Lyme Disease

I’ve treated many patients with Lyme disease over the past 13 years. Most of these people had come to my office complaining of a diversity of lingering symptoms. These include migratory joint pain, fatigue, forgetfulness (sometimes called “brain fog”), mood swings, constant headache, and sensory abnormality. When symptoms of Lyme disease persist or recur, it usually indicates that the infection has progressed from an early stage to a later, more entrenched stage. At this point, treatment often requires antibiotics, orally or intravenously, and sometimes in lengthy or repeated courses, I use antibiotics, but I add a variety of natural treatments.

These include: TOA Free Cat’s Claw, antioxidants, natural antibiotics, liver detoxifiers, immunological stimulators, hyperbaric oxygen, and probiotics and probiotics. Information about the natural treatments I’ve found helpful in Lyme appears under subheads further along in this article Lyme disease is difficult to treat in later stages. The Lyme pathogen has several ways of evading antibiotic kill and host immunity. It can invade intracellular sites, has a slow rate of growth, can remain dormant in atypical forms for long periods, and may sequester in areas antibiotics can’t easily penetrate. It’s imperative, then, to combine antibiotics with natural therapies.

Lyme Disease and Low Thyroid

Lyme researchers and clinicians have observed an association between Lyme infection and hypothyroidism (low thyroid).  The inci-dence of thy-roid invol-ve-ment in Lyme disease may be grea-ter than expec-ted from the normal population. In many of these patients, the thy-roid dys-func-tion was observed to ori-gi-nate in the pitui-tary or hypothalamus.  So it is vital in treating Lyme to test for low thyroid. There are a variety of tests for low thyroid. The one I use, the TRH Stimulation Test, can definitively show low thyroid in connection with Lyme disease. When the TRH test indicates low thyroid, I treat Lyme patients with natural thyroid hormones. Time and again, I’ve seen that this treatment has significant beneficial effects on numerous symptoms suffered by patients. It helps especially with the fatigue, muscle and joint pain, “brain fog,” and some neuropsychiatric issues.

Lyme Disease: Basic Information

The manifestations of Lyme disease are protean, suggesting the symptoms of numerous other illnesses. Lyme is such a mimicker of different conditions, it’s been called ”The Second Great Imitator” – the “first” great masquerader being syphilis, caused by a bacterium similar to the Lyme pathogen. For persons interested in what is solidly known about Lyme, the information that follows offers reliable basic information.

Cause and Transmission

The Borrelia genus consists of three different spirochetes (spiral-shaped bacteria). The third, identified in 1982 and named Borrelia burgdorferi (Bb), is responsible for Lyme disease in humans. Female ticks belonging to the Ixodes ricinus complex are the primary vector (carrier) of Bb to humans. The Centers for Disease Control and Prevention (CDC), believes that another tick species, Amblyomma americanum, transmits a spirochete-caused illness closely resembling Lyme in the US Southwest and Midwest. The CDC calls the spirochete involved in this illness Borrelia lonestari and the illness STARI (southern tick-associated rash illness). Ixodes and Amblyomma ticks coexist in many US regions. In

their larva, nymph, and adult stages, Ixodes ticks have one blood meal; larvae in late summer, nymphs the next spring and summer, and adults during the fall. Compared with the common dog tick, Ixodes ticks are smaller, their legs black, and the nymph form smaller than a poppy seed.  Larvae and nymphs prefer the white-footed mouse as a host in most of the US. Adults prefer the white-tailed deer. After attachment by a Lyme tick to a human, the time of transmission of Bb ranges from 12 to 72 hours, but there are documented cases where transmission has occurred in less than half a day. Pregnant women may also transmit Bb to fetuses.


Today, new Lyme cases make up 95 percent of the total number of vector-borne diseases reported annually to the CDC. In the past few years, all 50 states have reported Lyme or Lyme-like illnesses. The majority of new case reports have been pouring in from Northeastern, mid-Atlantic, and north-central states. Reports from California, Texas, and Florida are on the rise, indicating that Lyme disease in gaining a foothold in these highly populated states. And the incidence is soaring; over 12,000 nationwide in 1997, almost 17,000 in 1998, close to 24,000 cases in 2002. But the actual incidence of Lyme in the US is uncertain.

According to the CDC, it accepts only ten percent of reports of new Lyme cases. The chief limiting factor is the CDC case definition, utilizing very narrow criteria and developed not for clinical diagnosis but for surveillance alone. So in 2002, for instance, when the CDC reported 24,000 new cases, the true number of new Lyme cases around the country may have totaled 240,000!

STAGES Lyme disease may proceed through several stages, affect various organ systems, and persist or recur if not correctly diagnosed and treated early and properly. During the first stage of Lyme, many infected people develop a reddish rash, often roughly circular, at the site of the tick bite. Called erythema migrans (EM), normally the rash expands, clears in the center, and resolves in three or four weeks. Note:

the typical EM rash does not appear in a significant number of infected persons.

Or it may take an uncharacteristic form, or develop in a part of the body unlikely to be noticed by a Lyme-infected individual. Estimates on how frequently EM presents uncharacteristically or goes unnoticed or unrecognized range from 20 to 50 percent. Chills, a flu-like illness with fever, mild fatigue, or myalgia can be additional manifestations of Lyme during the first stage of infection.

The disseminated stage of Lyme disease begins when the spirochete passes into the blood or lymph. Signs and symptoms of dissemination vary greatly and can occur less than a month after infection or as much as a year or more following a bite by a tick carrying Bb. Whether in early disseminated Lyme (manifesting weeks or months after infection), or late, persistent Lyme (manifesting many months or even years after infection), the illness mostly affects the musculoskeletal system, the central nervous system, or the skin. Between five to ten percent of Lyme patients experience heart problems, which can be acute during the early disseminated stage. Incorrectly diagnosed and treated, up to 20 percent of patents in the late persistent stage develop neurological disease, which can also be acute In general, Lyme in the persistent stage presents with musculoskeletal or neurological involvement.


Diagnosing Lyme disease is a complex, often uncertain process .A large number of multisystem manifestations can cloud the picture, and Lyme signs and symptoms during both the early and late stages can appear like the clinical manifestations of many other conditions… The CDC advises physicians to make a clinical diagnosis if they suspect Lyme disease. There are two bases for such a diagnosis:

1. Identification of the EM rash in an early stage, or involvement of a major system backed by positive serology.

2. Recognition of clinical signs characteristic of Lyme, a history of exposure in a geographic area where Lyme ticks are endemic, and the use of lab tests as an adjunct to diagnosis.

Two lab tests are usually ordered to support a Lyme diagnosis: the ELISA and Western blot. These tests supply indirect evidence of the presence of Bb, measuring the immune system’s response to the spirochete.

ELISAs detect antibodies in the patient’s serum that react to antigens (proteins that evoke an immune response) present in the Lyme spirochete. A patient having such antibodies probably has been exposed to Bb. But Lyme ELISAs are notoriously deficient in two ways. They are not sensitive to certain true antibodies

of Lyme, and they are over sensitive to antibodies seen in many non-Lyme conditions, periodontal disease, for instance.

Western 20blots are used to distinguish between true and false positives on LISAs. The Western blot test looks at antibodies directed against a wide range of Bb proteins. In a patient with antibodies to a particular Bb protein, a “band” forms at a certain place on the blot. “Reading” the “band” patterns formed by the spectrum of Bb antibodies, labs are able to determine with greater specificity if a patient’s immune response is specific for the Lyme spirochete.

Indirect antibody detection has significant limitations. Patients vary considerably in their serologic reactions to Bb. Patients are expected to test negative in early Lyme because of the time required to develop detectable antibody levels. During the early period of disseminated Lyme, patients treated with antibiotics may have negative or equivocal serologies; presumably, the antibiotics nullified their immune response. In other patients, antibodies are detectable long after treatment, which makes it difficult to distinguish between active or past infection. Also, antibodies can form complexes with antigens, but current antibody tests only detect free antibodies.

Standard Treatment for Lyme Disease

Many cases of Lyme disease, diagnosed soon after infection, respond to relatively short-term antibiotic therapy and don’t recur. Diagnosed in a late stage, Lyme is much less responsive to antibiotics. Giving antibiotics orally or by IV in repeated longer courses or for lengthy periods appears to provide relief.

Natural Treatments for Lyme Disease

CAT’S CLAW: Cat’s Claw is an herb native to South America. This form of Cat’s Claw has been shown to help control inflammation and microbial balance and sooth irritated tissue in the GI tract. It also appears to have antioxidants which help modulate and support immunity. Cat’s Claw contains as well quinovic and glycosides, both natural precursors to quinolone antibiotics. (Quinolones are a family of synthetic broad-spectrum antibiotics that prevent bacterial DNA from unwinding and duplicating.)

GLUTATHIONE, A POWERFUL ANTIOXIDANT: Glutathione, given intravenously (IV) and orally, plays a vital role in liver detoxification; glutathione also seems to have a significant effect in neurological Lyme.

LAURICIDIN, A NATURAL ANTIBIOTIC: Derived from lauric acid, a fatty acid occurring in laurel, coconut, and palm oils, lauricidin appears to reduce Lyme neuro-toxicity.

AHCC, ACTIVATOR OF NATURAL KILLER CELLS: AHCC, derived from medicinal mushrooms grown on rice bran, stimulates the production of natural killer cells. Natural killer cells (NK cells) belong to the innate immune system. Their special function in immunity mostly involves targeting and killing cells infected with viruses or  host cells that have turned cancerous.

HYPERBARIC OXYGEN THERAPY: Hyperbaric oxygen increases the production of energy, blood flow, and production of ATP, a molecule essential for cellular energy production. Hyperbaric oxygen also appears to help in neurological Lyme issues.

PREBIOTICS AND PROBIOTICS: Long-term antibiotics can impair normal gastro-intestinal

(GI, or “gut”) functioning, I’m hyper-vigilant about monitoring and improving GI function. I give my patients probiotics and probiotics to maintain function. Probiotics are nutrients that help healthy GI bacteria to grow. In my clinical experience with Lyme, the most effective include inulin, oligofructose, betaglucan, and larcharabinogalactan. Inulins are a group of naturally occurring polysaccharides (several simple sugars linked together ) produced by many types of plants. Oligofructose is a subgroup of inulin. Betaglucan comes from a different group of polysaccharides. And larcharabinogalactan is a species of Echinacea. Betaglucan improves immunity generally. Larcharabinogalactan improves immune response, too.    Probiotics replace GI flora (microorganisms) reduced by antibiotics. I give Lyme patients various acidophilus cultures for replacement, but I’ve found saccharomyces boulardi (a tropical strain of yeast) to be more effective as a probiotics in the large and small intestines than the bacteria lactobacillus). S. boulardi seems particularly effective in auto-immune conditions, and Lyme can have an auto-immune component. Note: In monitoring GI function in Lyme patients, I’ve learned that it’s frequently necessary to test stools for overgrowth of certain gut bacteria.

OLIVE LEAF EXTRACT: This is a natural compound with apparent anti-Lyme activity. Clinical evidence shows that carefully produced extracts of olive leaf lower blood pressure. Bioassays at the lab level suggest that olive leaf extracts have antibacterial, antifungal, and anti-inflammatory effects. Recently, a liquid extract from olive leaves was shown to have an antioxidant capacity twice that of green tea extracts and an antioxidant capacity 400% higher than Vitamin C.

Lyme Research: Latest Findings

As the 21st century heads into its second decade, controversies and questions about Lyme disease still await resolution. Among them: Historically, Lyme emerged as a separate disease entity in the US from the mid-1970s to the early 1980s. A cluster of cases of children with severe arthritis in Lyme, CT, studied and reported by academic physicians associated with Yale University, is commonly taken as the starting point. Some 35 years later, every state in the Union has reported Lyme cases to the CDC, and with the true number of new cases most probably underreported annually, this tick-borne infection may have reached epidemic status. How does one account for the dramatic, rapid spread? It’s been recognized almost from the onset that the Lyme spirochete has a number of different strains. How many? Are the strains alike or dissimilar in their ways of affecting people? If Lyme infection can persist, as some clinicians and many patients say, how does the spirochete avoid detection and elimination by the host’s immune system? Studies have indicated that

antibiotics don’t eradicate infection in later stages in all cases? How do Lyme bacteria “hide” from antibiotics? Why does Lyme disease vary so greatly from patient to patient?  Pamela Weintraub, senior editor at Discover magazine, who’s covered medicine and science in the national media for 25 years, recently published a book about Lyme disease. Titled CURE UNKNOWN: Inside the Lyme Epidemic (St. Martin’s Press, NY, 2008), Weintraub’s book features recent research findings that are outdating 20th-century theories about the nature and treatment of Lyme. Studies of the Lyme spirochete’s genome and the proteins created to protect the spirochete are the “hot” fields in 21st-century Lyme science; these fields hold the greatest promise for improving diagnosis and treatment. I keep current on reports about Lyme disease in the medical literature. For people with little professional reason to read this literature, CURE UNKNOWN surveys most of the important findings, particularly on persistent or chronic Lyme.

Studies by Luft-Schutzer

On the apparent outbreak of Lyme in the US in the mid-1970s, Weintraub discusses one persuasive theory with Ben Luft, an infectious disease specialist at Stony Brook, Long Island. One of the big discoveries from research on the genome of the Lyme spirochete, she explains, is that the dominant strain, B31, is identical genetically in the US and in Europe, suggesting a transcontinental migration of the organism in recent years. Luft comments: “If the organisms had been separated longer, they would be different, because each would have been evolving in its own way.” Weintraub continues: “The data suggest that sometime before the epidemic took off, a strain from Europe may have arrived in the US on the back of a dog or a bird, lighting the forested suburbs like a match thrown on tinder wood.” She concludes: “But it wasn’t B31 alone that fanned the flames. In any given region, there could be a different mix of strains. The farther investigators traveled from the Northeast, the more variable and mixed the strains became, implying that the disease could produce different symptoms from person to person and different results from Lyme test to Lyme test.” Luft’s investigative team looked at 20 strains of the Lyme spirochete isolated from ticks collected from New Hampshire to the Carolinas, comparing differences

in their genes. The investigators determined that six strains don’t infect humans. Ten cause only a rash. But four strains can get past skin and invade other tissue. B31 proved the most virulent of these four. Recently, Luft’s team joined with Steven Schutzer, an immunologist at the University of Medicine and Dentistry, NJ, to see what causes B31 and the three other invasive strains different. The Luft-Schutzer teams discovered that the invasive Lyme strains can exchange genetic material with each other. (The non-invasive strains “reproduce” by cloning.) Luft-Schutzer is now designing studies that will sequence every gene in every strain of the Lyme spirochete from the Northeast, and genes in strains from the Midwest and Europe. Through recombinant biology, the team will get each gene to express its individual protein in the lab. The number of individual genes expressed could total 1,800 proteins altogether – every protein expressed by every protein. Then, instead of testing patients for antibodies to the very limited number of proteins that the CDC has called for since the late 1990s, Luft-Schutzer will coat all 1,800 Lyme proteins on a slide, making it possible to test patient sera against the whole spectrum of Lyme proteins in their entire variability.

Studies by Barthold and Norris

Weintraub’s chapter “Secrets of an Evil Genius: The Evidence for Persistence,” centers on animal research by Stephen Barthold, a veterinarian involved in gaining insights into the survival mechanisms of the Lyme spirochete, first at Yale back in the early 1980s, lately at the University of California, Davis. Barthold’s observations through his Yale years showed that the Lyme spirochete could persist in mice and other mammals even after aggressive antibiotic treatment. “You have a bacterium,” Barthold tells Weintraub, “with a relatively small and simple genome that can do incredibly complex things. It is a fascinating organism with a lot of evolutionary intelligence, consistently capable of creating persistent infection and evading host immunity.” Barthold published a paper in Antimicrobial Agents and Chemotherapy in 2008 on a controlled investigation in mice. One arm followed mice given ceftriaxone after three weeks of infection (early acute disease). A second arm followed mice treated with the same antibiotic after infection for four months (late, persistent disease). Paralleling the treatment arms, there was a control arm of mice on saline solution. All the mice were sacrificed to search for persistent infection, Weintraub reports that “Barthold found that after he treated acute or chronically infected mice with high-dose antibiotics, he achieved cure by virtually every ordinary measure, from clinical signs of disease to growth in culture. Yet three months later, small numbers of spirochetes remained, hunkered down in the collagen of the heart and joints. Moreover, in the chronic mice, these spirochetes remained infectious; they could be picked up by ticks and transmitted to other mice as active infections.” Weintraub notes a key new finding in Barthold’s paper. The treated spirochetes were attenuated in their ability to replicate. This finding, she remarks, opens “a window on the experience of human patients with chronic

infection…If spirochetes responsible for persistent disease can’t replicate, antibiotics that kill bacteria by hitting bacterial cells as they divide may not work. “And as long as these ‘attenuated’ spirochetes stay alive, they may not aggregate in a mass critical enough to cause the gross inflammatory signs of Lyme arthritis or meningitis. But they could cause the ‘constitutional’ symptoms suffered by chronic patients. Researchers term these symptoms ‘pro-inflammatory effects,’ and they include production of nitric oxide  and the activation of neutrophils and macrophages, which together could account for the fatigue and malaise so many of these patients report.” Turning next in this chapter on the evidence for persistence of Lyme to research by Steven Norris, a microbiologist at the University of Texas, Weintraub describes a discovery Norris made in the late 1990s, which he published in the journal Cell. In experiments with animals, Norris found a special DNA segment that creates new gene sequences. These new genes produce new Lyme spirochete proteins. As the proteins change, the spirochete coat also changes, and molecules spewed out by the host’s immune system to kill the Lyme spirochete lose their killing power. Through ‘promiscuous recombination’ of the genes, a “vast array of proteins”  (Norris’ language) swiftly generates into a system so extensive, it can “potentially create millions of antigenic variants in the  mammalian host” (Norris’s language again, emphasis added). In a follow up on this discovery, Norris reported in 2008 that this novel mechanism responds to cues in the environment, facilitating the Lyme spirochete’s survival “from locale to locale” (Weintraub’s words here). The process can also be “dialed up or down” (Weintraub’s language again) through fluctuations in the temperature and acid content of surrounding tissues and cells.

Studies by Weis

Janis Weis, an immunologist at the University of Utah, has studied why Lyme disease varies from individual to individual. Working with mouse tissue cultured in vitro, she exposed it to the Lyme pathogen and observed that while B and T cells generated by the immune system destroyed spirochetes, a more generalized inflammatory response, occurring before B and T cells appear, damaged the mice. Investigating further, Weis discovered a molecule, termed “Toll-like receptor 2,” which initiates the inflammatory reaction. Mice that lack this molecule develop little inflammation. Over time, the load of spirochetes grows huge, until these mice show inflammation more disabling than that in mice with more pro-inflammatory genes,    Noticing that some mice got much sicker than others, even when exposure to Lyme was exactly the same, Weis asked: Were some mice (and some people) simply less susceptible to inflammation? To answer her question, she crossed

severely and mildly arthritic mice over generations, so all kinds if intermediate combinations emerged. After years of interbreeding, she created 400 mouse lines, each line at a different point on the spectrum – from those prone to severe inflammation to those incapable of any inflammation. Infecting all 400 lines with Lyme, she found a full range of disease severity, which corresponded with the genetic background of the mouse. Depending on where mice fell on the spectrum, even a small number of spirochetes could induce and sustain their genetically predetermined variety of disease, No matter where on the spectrum an individual fell, when all the Lyme spirochetes were eliminated, the signs of the disease disappeared. So where an individual falls on the spectrum may not make a difference – unless that individual gets Lyme. The same system exists in humans, Weis believes, and probably accounts for why different people have such different disease outcomes.

Closing Note

In sharing this information on the latest research on Lyme disease, I chose findings on persistence of infection and variability in symptoms and outcomes because these areas are among the most debated issues and least resolved questions in Lyme. Bear in mind while reading this information that until these issues and questions are resolved, many people will continue to become infected with Lyme yet fail to receive early diagnosis and treatment. And late stage Lyme, experts estimate, is incurable in 20% of adults!