quite a change! I empirically prescribed a course of Levaquin and Tindamax. Her gyn and GI have been unable to diagnose the source of the pelvic pain.
A second patient, a 40 something neuroscientist, has been treated for Lyme with cognitive dysfunction for 6 months. Physical symptoms have improved, but cognitive difficulties remain.
She is unable to focus, concentrate or process. Her short memory is very poor. I asked her to have a brain MRI and a SPECT scan done, but she told me she "forgot." I bring this patient up because of her past medical history. Nine years ago she developed a bone infection- osteomyelitis, in an ankle following surgical repair of a fracture. She was treated with two courses of IV antibiotics, 9 weeks each. In addition, she was treated with extensive courses of oral antibiotics. All told, she took antibiotics for 4 consecutive YEARS. She finally improved after hardware was removed from her ankle. A consultant from the infectious disease department at Johns Hopkins University, where she was treated stated that she might require life-time antibiotic therapy.
A third patient, a 50 year old woman, with a history of ulcerative colitis developed acute Lyme disease in 2007. All 13 Western Blot Bands were present. She also has had a persistent, marked elevated ANA level. She saw me after failing standard treatment (3 weeks of doxycyline). She continued to have joint pain and fatigue. She improved over a couple of months and therapy was discontinued. She had recurrent symptoms over the next year: mostly joint pain. Further courses of antibiotics (short term) were prescribed with improvements. When I saw her in late 2008 she was well. Soon thereafter she experienced a recurrence of ulcerative colitis-- after a 10 year remission. This episode was controlled with steroids and maintenance Cloazol . At the end of 2009 she suffered a severe, uncontrolled relapse of her colitis. She was treated with: Remicaide, high doses of Colazol, 6-MP and steroids. The Remicaide, given at Johns Hopkins, was not effective. The Hopkins' GI recommeded a total colectomy (resection of colon) for non-responsive disease. Not done. Her local GI got the disease under control with high dose, tapered steroids. She remembered something I once told her. She recently sent colon biopsy fragment to Clongen. The PCR test of the biopsy specimen was POSITIVE FOR LYME. Be careful what you wish for! Flagyl has given her diarrhea in the past. I cautiously prescribed a course of Cipro--today. I spoke with Dr. Kilani. "We don't know what these results mean. The presence of DNA in the biopsy material does not tell us if viable organisms are present." The suffers with autoimmune disease. Did Lyme trigger her colitis or did the immunologial effects of treating Lyme trigger the disease. She will see her GI next week. I am sure he will have fun trying to make sense of the results.
I am really not trying to pick on Hopkins. It remains one of the best tertiary medical centers in the country--in most matters.
I saw her 4 weeks later; everything had resolved. In June 2009 she complained of new onset fatigue--severe, disabling for several months, brain fog and word retrieval difficulties. Lab testing was then performed. A CD57 count was 28. A standard Lyme Western Blot showed 41 bands. The Babesia WA 1 aby reacted 1:256, the lowest positive titer. A Clongen WB showed multiple bands, including IgM 23 and 41. A wet mount was performed. This showed numerous small round bacteria--presumptive of a Bartonella species and "numerous large elongated extracellular motile organisms(look like a protozoan or tiny round worm)." Contemporaneously, she developed pelvic pain. She was treated with: Amoxicillin, Zithromax, Rifampin and Tindamax. This was followed by a course of Levaquin. She improved nearly 100% within 7 months-- except for pelvic pain. At her request, a repeat wet mount was performed. This time scarce, elongated, curved, extracellular organisms were seen. The Bartonella like organisms were gone. Quite a change! I empirically prescribed a course of Levaquin and Tindamax. Her gyn and GI have been unable to diagnose the source of the pelvic pain.
A second patient, a 40 something neuroscientist, has been treated for Lyme with cognitive dysfunction for 6 months. Physical symptoms have improved, but cognitive difficulties remain.
She is unable to focus, concentrate or process. Her short memory is very poor. I asked her to have a brain MRI and a SPECT scan done, but she told me she "forgot." I bring this patient up because of her past medical history. Nine years ago she developed a bone infection- osteomyelitis, in an ankle following surgical repair of a fracture. She was treated with two courses of IV antibiotics, 9 weeks each. In addition, she was treated with extensive courses of oral antibiotics. All told, she took antibiotics for 4 consecutive YEARS. She finally improved after hardware was removed from her ankle. A consultant from the infectious disease department at Johns Hopkins University, where she was treated stated that she might require life-time antibiotic therapy.
A third patient, a 50 year old woman, with a history of ulcerative colitis developed acute Lyme disease in 2007. All 13 Western Blot Bands were present. She also has had a persistent, marked elevated ANA level. She saw me after failing standard treatment (3 weeks of doxycyline). She continued to have joint pain and fatigue. She improved over a couple of months and therapy was discontinued. She had recurrent symptoms over the next year: mostly joint pain. Further courses of antibiotics (short term) were prescribed with improvements. When I saw her in late 2008 she was well. Soon thereafter she experienced a recurrence of ulcerative colitis-- after a 10 year remission. This episode was controlled with steroids and maintenance Cloazol . At the end of 2009 she suffered a severe, uncontrolled relapse of her colitis. She was treated with: Remicaide, high doses of Colazol, 6-MP and steroids. The Remicaide, given at Johns Hopkins, was not effective. The Hopkins' GI recommeded a total colectomy (resection of colon) for non-responsive disease. Not done. Her local GI got the disease under control with high dose, tapered steroids. She remembered something I once told her. She recently sent colon biopsy fragment to Clongen. The PCR test of the biopsy specimen was POSITIVE FOR LYME. Be careful what you wish for! Flagyl has given her diarrhea in the past. I cautiously prescribed a course of Cipro--today. I spoke with Dr. Kilani. "We don't know what these results mean. The presence of DNA in the biopsy material does not tell us if viable organisms are present." The suffers with autoimmune disease. Did Lyme trigger her colitis or did the immunologial effects of treating Lyme trigger the disease. She will see her GI next week. I am sure he will have fun trying to make sense of the results.
I am really not trying to pick on Hopkins. It remains one of the best tertiary medical centers in the country--in most matters.
Sunday, February 21, 2010
The eye of the beholder: a specialist
Published studies do show that chronic Lyme improves with long term antibiotic therapy.
Donta, 1997, Boston University published a study of 277 patients with chronic Lyme disease.
He reported that patients frequently did not improve for several weeks. After 2 months 33% of patients had improved, after 5 months, 61% had improved. He claimed 20% of patients were cured, 10% did not improve, and 70% showed some improvement. The duration of the study was for 1 to 11 months. He concluded: CONTROLLED STUDIES NEED TO BE CONDUCTED TO VALIDATE THESE OBSERVATIONS.
In 2003, Donta published a study on the use of Biaxin, Biaxin with Plaquenil and Plaquenil alone.
The effective therapy was Biaxin and Plaquenil. Conclusion: THESE RESULTS SUPPORT THE HYPOTHESISIS THAT lYME BORRELIA RESIDE IN AN ACID ENDOSOME.....
Cameron, 2008, published a double-blind placebo controlled clinical trial.
He replaced the term chronic Lyme disease with Lyme disease with persistent symptoms (LDPS). He found a 46% improvement of subjective quality of life in treated patients and vs 18% in non treated patients. He concluded: WORTHY OF FURTHER STUDY.
Clarrisou et al, 2009, Med Mal Infect, published: Efficacy of long-term antibiotics in patients with a chronic Tick Associated Poly-organic Syndrome (TAPOS
Investigators keep inventing new terminology for the same disease. Why?
A cohort of 100 patients was followed. The study showed favorable results in subjective symptoms. The authors point out flaws and limitations of their study but recommend: RANDOMIZED, DOUBLE BLIND STUDY.
The number of patients studied in all of these studies was significantly higher than the number of patients studied in the 3 NIH sponsored studies. This has mostly to do with study design and patient selection limitations.
Hopkins-Harvard-Yale-IDSA-CDC: Where are you?
Those folks are sticking with the "Best science."
Problem: best science supports these conclusions (fatigue, qualitly of life) if you take another look at the Krupp and Fallon outcomes. A patient suffering with Lyme and chronic fatigue recently told me: " Hell, I would gladly go on 3 months of IV Rocephin if it only helped with fatigue."
I asked an esteemed professor(infectious disease) from Hopkins about his success with severe neruo-syphilis He told me with pride that he has treated it, (it is rare these days)--the penultimate expert. I asked him about patients with severe brain damage. "When the squash is gone there is no squash." Good answer. Even patients with persistent vegetative states have been shown to frequently have significant neurological and cognitive activity.
Patients with neuroborreliosis have recovered. SPECT scans, PET scans have improved. Patients with neuro-syphilis-dementia (general paresis) have been treated with only penicllin. These patients pathologically have blebs and cysts in their brains, similar to those seen in patients with neuroborrelosis. As stated, there are not many of these patients around anymore. There have been no studies since TUSKEGEE. How would neuro-syphilis patients do if they were treated with other therapies, including IV Flagyl? Not studied
How about this:
Why don't we let psychologists and psychiatrists evaluate cognitive functioning, radiologists evaluate objective, radigrophic signs of improvement and neurologist evaluate for evidence of neurological improvements. How about listening to our patients as well? I know--a novel concept.
Why does a professor of of infectious disease medicine, with little or no knowledge of these other fields, tell us about squash, a "fancy" designation for brain?-- what are his qualifications to tell us that chronic Lyme disease--including neuroborreliosis does not exist?
I went to medical school, internship and residency.
We made round, sometimes with esteemed attendings: we were intimidated: they knew everything, we were abysmally ignorant. We were ready to be chastised; we were swine waiting for pearls to be cast to our feet. I remember, Super-star attendings--Power, honor, prestige: with it comes a sense of infallibility--after all, you are the last word, the highest authority. You have to be self assured. Perfectly understandable. That is why I became a generalist, not a specialist. It is understandable. Nonetheless: sometimes you are wrong, dead wrong.
Donta, 1997, Boston University published a study of 277 patients with chronic Lyme disease.
He reported that patients frequently did not improve for several weeks. After 2 months 33% of patients had improved, after 5 months, 61% had improved. He claimed 20% of patients were cured, 10% did not improve, and 70% showed some improvement. The duration of the study was for 1 to 11 months. He concluded: CONTROLLED STUDIES NEED TO BE CONDUCTED TO VALIDATE THESE OBSERVATIONS.
In 2003, Donta published a study on the use of Biaxin, Biaxin with Plaquenil and Plaquenil alone.
The effective therapy was Biaxin and Plaquenil. Conclusion: THESE RESULTS SUPPORT THE HYPOTHESISIS THAT lYME BORRELIA RESIDE IN AN ACID ENDOSOME.....
Cameron, 2008, published a double-blind placebo controlled clinical trial.
He replaced the term chronic Lyme disease with Lyme disease with persistent symptoms (LDPS). He found a 46% improvement of subjective quality of life in treated patients and vs 18% in non treated patients. He concluded: WORTHY OF FURTHER STUDY.
Clarrisou et al, 2009, Med Mal Infect, published: Efficacy of long-term antibiotics in patients with a chronic Tick Associated Poly-organic Syndrome (TAPOS
Investigators keep inventing new terminology for the same disease. Why?
A cohort of 100 patients was followed. The study showed favorable results in subjective symptoms. The authors point out flaws and limitations of their study but recommend: RANDOMIZED, DOUBLE BLIND STUDY.
The number of patients studied in all of these studies was significantly higher than the number of patients studied in the 3 NIH sponsored studies. This has mostly to do with study design and patient selection limitations.
Hopkins-Harvard-Yale-IDSA-CDC: Where are you?
Those folks are sticking with the "Best science."
Problem: best science supports these conclusions (fatigue, qualitly of life) if you take another look at the Krupp and Fallon outcomes. A patient suffering with Lyme and chronic fatigue recently told me: " Hell, I would gladly go on 3 months of IV Rocephin if it only helped with fatigue."
I asked an esteemed professor(infectious disease) from Hopkins about his success with severe neruo-syphilis He told me with pride that he has treated it, (it is rare these days)--the penultimate expert. I asked him about patients with severe brain damage. "When the squash is gone there is no squash." Good answer. Even patients with persistent vegetative states have been shown to frequently have significant neurological and cognitive activity.
Patients with neuroborreliosis have recovered. SPECT scans, PET scans have improved. Patients with neuro-syphilis-dementia (general paresis) have been treated with only penicllin. These patients pathologically have blebs and cysts in their brains, similar to those seen in patients with neuroborrelosis. As stated, there are not many of these patients around anymore. There have been no studies since TUSKEGEE. How would neuro-syphilis patients do if they were treated with other therapies, including IV Flagyl? Not studied
How about this:
Why don't we let psychologists and psychiatrists evaluate cognitive functioning, radiologists evaluate objective, radigrophic signs of improvement and neurologist evaluate for evidence of neurological improvements. How about listening to our patients as well? I know--a novel concept.
Why does a professor of of infectious disease medicine, with little or no knowledge of these other fields, tell us about squash, a "fancy" designation for brain?-- what are his qualifications to tell us that chronic Lyme disease--including neuroborreliosis does not exist?
I went to medical school, internship and residency.
We made round, sometimes with esteemed attendings: we were intimidated: they knew everything, we were abysmally ignorant. We were ready to be chastised; we were swine waiting for pearls to be cast to our feet. I remember, Super-star attendings--Power, honor, prestige: with it comes a sense of infallibility--after all, you are the last word, the highest authority. You have to be self assured. Perfectly understandable. That is why I became a generalist, not a specialist. It is understandable. Nonetheless: sometimes you are wrong, dead wrong.
Thursday, February 18, 2010
Fallon and fatigue
An NIH study published in Neurology, 2008, lead investigator Brian Fallon has been misinterpreted by many in the Lyme community. The study was carefully performed using the highest level of scientific procedures. Patient selection was meticulous. The study was a randomized, placebo controlled study for Lyme encephalopathy (neuroborreliosis) and the results were published in a prestigious, peer reviewed journal. Dr. Fallon reported that the studied patient population suffered with... "moderate cognitive impairment, physical dysfunction comparable to patients with congestive heart failure, and fatigue comparable to patients with multiple sclerosis." The treatment arm of the study evaluated patients with established Lyme disease, seropositive by the CDC requirement of 5/10 positive IgG bands, who had previously been treated with 3 weeks of IV Rocephin. Patients were treated with 10 additional weeks of Rocephin. The study found significant short term improvements in cognitive dysfunction, but not memory in the treated group. A sustained improvement in fatigue was shown.
The investigators reported a 19% rate of complications. This does not comport with my clinical experience.
Dr Fallon recommended against the use of 10 weeks of Rocephin followed by 14 weeks of no therapy. He does report antibiotic associated improvement with regard to disabling symptoms such as pain and fatigue, particularly in patients who suffered the most at the outset of the trial. This was not a primary end point of the study, but the results were significant. Fallon also noted that the Krupp study showed significant improvement in fatigue.
"Conclusions regarding the benefit of repeated IV antibiotic therapy for this set of symptoms must await further investigation."
The IDSA still concludes that this study conclusively demonstrates that chronic Lyme disease does not exist. This is not true. Further study is needed. With regard to cognitive improvements several other conclusions might be suggested: the patients needed longer courses of antibiotic or perhaps gains could be sustained when IV therapy was followed up with oral therapy.
Of course, this study does not address the subject of co-infections. It does not address the need to treat L-forms and especially cyst forms which have been shown to be prominent in the brain.
Yesterday I had the opportunity to discus these issues with a Hopkins professor of infectious disease. He claimed that ALL the good science proves that chronic Lyme does not exist. He was steadfast in his opinion. When queried, he admitted he knows nothing about the Columbia/Fallon study. He asked if it was"good" science. He was oblivious to the fact that the Fallon study was third NIH-sponsored study cited by his colleagues to support the absolute belief that chronic Lyme does not exist. Apparently only the Klempner and Krupp studies are worthy of consideration. But what about that pesky Krupp study?
I have a simple question: how does Rocephin improve fatigue, demonstrated in clinical trials, the best science? If the patients do not have persistent infection with Borrelia burdorferi, what is the mechanism by which antibiotics help fatigue?
Sleep helps fatigue. Caffeine and stimulants help fatigue. Antibiotics?
Maybe when I needed to pull those all nighter to cram for chemistry finals in college I should have been popping penicillin instead of gulping down pots of coffee.
The investigators reported a 19% rate of complications. This does not comport with my clinical experience.
Dr Fallon recommended against the use of 10 weeks of Rocephin followed by 14 weeks of no therapy. He does report antibiotic associated improvement with regard to disabling symptoms such as pain and fatigue, particularly in patients who suffered the most at the outset of the trial. This was not a primary end point of the study, but the results were significant. Fallon also noted that the Krupp study showed significant improvement in fatigue.
"Conclusions regarding the benefit of repeated IV antibiotic therapy for this set of symptoms must await further investigation."
The IDSA still concludes that this study conclusively demonstrates that chronic Lyme disease does not exist. This is not true. Further study is needed. With regard to cognitive improvements several other conclusions might be suggested: the patients needed longer courses of antibiotic or perhaps gains could be sustained when IV therapy was followed up with oral therapy.
Of course, this study does not address the subject of co-infections. It does not address the need to treat L-forms and especially cyst forms which have been shown to be prominent in the brain.
Yesterday I had the opportunity to discus these issues with a Hopkins professor of infectious disease. He claimed that ALL the good science proves that chronic Lyme does not exist. He was steadfast in his opinion. When queried, he admitted he knows nothing about the Columbia/Fallon study. He asked if it was"good" science. He was oblivious to the fact that the Fallon study was third NIH-sponsored study cited by his colleagues to support the absolute belief that chronic Lyme does not exist. Apparently only the Klempner and Krupp studies are worthy of consideration. But what about that pesky Krupp study?
I have a simple question: how does Rocephin improve fatigue, demonstrated in clinical trials, the best science? If the patients do not have persistent infection with Borrelia burdorferi, what is the mechanism by which antibiotics help fatigue?
Sleep helps fatigue. Caffeine and stimulants help fatigue. Antibiotics?
Maybe when I needed to pull those all nighter to cram for chemistry finals in college I should have been popping penicillin instead of gulping down pots of coffee.
Tuesday, February 16, 2010
A proposal for a clinical study
Medical science--clinical studies, must be taken with a grain of salt. It is nearly impossible to do science when the thing being studied is as complex and multi-faceted as a human. Such studies attempt to prove that treatment A is better than a placebo (a pretty low standard) or that treatment A is superior to treatment B. The group under study is supposed to be homogeneous--a cohort with the same disease process. I would suggest it is nearly impossible to find a cohort of patients with exactly the same disease. Ultimately, many confounding variables make this sort of science difficult to do and to validate.
All the randomized-placebo-double blind-peer reviewed studies for chronic or post Lyme disease look at lot alike. All patients had prior, treated Lyme disease. All had had received "standard" therapy. And, all had persistent symptoms in the face of prior therapy. "Long term therapy" was defined as limited courses of Rocephin with or without courses of doxycyline. Generally, patient selection required CDC-IgG positivity, 5/10 bands. Of interest, Klempner also studied "sero-negative" patients. This is anomalous since the IDSA has generally claimed that seronegative patients do not suffer with Lyme disease.
Insanity has been defined as: doing the same thing over and over again-- expecting a different result.
I would suggest that another kind of study be designed and carried out. Patients with the same general set of symptoms, for example: migratory joint pains, fatigue and cognitive impairment plus positive Lyme Western Blocks by IgM or IgG standards should be studied. Patients from this cohort should be randomized into two arms: a head-to-head study. Group A would receive IDSA recommended therapy and group B would receive LLMD style therapy. Objective measurements of progress would be agreed upon. These might include: symptom lists, psychometric testing, physical exams and perhaps lab parameters such as a highly sensitive C-reactive protein. Patients would be periodically assessed over a prolonged period of time. For example, patients could be assessed every 3 months for a period of one to two years.
LLMDS in the study could agree upon some general standards, for example, Babesia could be treated with Mepron and Zithromax for 8 weeks. If there were no clinical response, a second course might be Larium plus Artemesin. In general, the physicians would be given flexibility to treat patients differently, based on clinical experience.
This is the sort of study which might provide convincing evidence that treatment for chronic Lyme disease is effective. The disease is different in every patient. It is nuanced. It is complex. Standard study designs which look at only one variable, will never prove the benefits of long term treatment for Lyme disease.
I hear a lot of talk about the need for Lyme studies.
I think, first potential investigators need to develop a study design. The teams needs then to find a partner with credibility and prestige, such as NIH. The cost could be low, particularly if this sort of head to head study could be "piggy-backed" onto another planned or ongoing study. Results, hopefully favorable ones, could be published in a major, peer reviewed journal.
All the randomized-placebo-double blind-peer reviewed studies for chronic or post Lyme disease look at lot alike. All patients had prior, treated Lyme disease. All had had received "standard" therapy. And, all had persistent symptoms in the face of prior therapy. "Long term therapy" was defined as limited courses of Rocephin with or without courses of doxycyline. Generally, patient selection required CDC-IgG positivity, 5/10 bands. Of interest, Klempner also studied "sero-negative" patients. This is anomalous since the IDSA has generally claimed that seronegative patients do not suffer with Lyme disease.
Insanity has been defined as: doing the same thing over and over again-- expecting a different result.
I would suggest that another kind of study be designed and carried out. Patients with the same general set of symptoms, for example: migratory joint pains, fatigue and cognitive impairment plus positive Lyme Western Blocks by IgM or IgG standards should be studied. Patients from this cohort should be randomized into two arms: a head-to-head study. Group A would receive IDSA recommended therapy and group B would receive LLMD style therapy. Objective measurements of progress would be agreed upon. These might include: symptom lists, psychometric testing, physical exams and perhaps lab parameters such as a highly sensitive C-reactive protein. Patients would be periodically assessed over a prolonged period of time. For example, patients could be assessed every 3 months for a period of one to two years.
LLMDS in the study could agree upon some general standards, for example, Babesia could be treated with Mepron and Zithromax for 8 weeks. If there were no clinical response, a second course might be Larium plus Artemesin. In general, the physicians would be given flexibility to treat patients differently, based on clinical experience.
This is the sort of study which might provide convincing evidence that treatment for chronic Lyme disease is effective. The disease is different in every patient. It is nuanced. It is complex. Standard study designs which look at only one variable, will never prove the benefits of long term treatment for Lyme disease.
I hear a lot of talk about the need for Lyme studies.
I think, first potential investigators need to develop a study design. The teams needs then to find a partner with credibility and prestige, such as NIH. The cost could be low, particularly if this sort of head to head study could be "piggy-backed" onto another planned or ongoing study. Results, hopefully favorable ones, could be published in a major, peer reviewed journal.
Sunday, February 14, 2010
Lyme 2010: A brief update
Diagnosis remains clinical. Laboratory data should not be over-emphasized. Lyme Western Blots from Igenex, MDL and Clongen are helpful. I prefer Clongen. They provide quality pictures of blot strips which quantitatively compare patient reactivity to controls. C4a is a good marker of infection, better than CD57. Other clues include: reversed vitamin D levels, elevated CRP, low/normal B12 and folic acid levels, and low white blood cell counts. Blood wet mounts reliably show motile round bacteria---presumptive Bartonella species. A large percent of patient have the BBB triad: Borrelia, Bartonella, Babesia.
Primary oral therapy with Doxycycline and Tindamax is excellent. Killing cysts early seems to improve outcomes. Tindamax is clearly better than Flagyl and Albendazole. Biaxin is a second choice in patient's who cannot tolerate Doxy. When Biaxin is used patients seem to do better when a beta lactam is added:Amoxicillin/Ceftin/Omnicel. The benefits of Plaquenil are not clear. Rather than having an anti-cyst effect, it promotes cyst formation. Many antibiotics used for Lyme also have mild effects against Bartonella as well. In patients with neurocognitive deficits, Lyme and Bart are generally both a factor. Bartonella/brain Herxes can be extremely severe. Anti-Bart therapy is such patients needs to be gradually ramped up. Drugs with low anti-Bart activity include: Doxy and Biaxin even though these drugs are thought to be only Lyme drugs. Minocycline is a little more active against Bart. Zithromax orally is a poor Lyme drug and has mild anti-Bart effects. Rifampin is somewhat more active against Bart. Bactrim is quite effective and quinolones are very active: Cipro followed by Levaquin and then Factive. Cipro and especially Factive are also good Lyme drugs. Factive is a fabulous Lyme drug.
Many strains of Babesia appear to be very resistant. I suspect like malaria, these bugs have a propensity for developing resistance. When Mepron, Malarone and Artemesin are relatively ineffective, Larium may be surprisingly effective. I generally like to treat Lyme first. The exception is patients with dramatic Babesia symptoms: drenching sweats. As a rule, patients respond quickly once the sweating stops.
I agree with the Martz approach to IV antibiotics: layering. I start with Rocephin, add Zithromax and then Flagyl. Works very well. Other IV antibiotics may be helpful but responses are more variable. Tigacyl has been disappointing in my practice.
Patient should be treated with IV antibiotics for at least 12 weeks, longer if possible. Gains from IV therapy require ongoing therapy with potent oral antibiotics or the gains will vanish. Factive and Tindamax are superb. Factive is costly. Doxy is a good alternative. A subset of patients only do well when beta lactams are continued. Biaxin and Amoxicillin remains an excellent choice of therapy.
Supplements? vitamin D3, 2000-4000IU seems helpful. Probiotics are critical. A good mix of acidophilus type, 30 billion twice daily and Sacchromyces works well. Supplementation with yogurt is better yet. A balanced diet is helpful: fruits, berries, nuts, fish and a wide variety of vegetables of different colors--broccoli to red peppers. Sugar is always bad. I am not yet sold on other supplements. Transfer factor which is basically colostrum may be helpful. If B12 and folic acid are low-- supplement. These patients are probably nutritionally depleted and should also be given B complex and multivitamins.
The body cannot be sterilized of Lyme bacteria. Intracellular bacteria will always persist.
Unfortunately, many patients require maintenance therapy. I have seen many patients who have been "cured" by other physicians, but complain of incomplete recovery or relapse.
Not all Lyme infected patients required treatment. I only test patients who are symptomatic.
No--it is not sexually transmitted or transmitted by mosquitoes or flies. It may be transmitted via placenta to newborns. This can be very problematic. I treat pregnant Lyme patients with low dose Amoxicillin.
There is no one right way to treat Lyme disease. At times you have to be creative--and, never give up. Individual responses to therapy are impossible to predict.
Patients with autoimmune neuropathy may get much worse with therapy. This is one of the most challenging group of patients. IViG should be considered if possible. Sometimes steroids are needed, despite all the caveats. Antibiotic therapy must be titrated very gingerly.
Welchol works very well in some patients--especially with neurocognitive issues. Long term therapy may be required. It also lowers CRP and inflammation.
Straight IV fluids, normal saline solution may be given to patients on IV antibiotics to flush out toxins? or circulating immune complexes. It may reduce Herxes and make patients feel better.
Politics: no change except Connecticut. Patients must understand that doctors who treat Lyme disease face ridicule from their colleagues and possible censure from medical boards.
Primary oral therapy with Doxycycline and Tindamax is excellent. Killing cysts early seems to improve outcomes. Tindamax is clearly better than Flagyl and Albendazole. Biaxin is a second choice in patient's who cannot tolerate Doxy. When Biaxin is used patients seem to do better when a beta lactam is added:Amoxicillin/Ceftin/Omnicel. The benefits of Plaquenil are not clear. Rather than having an anti-cyst effect, it promotes cyst formation. Many antibiotics used for Lyme also have mild effects against Bartonella as well. In patients with neurocognitive deficits, Lyme and Bart are generally both a factor. Bartonella/brain Herxes can be extremely severe. Anti-Bart therapy is such patients needs to be gradually ramped up. Drugs with low anti-Bart activity include: Doxy and Biaxin even though these drugs are thought to be only Lyme drugs. Minocycline is a little more active against Bart. Zithromax orally is a poor Lyme drug and has mild anti-Bart effects. Rifampin is somewhat more active against Bart. Bactrim is quite effective and quinolones are very active: Cipro followed by Levaquin and then Factive. Cipro and especially Factive are also good Lyme drugs. Factive is a fabulous Lyme drug.
Many strains of Babesia appear to be very resistant. I suspect like malaria, these bugs have a propensity for developing resistance. When Mepron, Malarone and Artemesin are relatively ineffective, Larium may be surprisingly effective. I generally like to treat Lyme first. The exception is patients with dramatic Babesia symptoms: drenching sweats. As a rule, patients respond quickly once the sweating stops.
I agree with the Martz approach to IV antibiotics: layering. I start with Rocephin, add Zithromax and then Flagyl. Works very well. Other IV antibiotics may be helpful but responses are more variable. Tigacyl has been disappointing in my practice.
Patient should be treated with IV antibiotics for at least 12 weeks, longer if possible. Gains from IV therapy require ongoing therapy with potent oral antibiotics or the gains will vanish. Factive and Tindamax are superb. Factive is costly. Doxy is a good alternative. A subset of patients only do well when beta lactams are continued. Biaxin and Amoxicillin remains an excellent choice of therapy.
Supplements? vitamin D3, 2000-4000IU seems helpful. Probiotics are critical. A good mix of acidophilus type, 30 billion twice daily and Sacchromyces works well. Supplementation with yogurt is better yet. A balanced diet is helpful: fruits, berries, nuts, fish and a wide variety of vegetables of different colors--broccoli to red peppers. Sugar is always bad. I am not yet sold on other supplements. Transfer factor which is basically colostrum may be helpful. If B12 and folic acid are low-- supplement. These patients are probably nutritionally depleted and should also be given B complex and multivitamins.
The body cannot be sterilized of Lyme bacteria. Intracellular bacteria will always persist.
Unfortunately, many patients require maintenance therapy. I have seen many patients who have been "cured" by other physicians, but complain of incomplete recovery or relapse.
Not all Lyme infected patients required treatment. I only test patients who are symptomatic.
No--it is not sexually transmitted or transmitted by mosquitoes or flies. It may be transmitted via placenta to newborns. This can be very problematic. I treat pregnant Lyme patients with low dose Amoxicillin.
There is no one right way to treat Lyme disease. At times you have to be creative--and, never give up. Individual responses to therapy are impossible to predict.
Patients with autoimmune neuropathy may get much worse with therapy. This is one of the most challenging group of patients. IViG should be considered if possible. Sometimes steroids are needed, despite all the caveats. Antibiotic therapy must be titrated very gingerly.
Welchol works very well in some patients--especially with neurocognitive issues. Long term therapy may be required. It also lowers CRP and inflammation.
Straight IV fluids, normal saline solution may be given to patients on IV antibiotics to flush out toxins? or circulating immune complexes. It may reduce Herxes and make patients feel better.
Politics: no change except Connecticut. Patients must understand that doctors who treat Lyme disease face ridicule from their colleagues and possible censure from medical boards.
The IgM question: Is it chronic Lyme disease?
Many patients have been told by their physicians they do not have chronic Lyme disease because Western blot antibodies are in the IgM class, not the IgG class. The doctors themselves may be confused -- or adamant. The adamant ones very likely don't believe chronic Lyme exists. If you, on the other hand, believe chronic Lyme is real, you may want to discount opinions proffered by those who do not share those beliefs.
Lyme acts differently immunologically than many other germs. Patients with only IgM antibodies may have Lyme and or/ chronic Lyme. In the typical scenario of antibody response to infection the immune system makes IgM antibodies in early infection and then makes IgG antibodies in late infection. As the amount of IgG increases IgM decreases and then goes away. This is not always the case. Lyme is a clear exception to this rule.
Peer reviewed medical studies have contributed to the confusion. Selection bias inherent to published studies is one problem. The only patients selected for NIH sponsored clinical trials have had IgG, not IgM antibodies. One investigator, Brian Fallon, who treats a lot of Lyme patients, found it challenging to find patients with the 5/10 IgG band requirement; less than 5% of his patients fulfilled the study entry requirement. All studies require certain criteria for inclusion in the study. These criteria were used for standardization and in no way suggest or prove that a particular IgG response is needed for the diagnosis.
A large chunk of chronic Lyme patients have only IgM responses. Some have mixed IgM and IgG responses. In some cases IgG responses are favored and in others IgM.
Those from the no-such-thing as chronic Lyme camp stake out the position that persistent IgM responses without later production IgG antibodies represent false positive responses. Patients with only IgM responses are told that they in fact never had Lyme, or they may be told they have Lyme but it must have a new case. Science tells us something else. Some patients make only IgM antibodies. And it is known that IgM and/or IgG antibodies may persist for years after acute infection.(Steere). The CDC has not been helpful. The CDC two tier test, ELISA followed by Western Blot standard was developed for surveillance, not clinical diagnosis. The claim that the test lacks accuracy in early Lyme but is virtually 100% accurate in late stage Lyme is crazy and has no basis in science -- or published evidence. This unfounded statement unfortunately lends credence to the Lyme deniers who push the falsehood that IgM bands equal false positive.
IgeneX has published its finding that 2 specific IgM or IgG are diagnostic of the disease, stage of the illness not withstanding. Aucott has found that 20% of patients with treated acute Lyme are unable to produce IgG antibodies, likely a genetic variable. Steere published data showing persistence of IgM antibodies in late Lyme in the 1990s. This knowledge is not new. Existing literature supports the idea that certain Western Blot antibodies are highly specific for Lyme. If specific antibodies are present it is unlikely they are the product of a false positive test, irrespective of antibody class. When only IgM antibodies appear there is a alternate hypothesis. The persistence of IgM antibodies may suggest the immune system is "chronically" seeing Borrelia as an acute--new infection. This interpretation is applied by doctors in other situations. For example EBV. IgM EBV antibodies are frequently interpreted as evidence of reactivation of the infection.
Antibodies are the result of "humoral" immunity or acquired immunity. The immune system "reads" the pathogenic germ and turns the information over to the body's antibody factory. IgM and IgG antibodies are produced by the same cells: B lymphocytes. These lymphocytes may become plasma cells. The change from IgM to IgG is due to a genetically directed molecular switching mechanism. This class switching--IgM to IgG-- may not occur or occur poorly. We don't know why but these facts have been established by evidence based science.
In my experience, Lyme patients, on average, produce slightly more IgM than IgG antibodies. This may be hard to see since most IgM assays present limited data (few bands). Certain antibodies, for example: 18, 23, 31, 34, 39 41 and 93 are HIGHLY specific for exposure to Lyme bacteria and this is well described in many places.
Doctors known as LLMDs have know for decades that the IgM vs IgG class distinction does not apply to Lyme.
Addendum: Antibodies are Y shaped molecules/proteins made up of heavy chain and light chains. Some portions are variable and some portions are invariable. Binding to antigen occurs when a variable portion at the end of one leg of the Y has a structure reconfigured (controlled by gene modification). This is the part which is analogous to taking a key to hardware store to have it copied. A generic antibody is like the blank key. The key (specific antibody) is formed through a complex process. The same cells, B lymphocytes/plasma cells that make IgM antibodies also make IgG antibodies. When the class of antibody is changed it is referred to as isotopic switching. Here is the critical piece of information: the key - the variable portion of the antibody is unchanged when IgM is changed to IgG. Rather an invariant heavy chain is swapped out. Meaning: the specificity of IgM antibodies is identical to the specificity of IgG antibodies. Remember, the immune system is controlled by mediators, cytokines. The switch from one class to the next is controlled by cytokines. IgM antibodies induce cytokines which differ from those of IgG antibodies. This is why IgM and IgG antibodies have different biological properties. The cytokines communicate with different parts of the most complex system (immune system) in the body outside of the brain and the wide array of moving parts are given different tasks. IgM signals are different from IgG signals. It should all work together for the most effective killing of unwanted pathogens. The operative word is should.
Germs evolve. Germs are smart. If a pathogen can modify the signals and confuse the cells, if gives the highly motivated germ a leg up, a survival advantage, and we know that Lyme infection can modify cytokine responses. Maybe that is why isotopic switching, IgM to IgG fails for many patients.
Take home point: the part of the antibody that specifically binds to the antigen is 100% unchanged when IgM antibodies are replaced by IgG counterparts.
If you suspect you suffer with manifestations of Lyme disease only an experienced knowledgeable doctor can make the diagnosis.
Please see other BLOG posts for more information regarding this issue.
Monday, February 8, 2010
Post-Lyme syndrome
A 68 year old female consulted with me one year ago. She had been ill for over 4 years. At the outset she had flu like symptoms and a rash on her neck. A 2 tier Lyme WB was positive by CDC criteria. She was treated with antibiotics 4 four months by her primary care physician. The physician pronounced her cured and refused to extend the course of therapy. Her symptoms returned with a vengeance. She developed more pains, joint swelling, numbness and tingling, fatigue, and cognitive dysfunction. She had progressive memory loss. She could not focus, concentrate, process or retrieve words and thoughts. She had episodes of confusion and disorientation. She saw numerous doctors, all of whom were dismissive, if not rude. She was told her symptoms were normal for a woman her age. Then after doing her own research on the Internet she ordered an IgeneX test.
The Lyme IgM Western showed bands: 18 28, 30, 39, 41 and 58. A C6 peptide antibody was 0.86. Her CD57 was 18.
When I first saw her the physical exam showed difficulty with word search and moderate short term memory deficits. Positive findings included: bilateral weakness in the upper extremities, absent deep tendon reflexes in the knees and ankles, decreased pin-prick sensations in 4 extremities and decreased vibratory sense in the feet and lower extremities.
The brain MRI showed scattered white matter lesions-non-specific. The brain SPECT showed decreased activity in the the left anterior temporal region.
After one year of treatment she is about 90% better. Her cognitive functions are nearly normal. Her treatment included: Omnicef, Biaxin, Plaquenil, Tindamax, Zithromax, Mepron, Malarone, Artemesin, Bactrim, Amoxicillin, and Doxycyline.
Comments:
This patient's story is illustrative of care given to similar patients by many LLMDs.
There is good evidence: patient's history, physical exam, laboratory test result and brain imaging all support the diagnosis of CNS Lyme/Lyme encephalopathy/neuroborreliosis etc --even to well informed IDSA physicians. The science suggests that all such patients should be considered for intravenous antibiotics, no matter which side of the fence you are on. In this case, the patient improved with only oral (extended-plus-co-infection) anti-microbials.
The IDSA view is that chronic Lyme disease does not exist. The IDSA has no argument with the existence of a post-Lyme syndrome. The authors of NIH sponsored studies have expressed empathy for such patients. Their suffering is real. The investigators and CDC claim current evidence does not support the use of long term antibiotics for such patients. It recognizes the genuine suffering of such patients and that this suffering is causally related to previous, (treated) Lyme disease. Fair enough. (I disagree).
But something strange has happened. Patients who seek the attention of ID doctors and rhematologist, even those with "CDC positive" results are treated as pariahs. Despite hard evidence, the patients are herded out of these physicians offices as quickly as possible. They are still told: you are depressed, you just need to exercise and loose weight, you have fibromyalgia, you are just imagining your symptoms, you spend too much time on the Internet, there is nothing wrong with you, I don't care what the tests say--you don't have Lyme and so on.
I went to medical school--admittedly some time ago. I thought doctors are supposed to be empathetic and kind to patients. Instead, many doctors are belittling, dismissive and bellicose.
They don't have to agree with the ILADS/LLMD approach, but for heaven's sake, they have a diagnosis to rest their hats on: post-Lyme syndrome-"a poorly characterized autoimmune syndrome."
They should at least read their own literature. These physicians should be supportive, offer a diagnosis, explain the diagnosis, its pathogenesis prognosis and therapy.(If they believe the party line?). These understanding physicians should prescribe therapies to alleviate or ameliorate the suffering of their patients. Instead, they appear to be taking out their disdain for LLMDS on their patients. Ironically, this may be a good thing because the patients keep looking until they find us. (I don't want to give "the other side" any good ideas).
The Lyme IgM Western showed bands: 18 28, 30, 39, 41 and 58. A C6 peptide antibody was 0.86. Her CD57 was 18.
When I first saw her the physical exam showed difficulty with word search and moderate short term memory deficits. Positive findings included: bilateral weakness in the upper extremities, absent deep tendon reflexes in the knees and ankles, decreased pin-prick sensations in 4 extremities and decreased vibratory sense in the feet and lower extremities.
The brain MRI showed scattered white matter lesions-non-specific. The brain SPECT showed decreased activity in the the left anterior temporal region.
After one year of treatment she is about 90% better. Her cognitive functions are nearly normal. Her treatment included: Omnicef, Biaxin, Plaquenil, Tindamax, Zithromax, Mepron, Malarone, Artemesin, Bactrim, Amoxicillin, and Doxycyline.
Comments:
This patient's story is illustrative of care given to similar patients by many LLMDs.
There is good evidence: patient's history, physical exam, laboratory test result and brain imaging all support the diagnosis of CNS Lyme/Lyme encephalopathy/neuroborreliosis etc --even to well informed IDSA physicians. The science suggests that all such patients should be considered for intravenous antibiotics, no matter which side of the fence you are on. In this case, the patient improved with only oral (extended-plus-co-infection) anti-microbials.
The IDSA view is that chronic Lyme disease does not exist. The IDSA has no argument with the existence of a post-Lyme syndrome. The authors of NIH sponsored studies have expressed empathy for such patients. Their suffering is real. The investigators and CDC claim current evidence does not support the use of long term antibiotics for such patients. It recognizes the genuine suffering of such patients and that this suffering is causally related to previous, (treated) Lyme disease. Fair enough. (I disagree).
But something strange has happened. Patients who seek the attention of ID doctors and rhematologist, even those with "CDC positive" results are treated as pariahs. Despite hard evidence, the patients are herded out of these physicians offices as quickly as possible. They are still told: you are depressed, you just need to exercise and loose weight, you have fibromyalgia, you are just imagining your symptoms, you spend too much time on the Internet, there is nothing wrong with you, I don't care what the tests say--you don't have Lyme and so on.
I went to medical school--admittedly some time ago. I thought doctors are supposed to be empathetic and kind to patients. Instead, many doctors are belittling, dismissive and bellicose.
They don't have to agree with the ILADS/LLMD approach, but for heaven's sake, they have a diagnosis to rest their hats on: post-Lyme syndrome-"a poorly characterized autoimmune syndrome."
They should at least read their own literature. These physicians should be supportive, offer a diagnosis, explain the diagnosis, its pathogenesis prognosis and therapy.(If they believe the party line?). These understanding physicians should prescribe therapies to alleviate or ameliorate the suffering of their patients. Instead, they appear to be taking out their disdain for LLMDS on their patients. Ironically, this may be a good thing because the patients keep looking until they find us. (I don't want to give "the other side" any good ideas).