“Lyme disease is the most common vector-borne illness in the United States and is also endemic in Europe and Asia(ref).” Recently, a close member of my family contracted an acute case of Lyme Disease (LD), leading me to review the recent literature relevant to the disease. I discovered that there is a conventional wisdom related to the disease that is prevalent in the medical profession but a significant body or research and informed opinion indicates this conventional wisdom is wrong. I share some of my observations here.
The medical community appears to be divided when it comes to Lyme Disease
For a number of years now there appears to be two different frameworks for viewing LD.The traditional narrative about LD pursued by most medical practitioners holds that it is a fairly simple regional disease confined to limited parts of the country, that is transmitted by a specific carrier tic that is carried by deer, that it is caused by a particular strain of bacterium Borrelia burgdorferi, that LD can usually be identified by a certain bull’s-eye pattern of redness on the skin, that diagnosis can reliably be confirmed using simple clinical tests, that LD is easy to cure with a single bout of antibiotics once diagnosed, and that rarely is a serious life-threatening medical condition. This traditional narrative has for many years been advocated by the Infectious Diseases Society of America (IDSA). It is the basis for the 2006 and current IDSA Lyme Disease Guidelines. It therefore governs how a great many medical practitioners continue to view and treat Lyme Disease.
The alternative narrative about LD that I articulate further here sees the above narrative as too simplistic and plain wrong on several key dimensions. This alternative narrative is strongly supported by the International Lyme & Associated Diseases Society (ILADS) and an international group of medical practitioners who have become knowledgeable about LD and have focused practices in this area. According to this view LD can be a number of related disease conditions resulting from multiple species of the Borrelia burgdorferi bacterium carried by multiple kinds of tic hosts that may feed upon multiple kinds of animal hosts. LD is far more commonplace and geographically dispersed than generally acknowledged. The disease is devilishly difficult to diagnose and laboratory tests are far from reliable. LD infection may be chronic. Very long bouts of antibiotics may be needed to cure LD. The bacterium has developed means to disguise itself and hide in the body and survive rounds of antibiotic treatment. And LD is incurable and lifelong-recurrent in some patients.
So, there appears to be great persistent controversy in the medical community about LD. What is so with regard to LD is unfortunately now a political issue between ensconced camps. Conflict between the conventional and alternative narratives goes back some time. Important elements of the new narrative were laid out in the 2004 publication LYME DISEASE (Borreliosis) A Plague of Ignorance Regarding the Ignorance of a Plague.
The IDSA review panel on LymeDisease conducted a review panel hearing in 2009 but basically retained the 2006 guidelines based on the traditional narrative. A number of presentations made at that hearing resenting evidence for the alternative narrative can be found on this ILADS website. These presentations clearly challenge the traditional IDSA narrative.The 2011 review article Lyme disease: the next decade effectively articulates this alternative narrative. “The controversy over Lyme disease came to a head in November 2006 when IDSA released new guidelines severely limiting treatment options for patients with persistent Lyme symptoms.3 The guidelines were so restrictive that the Attorney General of Connecticut initiated an unprecedented investigation into potential antitrust violations by IDSA, the dominant infectious disease society in the United States, in its formulation of the guidelines.6–8 The investigation found significant conflicts of interest and suppression of data in the guidelines development process.6,7 As a result, IDSA created a new scientific panel to review its Lyme guidelines in a process under the complete control of IDSA.8,9 The review panel held a hearing in July 2009 that was broadcast live over the internet and featured more than 300 peer-reviewed articles and 1600 pages of analysis supporting the concept of persistent infection despite short-course antibiotic therapy of 2 to 4 weeks in patients with persistent Lyme disease symptoms.8,9 Despite this extensive evidence, the IDSA review panel voted unanimously to uphold the flawed Lyme guidelines. This result was not surprising given that seven of the eight members of the review panel were members of IDSA, which selected the panel.8,9”I draw here from the above-mentioned and a number of other recent publications.
LD is far more common than generally acknowledged
“The true prevalence of Lyme disease is much higher than is being reported by health officials. It is difficult to know how many cases are unreported but estimations suggest that the prevalence is actually 10-15 times higher than what is actually being reported. I personally believe it is much higher than that. Why are health officials under-reporting cases of Lyme disease? Again, the answer is because physicians don’t recognize and report most cases. These misdiagnosed cases go unreported even though Lyme disease is a mandatory reportable disease (in the state of Iowa). So, a futile cycle exists causing numerous cases of Lyme disease to be misdiagnosed and unreported. That is, since most cases of Lyme disease go undiagnosed, health officials under-report Lyme disease; thus, physicians that read their official reports believe that the prevalence of Lyme is rare and place it low on their list of possibilities when faced with clinical cases that could be caused by Borrelia(ref).”
Lyme Disease is a family of different diseases caused by related bacterial species
“LD is caused by many borrelia species. — there are many pathogenic borrelia strains; many of which cause borreliosis (Lyme-like disease). The causative agent, Borrelia burgdorferi, is a type of spirochete. When Bb was first discovered in 1982 it was thought that there was just one strain. Since then, about 100 U.S. and 300 worldwide strains of the bacterium have been discovered. — Borrelia burgdorferi sensu lato is name given to the overall category. In North America there is just one genospecies variant – Bb sensu stricto. In Europe there are three categories Bb sensu stricto, B. garinii, and B. afzelii. Asia has B. garinii and B. afzelii. Japan has B. japonica and B. miyamoto. These groups are evolving as new research discoveries occur(ref).”
LD is frequently misdiagnosed
“Physicians frequently overlook cases of Lyme disease simply because they don’t know the complex pathogenesis of the disease. They don’t understand that Lyme disease causes well over 100 different symptoms; the common arthralgia (the medical term for joint pain) is a LD symptom that most physicians are familiar with; however, it is only one of many symptoms caused by Lyme disease. The clinical presentation of Lyme disease can be very subtle and complex. Most doctors don’t know that laboratory tests are often useless and misleading. Results are frequently negative or inconclusive in individuals with borreliosis. — . The criteria being used to report Lyme disease by physicians is often set by state health officials and is often based upon the rigid criteria established by the Center for Disease Control and Prevention (CDC). This CDC criteria was established for an epidemiological survey, which was designed to study the distribution of Lyme disease. The two-step method of the CDC uses a screening immunoassay for all patients followed by a more sensitive and specific Western blot only if the screening test was positive. Unfortunately, this approach was originally intended for surveillance of Lyme disease in potentially asymptomatic patients, not for diagnostic purposes in patients with symptoms that are potentially related to Lyme disease. This criteria was not intended to be used as a standard for the clinical diagnosis of Lyme disease; the CDC has clearly stated this. Unfortunately, ignorant health officials and physicians continue to use these criteria for the clinical diagnosis of Lyme disease. 2. Unfamiliar pathogenesis. Lyme disease has a complex pathogenesis — Only a few medical professionals understand the pathogenesis of Lyme disease. Actually, very few MDs that specialize in Lyme disease understand this pathogenesis very well. This detailed information is not taught in medical schools or even in the general medical conferences or in post-resident seminars. Thus, most clinicians practicing medicine don’t understand how borrelia causes disease. Without this knowledge, it is difficult to properly recognize, diagnose, and treat Lyme disease(ref).”
Disease manifestations are different for different species of the Lyme disease and disease colonization in infected cells is affected by complex binding proteins and processes
The 2011 publication Allelic variation of the Lyme disease spirochete adhesin DbpA influences spirochetal binding to decorin, dermatan sulfate, and mammalian cells reports “After transmission by an infected tick, the Lyme disease spirochete, Borrelia burgdorferi sensu lato, colonizes the mammalian skin and may disseminate systemically. The three major species of Lyme disease spirochete, B. burgdorferi sensu stricto, B. garinii and B. afzelii, are associated with different chronic disease manifestations. Colonization is likely promoted by the ability to bind to target tissues, and Lyme disease spirochetes utilize multiple adhesive molecules to interact with diverse mammalian components. The allelic variable surface lipoprotein decorin binding protein A (DbpA) promotes bacterial binding to the proteoglycan decorin and to the glycosaminoglycan (GAG) dermatan sulfate.”
More is being learned about the binding processes of different Lyme species, such as described in the 2011 publication Decorin Binding by DbpA and B of Borrelia garinii, Borrelia afzelii, and Borrelia burgdorferi Sensu Stricto.
Most species of Borrelia causing LD are not tracked by the CDC
“A new pathogen causing Lyme or “Lyme-like” disease has been reported. While not culturable, it has been named B. lonestari sp. — B. andersonii, B. lonestari and B. miyamotoi have been identified by PCR and DNA sequence analysis as likely human pathogens in the U.S. Unfortunately, the criteria for clinical Lyme are set for only Borrelia burgdorferi; they were not designed for any other borrelia species. The reason that Borrelia burgdorferi is tracked by health officials but not other species is because it’s the primary borrelia species that laboratories are able to identify and study. I admit that Borrelia species are very difficult to grow (fastidious) and work with in the laboratory. In most cases, laboratories are not even able to isolate and identify Borrelia species. Some other known strains of borrelia include: B. valaisiana, B. lusitaniae and B. bissettii(ref).”
Besides deer, several other vertebrates can serve as hosts for LD-infected tics
Tics carrying Borrelia burgdorferi can feed on birds, dogs, cats, mice, rats, horses and cows among other animals . Even voles and Siberian chipmunks may be involved as important carriers(ref)(ref). “There are reports of the Lyme organism being found in fleas, horseflies and mosquitoes, and possible associations between fleas and Lyme cases (ref).” “There is a tremendous misunderstanding regarding the vector (carrier) that transmits Lyme disease. First of all, the familiar tick vector called the deer tick (Ixodes dammini) and black-legged ticks (commonly called deer ticks) (Ixodes scapularis) are more prevalent and spreading wider than reported. Secondly, these ticks are not the only vector able to transmit Borrelia species. Several other tick species such as the Lone Star ticks (Ammblyoma americanum), western black-legged ticks (Ixodes pacificus), and wood ticks or dog ticks (Dermacentor variabilis) can transmit it too. Unfortunately, this critical information is not being reported by health officials to the public and medical community. The widespread distribution of these tick vectors greatly increases the prevalence of Lyme disease well beyond that of official reports(ref).”
“The 2008 publication Borrelia burgdorferi sensu lato, the agent of lyme borreliosis: life in the wilds reported: “In Europe, Borrelia burgdorferi sensu lato (sl) the agent of Lyme borreliosis circulates in endemic areas between Ixodes ricinus ticks and a large number of vertebrate hosts upon which ticks feed. Currently, at least 12 different Borrelia species belonging to the complex B. burgdorferi sl have been identified among which seven have been detected in I. ricinus: B. burgdorferi sensu stricto (ss), B. garinii, B. afzelii, B. valaisiana, B. spielmanii and B. bissettii. A few dozens of vertebrate hosts have been identified as reservoirs for these Borrelia species. Specific associations were rather early observed between hosts, ticks and borrelia species, like for example between rodents and B. afzelii and B. burgdorferi ss, and between birds and B. garinii and B. valaisiana. The complement present in the blood of the hosts is the active component in the Borrelia host specificity. Recent studies confirmed trends toward specific association between Borrelia species and particular host, but also suggested that loose associations may be more frequent in transmission cycles in nature than previously thought.”
The genome of the LD spirochete is rather unique and lends itself to substantial genomic variation
The 1011 publication BB0844, an RpoS-regulated protein, is dispensable for Borrelia burgdorferi infectivity and maintenance in the mouse-tick infectious cycle relates “The genome of Borrelia burgdorferi, the causative agent of Lyme disease, is comprised of a large linear chromosome and numerous smaller linear and circular plasmids. B. burgdorferi exhibits substantial genomic variation, and previous studies revealed genotype-specific variation at the right chromosomal telomere. A correlation has also been established between genotype and invasiveness. The correlation between chromosome length and genotype and between genotype and invasiveness suggested that a gene(s) at the right chromosome telomere may be required for virulence.”
The tic-host-disease- interactions in LD can be quite complex
These interactions have been studied for some time and are still being decoded. For example the 2011 publication The Borrelia burgdorferi linear plasmid lp38 is dispensable for completion of the mouse-tick infectious cycle reports: “Borrelia burgdorferi, the causative agent of Lyme disease, exists in a complex enzootic cycle, transiting between its vector, Ixodes ticks, and a diverse range of vertebrate hosts. The B. burgdorferi linear plasmid 38 (lp38) contains several genes that are differentially regulated in response to conditions mimicking the tick or mouse environments, suggesting that these plasmid-borne genes may encode proteins important for the B. burgdorferi infectious cycle. Some of these genes encode potential virulence factors, including hypothetical lipoproteins as well as a putative membrane-transport system.”
Lyme Disease is a complicated inflammatory disease that is a great imitator of many other diseases
“Lyme disease (LD) is a seriously complex multi-system inflammatory disease that is triggered by the bacterial lipoproteins (BLPs) produced by the spiral-shaped bacteria called Borrelia. Borrelia are difficult to isolate, grow, and study in the laboratory. So, our technical knowledge of this pathogen is poor compared to our understanding of most bacteria that cause disease. ransmission of Borrelia occurs primarily through the bite of ticks. The disease affects every tissue and every major organ system in the body. Clinically, it can appear as a chronic arthalgia (joint pain), fibromyalgia (fibrous connective tissue and muscle pain), chronic fatigue, immune dysfunction and as neurological disease. LD may even be fatal in severe cases. – BLPs are fat-soluble toxins that are part protein and part lipid. They are often a structural part of the borrelia cell membrane and can be found within the outer surface proteins of borrelia. They are very potent immunomodulators even in small amount Thus, a few borrelia can produce enough BLPs to initiate significant disease. — These BLPs trigger many harmful responses in any tissues and organ system of the human body. These responses, produce complex symptoms of fibromyalgia, arthritis, neurological signs, psychiatric disorders, immunologic dysfunctions, and endocrine deficiencies(ref).” It is standard laboratory practice to use lipoproteins to create serious disorders in laboratory animals.“
“At the molecular level, the BLPs cause a dysfunction in the immune system by triggering a complex imbalance of chemical immune mediators (cytokines). These cytokines regulate the immune system and when they are over stimulated, they produce harmful reactions from the immune system, such as pain, inflammation, and even apoptosis (cell death). Some of the cytokines involved include: tumor necrosis factor-alpha (TNF-α), interleukins-6 (IL-6), fatty acid products (eicosanoids such as inflammatory prostaglandins, thromboxanes, and leukotrienes) that have potent inflammatory/physiological properties and many other cytokines play a role in the pathogenesis of borreliosis. These BLPs have a key component, Pam3cys, which triggers an innate immune response that cascades into the disease borreliosis(ref).”
Because LD clinical tests are not reliable and because LD is such a great imitator of other inflammatory diseases, it is often initially misdiagnosed, allowing the Borrelia to become ensconsed in the body and thereafter very difficult or impossible to be removed
“As we enter a new decade, clinical testing for Lyme disease remains abysmal.110–115 The two-tier algorithm recommended by the Centers for Disease Control and Prevention utilizes a screening enzyme-linked immunosorbent assay (ELISA) or immunofluorescence assay followed by a confirmatory Western blot. Although this approach has a high test specificity, the sensitivity of the two-tier approach in Lyme disease patients tested at least 4 to 6 weeks after infection is only 44% to 56%, which is inadequate for a clinical diagnostic test and, by comparison, far below the 99.5% sensitivity of diagnostic HIV testing.110,114,115 Furthermore, the misconception that two-tier testing is highly sensitive for Lyme disease patients with persistent arthritic or neurologic symptoms derives from a study that selected patients based on positive Lyme testing and then showed high levels of two-tier test positivity.115 This circular reasoning is a systematic problem with the evaluation of Lyme testing. — There are a number of reasons for the inaccuracy of Lyme testing, including use of less antigenic laboratory spirochetal strains in the commercial test kits, elimination of important spirochetal target proteins from those kits, and lack of standardization of the commercial Lyme assays.111–113(ref)”
“The diagnosis of Lyme disease is primary based upon clinical evidence. There is currently no laboratory test that is definitive for Lyme disease. Many tests give false negative results. Physicians not familiar with the complex clinical presentation of Lyme disease frequently misdiagnose it as other disorders such as: Fibromyalgia or Chronic Fatigue Immune Dysfunction Syndrome (CFIDS), Multiple Sclerosis, Lupus, Parkinson’s, Alzheimer’s, Rheumatoid Arthritis, Motor Neuron Disease (ALS, Amyotrophic Lateral Sclerosis -Lou Gherig’s disease), Multiple Chemical Sensitivity Syndrome (MCS) and numerous other psychiatric disorders such as depression and anxiety(ref).”“Lyme disease is an extremely challenging infectious/toxic disease for both doctor and patient. It can exhibit many different symptoms. The clinical picture of LD can be similar to fibromyalgia, including: chronic fatigue, joint pain (arthralgias), muscle, fibrous tissue and tendon pain. Lyme disease can also manifest primarily as a neurological disorder, including fatigue and many neurological symptoms. It is important to remember that there are hundreds of symptoms that are caused by LD and it can mimic many diseases; for this reason, LD is often called, “the great imitator(ref).”
Borrelia can generate biofilms and hide behind them thus evading body defenses and antibiotics
“Another mechanism of chronic infection involves the formation of biofilms.92–98 These adherent polysaccharide-based matrices protect bacteria from the hostile host environment and facilitate persistent infection. Biofilms are responsible for a number of chronic infections, including periodontitis, chronic otitis media, endocarditis, gastrointestinal infection, and chronic lung infection.92–98 Sapi and MacDonald raised the possibility of biofilm formation by B. burgdorferi, and subsequent work has demonstrated these spirochetal formations in culture and
in the tick gut.99,100 Combinations of borrelial cysts and putative biofilms have also been noted in patient skin biopsies using focus floating microscopy.101 Biofilm formation is dependent on cyclic di-GMP expression,102,103 and recent studies have shown that B. burgdorferi expresses this regulatory molecule.104,105 Coordinated steps in the elaboration of biofilms have been demonstrated in other bacteria, and it remains to be seen whether similar molecular processes occur in borrelial strains and whether these processes play a role in persistent infection.106,107(ref).”
Another protective strategy used by LD for survival in host bodies is migration of borrelia spirochetes into lymph glands where they are protected against specific host antibodies
The 2011 publication Lymphoadenopathy during Lyme Borreliosis Is Caused by Spirochete Migration-Induced Specific B Cell Activation reports “The present study demonstrates that extracellular, live spirochetes accumulate in the cortical areas of lymph nodes following infection of mice with either host-adapted, or tick-borne B. burgdorferi and that they, but not inactivated spirochetes, drive the lymphadenopathy. — Together, these findings suggest a novel evasion strategy for B. burgdorferi: subversion of the quality of a strongly induced, potentially protective borrelia-specific antibody response via B. burdorferi’s accumulation in lymph nodes.”
A July 2011 Science Daily article on this research reports “Results from this groundbreaking study involving mice may explain why some people experience repeated infections of Lyme disease. The study appears online in the journal Public Library of Science Pathogens. — “Our findings suggest for the first time that Borrelia burgdorferi, the bacteria that cause Lyme disease in people, dogs and wildlife, have developed a novel strategy for subverting the immune response of the animals they infect,” said Professor Nicole Baumgarth, an authority on immune responses at the UC Davis Center for Comparative Medicine. — “At first it seems counter intuitive that an infectious organism would choose to migrate to the lymph nodes where it would automatically trigger an immune response in the host animal,” Baumgarth said. “But B. burgdorferi have apparently struck an intricate balance that allows the bacteria to both provoke and elude the animal’s immune response.””
LD can often become a chronic infection
“The comprehensive review of the IDSA Lyme guidelines provided strong evidence for chronic spirochetal infection in patients with persistent Lyme symptoms (Appendix 1).48–58 This evidence was supported by ongoing studies showing failure of ‘standard’ antibiotic therapy in mice infected with the Lyme spirochete.20–24 Coupled with previous animal and human studies of persistent infection and antibiotic failure, this evidence underscores the importance of chronic infection in Lyme disease. It also raises many questions about the mechanism(s) and optimum therapy for persistent spirochetal illness. — Complementing the evidence in favor of chronic B. burgdorferi infection, clinical and experimental studies have shown that tick-borne coinfections may also have chronic phases.59–67 In the past, reports of pathology due to Babesia, Anaplasma, Ehrlichia, and Bartonella species have focused on the fulminant acute forms of infection that are relatively easy to diagnose and often fatal in immunocompromised patients.61,63,67 More recently, these organisms have been associated with chronic persistent infection in animal models and humans.59–67 The presence of coinfecting organisms has been shown to enhance the symptoms and exacerbate the severity of Lyme disease.68–73 Thus recognition of chronic coinfections supports the concept of unresolved illness due to persistent infection with the Lyme spirochete(ref).”
Liver function test scores are often elevated in patients with early Lyme Disease
The 2007 publication Liver function in early Lyme disease reports “To evaluate the frequency, pattern, and severity of liver function test abnormalities in patients with Lyme disease associated with erythema migrans (EM), 115 individuals with no other identifiable cause for liver function test abnormalities who presented with EM between July 1990 and September 1993 were prospectively evaluated. For individuals with abnormal liver function tests, common causes of hepatitis, including hepatitis A, B, and C, were excluded. A local control group was used for comparison. Forty-six (40%) patients had at least one liver test abnormality, and 31 (27%) had more than 1 abnormality compared with 19 (19%) and 4 (4%) of controls, respectively (P < .01 for each comparison). gamma-Glutamyl transpeptidase (28%) and alanine transaminase (ALT) (27%) were the most frequently elevated liver function tests among Lyme disease patients. Anorexia, nausea, or vomiting was reported by 30% of patients, but did not occur more frequently in patients with elevated liver function tests compared with those with normal values. Patients with early disseminated Lyme disease were more likely to have elevated liver function studies (66%) compared with patients with localized disease (34%) (P = .002). After antibiotic treatment, elevated liver function tests improved or resolved in most patients. Liver function test abnormalities are common in patients with EM but were mild, most often not associated with symptoms, and improved or resolved by 3 weeks after the onset of antibiotic therapy in most patients.”
The length of antibiotic treatment specified in the conventional IDSA LD guidelines can be inadequate
“The standard therapy of 4 -6 weeks of antibiotic treatment is not sufficient to treat chronic Lyme disease. Chronic Lyme disease is often a life-long illness. Months, years, and often indefinite antibiotic therapy may be necessary to manage the disease. Ignorant physicians often use the standard treatment and consider the patient cleared of Lyme disease afterwards. Often these patients are not treated long enough to clear the stubborn Borrelia from the body. So, when the standard regimen of antibiotics is finished, the patients relapse with Lyme symptoms soon after the residual Borrelia reemerges. Unfortunately, the relapse is often not recognized by doctors and the patients are misdiagnosed with a different disorder(ref).”
The 2007 publication Counterpoint: long-term antibiotic therapy improves persistent symptoms associated with lyme disease reports “Controversy exists regarding the diagnosis and treatment of Lyme disease. Patients with persistent symptoms after standard (2-4-week) antibiotic therapy for this tickborne illness have been denied further antibiotic treatment as a result of the perception that long-term infection with the Lyme spirochete, Borrelia burgdorferi, and associated tickborne pathogens is rare or nonexistent. – METHODS: I review the pathophysiology of B. burgdorferi infection and the peer-reviewed literature on diagnostic Lyme disease testing, standard treatment results, and coinfection with tickborne agents, such as Babesia, Anaplasma, Ehrlichia, and Bartonella species. I also examine uncontrolled and controlled trials of prolonged antibiotic therapy in patients with persistent symptoms of Lyme disease. — RESULTS: The complex “stealth” pathology of B. burgdorferi allows the spirochete to invade diverse tissues, elude the immune response, and establish long-term infection. Commercial testing for Lyme disease is highly specific but relatively insensitive, especially during the later stages of disease. Numerous studies have documented the failure of standard antibiotic therapy in patients with Lyme disease. Previous uncontrolled trials and recent placebo-controlled trials suggest that prolonged antibiotic therapy (duration, >4 weeks) may be beneficial for patients with persistent Lyme disease symptoms. Tickborne coinfections may increase the severity and duration of infection with B. burgdorferi. CONCLUSIONS: Prolonged antibiotic therapy may be useful and justifiable in patients with persistent symptoms of Lyme disease and coinfection with tickborne agents.”
Besides antibiotic treatment, use of aggressive anti-inflammatory treatment is justified in the case of LD, but not the use of prednisone
Debilitating arthritis and many other inflammatory conditions may suddenly arise in LD patients as a result of the bacterial lipoproteins let loose by Borrelia. However, unsuspecting physicians may not recognize that the cause of the inflammation is LD. “Wrong diagnosis leads to wrong treatment. Another critical point that needs to be highlighted is that Lyme ignorant physicians often administer medication that is contraindicated in patients with Lyme disease. The therapy most often prescribed that is extremely contraindicated is the use of steroidal anti-inflammatories; usually the glucocorticosteroids (such as prednisone). Lyme patients suffer with many painful inflammatory symptoms. MDs, not knowing that the patient has Lyme disease, think it is appropriate to treat these patients with steroids to reduce the pain and inflammation. Unfortunately, steroidal therapy is very deleterious to Lyme patients because it suppresses the patient’s immune system causing it to tolerate the presence of Borrelia instead of attacking and killing it. This harmful treatment significantly diminishes the prognosis of Lyme patients; it prolongs the course of the disease and makes it more severe in the long run(ref).”
Fortunately, a number of antioxidants and natural substances can be used to control inflammation in LD without such immune system suppression including NAC (N-acetyl cysteine} , curcumin, ginger root, quercetin, garlic, olive leaf extract, resveratrol, boswellia and vitamins D-3 and B-6. I have discussed these substances in other blog entries and in the firewall against chronic inflammation in my treatise.
FROM TIME TO TIME, THIS BLOG DISCUSSES DISEASE PROCESSES. THE INTENTION OF THOSE DISCUSSIONS IS TO CONVEY CURRENT RESEARCH FINDINGS AND OPINIONS, NOT TO GIVE MEDICAL ADVICE. THE INFORMATION IN POSTS IN THIS BLOG IS NOT A SUBSTITUTE FOR A LICENSED PHYSICIAN’S MEDICAL ADVICE. IF ANY ADVICE, OPINIONS, OR INSTRUCTIONS HEREIN CONFLICT WITH THAT OF A TREATING LICENSED PHYSICIAN, DEFER TO THE OPINION OF THE PHYSICIAN. THIS INFORMATION IS INTENDED FOR PEOPLE IN GOOD HEALTH. IT IS THE READER’S RESPONSIBILITY TO KNOW HIS OR HER MEDICAL HISTORY AND ENSURE THAT ACTIONS OR SUPPLEMENTS HE OR SHE TAKES DO NOT CREATE AN ADVERSE REACTION.