The Rise of Chronic Lyme—and What to Do About It
Amiram Katz, M.D. was the director of the epilepsy center at Norwalk Hospital in Connecticut in the 1990’s when he started seeing patients whose seizures were not epileptic, but something different—involuntary movements which turned out to be autoimmune complications of Lyme disease. “When the Lyme community hears about a doctor willing to listen to them, that information spreads like wildfire,” says Katz. He began seeing more and more Lyme patients and opened a private practice in 2002.
Katz’s approach to treating chronic Lyme reflects his decades of experience, and his open mind: He disagrees with what he sees as extreme approaches (zero antibiotic use, or prescribing antibiotics long-term), and he’s cautious when it comes to shiny new treatments (unless he’s sure they are safe for his patients—and their pocketbooks), but he also sees a place for ancient methods of healing, too. Where Katz looks to go above and beyond is in the relationship he cultivates with patients. The most important thing? Believing your patient, he says.
Here, Katz shares his stance on chronic Lyme, and illuminates a way to navigate through it that has proved immensely helpful for many. (For multiple other perspectives on Lyme disease, see here.)
A Q&A with Dr. Amiram Katz
How do you define chronic Lyme disease?
There is no debate about defining acute Lyme infection. Chronic Lyme disease is more complicated. The majority of the medical community denies the existence of chronic Lyme disease; patients who continue to be ill after the standard 30 days of antibiotics treatment that the Infectious Disease Society of America recommends are referred to as “Post Treatment Lyme Disease” (PTLD).
Chronic Lyme is a disease that continues either after the acute spirochetal infection is recognized and treated appropriately in a timely manner, or, if the initial infection is not identified, it may develop into chronic illness insidiously. Even from a microbiological standpoint, one of the characteristics of chronic Lyme disease is the persistence of the spirochetes (bacteria that cause Lyme) that can never be totally eliminated from the body. Their defense mechanisms allow them to turn into persisters; they may go dormant in the body for long periods of time, but they are still there.
What are the symptoms?
Patients with chronic Lyme have a mega-list of symptoms. I hate when patients come with a list of 100 symptoms checked on a questionnaire issued by one of the Lyme organizations, because it can be every possible illness, is vague, and makes it hard for the doctor to understand the main problems. But the reality is that Lyme is a multisystemic disease that can lead to a variety symptoms due to a persistent damage from the original infection or the development of secondary autoimmune conditions. It attacks the central and peripheral nervous system, the joints, and sometimes muscles. Symptoms are generally neurological, rheumatological, and psychiatric, and more rarely, cardiac-related.
People typically report joint and muscle pain; non-specific fatigue; sleep difficulties; “brain fog,” which includes memory problems, difficulties in attention and concentration, loss of sense of direction, and loss of executive functions. Patients frequently complain of ringing in the ears, vertigo, light and sound sensitivity, numbness and tingling in different parts of their body, a sense of internal vibration, change in bowel habits, night sweats, sometimes bizarre cutaneous manifestations, and many more symptoms. I will often ask patients who come with the prepared mega-list of symptoms to tell me their main problems, in order to know which should be managed first.
“We have at least a million patients suffering from a chronic condition that was initiated by Lyme, and probably a minute fraction of them are getting the right attention and recognition.”
I always thought that the autoimmune explanation of chronic Lyme would make sense to the mainstream medical community, but many shy away from it. The autoimmune etiology of chronicity should be accepted and further research should continue in this direction. Unfortunately, I think that the NIH doesn’t push enough in this direction and is focused on the early diagnostic testing while not giving enough weight to the chronic problem. Meanwhile, in mainstream literature, it’s agreed that 10 percent of patients who are diagnosed with Lyme and treated in a timely manner go on to develop a chronic illness, and that every year, 30,000 people are added to the pool of chronically ill patients—and we really don’t know what to do with them. We have at least a million patients suffering from a chronic condition that was initiated by Lyme, and probably a minute fraction of them are getting the right attention and recognition.
What do we know about the sources of Lyme disease, the risk of contracting it, and why it develops into a chronic issue in some people?
Beside ticks (mainly the deer tick, Ixodes scapularis), there is some evidence that Lyme can be carried by mosquitoes and avian parasites, like fleas, along with other potential carriers. There are no geographic boundaries to the disease. What determines where Lyme is more prevalent is a humid temperate climate conducive to the survival and multiplication of a big reservoir of ticks on the ground, like what we have in New England. In the desert, there are animals like deer and mice, but the dry conditions won’t allow the larvae (first cycle of reproduction of the tick) to survive on the ground.
It’s a two-year cycle: The stage from larvae to nymph takes one season. The larvae typically attaches to the white-footed mouse, transforms to a nymph, which then sheds to the ground, and is dormant for one year before moving to deer. The nymph then matures sexually, mates/lays eggs, which will be shed on the ground and stay dormant until the next spring, when they will develop into larvae who will be looking for mice or other rodents.
It’s possible that some people are more prone to contracting Lyme than others, as some people’s perspiration, or pheromones, may attract ticks or other carriers more so than others.
We don’t know exactly why chronic Lyme develops in some people but not others, but it’s likely that it develops more readily in people who are prone to developing autoimmune conditions when they encounter this particular trigger (the invading Lyme spirochete). It’s also thought that people with robust immune systems are more likely to develop the “bullseye rash” after being infected, which also makes early detection (and treatment) more likely.
How do microorganisms like spirochetes evolve to live in our bodies? (They’ve been able to for quite some time: You might be aware of the 5,300-year-old frozen body that was discovered in the Alps in the early 1990’s. When they performed his autopsy, some twenty years later, they found Lyme spirochetes in the man’s brain.) It’s likely that spirochetes evolved some of their outer surface proteins through mutations to look like our own body proteins, which would cause the autoimmunity associated with Lyme: The body fails to recognize the invader, and instead, can end up attacking its own proteins, which look similar, along with the foreign invader in an attempt to fight the invader off. (This mechanism of forming autoimmunity is called “molecular mimicry”).
If you suspect you’ve been bitten and/or contracted Lyme, what should you do?
If you find a tick attached, remove it, and seek treatment from a doctor right away (and a blood test 3 to 4 weeks later). For the treatment to be most effective, the tick should be removed within twenty-four hours.
My approach is a little different from the mainstream. If someone develops symptoms a few days after a bite, I treat them, rather than waiting for the tick analysis results to see if it is positive for Lyme (the test can take weeks in some cases). For prevention after finding and removing a tick, I have a rule of 3 x 3, where I give three doses of the antibiotic doxycycline—100mg, each day, over the course of three days. Typically, you’d get two doses (100mg each) for one day—based on current medical literature—but I’ve seen cases where this was not enough.
What are the testing methods?
Per CDC recommendations (the outcome of the famous meeting in Dearborn, MI in 1993), laboratory testing for Lyme disease should follow a two-tier approach. It’s important to note that these CDC guidelines were set for the purpose of reporting, research, and surveillance, and not as diagnosis and treatment guidelines. The first blood test that is usually ordered as a screening is called ELISA (enzyme-linked immuno sorbent assay), which is generally reliable (except for having false positives in some autoimmune diseases), and measures quantitatively the total amount of antibodies against the different proteins (antigens) of the spirochete.
If the ELISA is positive, a Western blot is typically ordered, or is automatically checked by the lab (although you can also request a Western blot regardless of the ELISA). The blot is problematic in that it is qualitative. It measures the response of different antibodies in the blood against the different proteins (antigens) of the spirochete, separated and prepared on a stripe of gel. A positive response against a specific spirochetal protein will appear as a band, rather than a number. So technicians and doctors are looking at what appears to be a set of bar codes, shaded in to different degrees. In essence, the FDA instructs the performing lab to compare the patient’s band density of the blot to a positive control blot; if it’s 40 percent as strong (or more), then the patient is said to have a band; and a certain number and type of bands are required to be counted as a positive Lyme test.
“A minor fluctuation in subjective visual interpretation can entirely alter a patient’s health outcome—potentially leading to chronic illness, which is then denied as a chronic illness.”
Since this visual inspection is subjective and varies from one technician to the other, it is not surprising that sometimes I’ll get three different blot results of the same patient’s blood sample (one ordered directly and the other two by the automatic Western blot testing following a positive ELISA, or a C6 peptide test, which is a more specific quantitative test).
I use a laboratory that analyzes the optic density of the band with a machine, so it’s more reliable, and I also have a picture of the blot sent to me so I don’t have to solely rely on someone else’s interpretation. Still, as mentioned, I’ve seen three Western blot tests from the same patient come back with three different bands reports that indicate alternating positive and negative results. This test is supposed to be what doctors use to determine how and whether to treat patients or not! A minor fluctuation in subjective visual interpretation can entirely alter a patient’s health outcome—potentially leading to chronic illness, which is then denied as a chronic illness. So, I read those blots a little more liberally when patients are presenting with symptoms—I’m looking for shadows, visible lines, that might indicate that there was some antibody activity against spirochetes. A band cannot be there unless there are antibodies against the particular spirochetal protein. So if it is 1 percent below the cutoff number, shouldn’t it be counted? This can make all the difference for a patient.
What’s your approach to treating Lyme?
I don’t think that any of the extreme approaches to Lyme disease diagnosis and treatment are justified: Ignoring its presence completely and denying antibiotics across the board, or, on the other hand, diagnosing anyone with Lyme disease and bombarding patients’ systems with multiple antibiotics for years—these extreme approaches should be avoided in favor of a middle-road approach.
If there is evidence of acute or subacute illness and the Western blot looks positive, I will treat aggressively: If there is no response to oral antibiotics and there is clinical evidence of neurologic involvement, I will proceed with intravenous antibiotics within a few weeks, following a spinal tap. (The spinal tap doesn’t need to be positive for Lyme, but should show that something related is going on—elevated protein or increased white blood cell count—along with the positive serology. Many mainstream physicians expect to find positive Lyme indicators in the spinal fluid, but these are rarely found even when there is a clear Lyme involvement of the central nervous system.)
“I don’t think that any of the extreme approaches to Lyme disease diagnosis and treatment are justified.”
If the disease is chronic and there are neuropsychiatric manifestations, I use a test panel that detects antibodies against several elements of the central nervous system. (This was developed by a PANDAS—Pediatric Autoimmune Neuropsychiatric Disorder Associated with Streptococcus—researcher, Madeleine Cunningham. I found that patients with chronic Lyme develop the same antibodies as patients with PANDAS). I treat those patients with a low dose of penicillin by weekly injection. It’s a benign treatment that has a lot of success if it’s given as a monotherapy, without any other antibiotics. (I’ve seen, for instance, young teenagers with positive Lyme tests and positive antibodies on the Cunningham panel, presenting with acute psychiatric symptoms—anxiety, OCD, and sometimes self-mutilating behavior—who return to their normal health after four penicillin injections.)
We don’t know exactly why this treatment works, but one of the theories is that the residual spirochetes in our body that probably perpetuate the autoimmune process are not detecting the low-dose penicillin. So, it’s a stealth method of killing the spirochetes that upregulate the autoimmune process.
It is very important to treat patients’ symptoms and support them emotionally. Many times the emotional support will combine counseling and psychopharmacology. It is also important to send patients with sleep complaints for a sleep study. I’ve found late onset narcolepsy in some of my Lyme patients. Late development of attention deficit confirmed by neuropsychological testing should be addressed pharmacologically with stimulants. Pain management is important and should be done properly, avoiding opiates as much as possible.
What about boosting the immune system?
It’s always beneficial for patients to maintain good health. This includes eating a balanced diet high in antioxidants, taking rich supplements, a multivitamin, probiotics of various kinds, good bacteria and good yeast. It’s also beneficial to take other agents that are believed to boost the immune system, like colostrum (which has immune transfer factors) and the Maitake mushroom (which was found to boost the immune system of AIDS patients in Japan)—both of which you can get over the counter. You want to be sure you have good levels of vitamin B12 and vitamin D (low levels of D have been linked to autoimmunue conditions). For vitamin D, I mean having levels well beyond the standard range of 30-50 ng/ml, and closer to 70-100 ng/ml.
It’s also important to look for other things that can contribute to the chronicity of illness, like the inability to detoxify efficiently. Consider testing for MTHFR genetic mutations, which disrupts the methylation process (your body needs to convert folate into its usable form, methylfolate, in order to carry out important biochemical reactions), and may inhibit detoxification. If you have the MTHFR genetic mutation, then the forms of B12 and folic acid that you’re taking need to be methylated so that they can be used by the body.
For some of my patients with neurologic autoimmune complications or immune deficiency, IVIg (intravenous immunoglobulin) therapy may be an option. The problem with autoimmunity is that most of the treating agents we have that quiet down the autoimmune process also suppress the immune system. One agent that doesn’t suppress the immune system is IVIg, which is a pulled plasma protein collected from thousands of donors that is infused into patients. It’s a passive immunization by delivering pure antibodies. For people born with, or who develop, an immune deficiency, IVIg can replenish the blood and boost the immune system. Furthermore, the antibodies from the donors are thought to counteract autoimmunity by binding to the patient’s auto-antibodies, which are the patient’s antibodies responsible for the autoimmune process.
How does the patient-doctor relationship come into play in treating Lyme?
In our current practice system, it’s near-impossible to deal with patients that are presenting with the multitude of symptoms and the big medical history file as is often the case with chronic Lyme. I don’t blame doctors that they don’t have time—that is the face of medicine today. It is a checklist system that creates a game of ping pong: Tell me your symptoms and I’ll throw back some medicine. It’s getting worse and worse.
“Autoimmune diseases are more prevalent in women, towards whom there is a discarding attitude, that unfortunately continues to this day where chronic illness in women is written off as solely an emotional matter.”
But we need to give these patients time. At my practice, I give patients two hours for an initial visit and sometimes it lasts longer. For follow-ups, it is at least an hour. We need to be able to communicate—especially with neuropsychiatric Lyme patients who might also need some therapy and counseling, whose family we might need to work with, too. As a doctor, you need to be close to your patients. Patients need to feel comfortable with you and know that you will listen to all their problems and take them seriously. That’s the most important thing: You need to believe that the patient’s symptoms are real and the patient needs to feel it.
There is an attitude among a few doctors that some patients’ symptoms are not valid. If there is no immediate explanation for symptoms, patients are sometimes sent to a psychiatrist, under the assumption that their problems are emotional (and not because an organic neuropsychiatric disorder has also been diagnosed). Autoimmune diseases are more prevalent in women, towards whom there is a discarding attitude, that unfortunately continues to this day where chronic illness in women is written off as solely an emotional matter.
It’s also important for doctors to follow patients longitudinally, and to try to integrate all the information they bring you, rather than just referring them to different sub-specialists. With chronic Lyme patients, I think we physicians don’t always integrate all the information we have—another problem in medicine today. If something isn’t in our area of expertise, we are too quick to send the patient to someone else. I think we need to remember that we all begin as general practitioners, and then we become specialists. We need to utilize our knowledge and try and understand the WHOLE picture, rather than looking at only the fragments.
Can you explain your stance on alternative therapies?
A good rule to follow is: If doesn’t hurt your body and it doesn’t hurt your pocketbook, you can try it. If some treatment has no peer-reviewed articles supporting it, despite how desperate a patient may feel, it’s important to consider whether the treatment could be harmful or not. Also, some very expensive treatments can be successful only temporarily, which is another thing to consider before mortgaging your home. (This is not entirely different from some FDA-approved medications—sometimes in the first year of their release, things look great and then, the next year, it turns out that there are serious complications, and a treatment that seemed promising doesn’t actually lead to long-term improvements.)
“These are traditions that have been around for thousands of years and we need to respect them.”
At the same time, if patients want to try an “alternative” treatment, like acupuncture, I support that. Acupuncture plays a big role in the modulation of body function and restoring homeostasis, which is disrupted with autoimmunity and chronic illness. These are medical traditions that have been around for thousands of years and we need to respect them. Other forms of ancient medicine can be beneficial, too. Some of my patients have been helped by herbal treatments, in particular those prepared by Dr. Qingcai Zhang, who is extremely knowledgeable and combines acupuncture with Chinese herbal medicine.
Where do you see treatment for Lyme disease going in future?
I think that immunotherapy is the answer, but in a different way than it is currently practiced: We talk about certain proteins of microorganisms triggering autoimmunity via molecular mimicry (the body mistakes the invader’s proteins for its own). We could identify these proteins (like those of the spirochetes) and give them to patients in very, very small doses to serve as a desensitization. In small dosages, the immune cells will attack these proteins rather than its own. In addition, we can develop monoclonal antibodies against targets on the spirochetes, and can eliminate them by this mechanism, rather than giving high doses of antibiotics. So this would be an immunological attack on the invader—not immunotherapy by definition, but immuno-elimination of the microorganism that would solve the problem effectively without using antibiotics.
Amiram Katz, M.D. started the Epilepsy Center at Norwalk Hospital in Connecticut in 1993. In his ten years at the hospital, he also served as co-director of the Sleep Disorder Center. In 2002, Katz opened his own practice, based out of Orange, Connecticut, where he focuses on the treatment of the neurological complications of Lyme disease and neuroinflammatory and neurodegenerative conditions associated with Lyme disease.
The views expressed in this article intend to highlight alternative studies and induce conversation. They are the views of the author and do not necessarily represent the views of goop, and are for informational purposes only, even if and to the extent that this article features the advice of physicians and medical practitioners. This article is not, nor is it intended to be, a substitute for professional medical advice, diagnosis, or treatment, and should never be relied upon for specific medical advice.