Turmeric and Lyme disease
For example, in one case with which the author is personally familiar, a young woman with a recent diagnosis of Lyme disease went to the emergency room for help with her extreme pain. The intake nurse wrote that she "claimed to have 'end stage Lyme Disease.'" The woman protested that she had said no such thing, that there is no 'end stage Lyme Disease,' that she was simply providing information on her diagnosis. The nurse finally changed the wording, but her attitude made it plain that the young woman's previous antidepressant use was likely to invalidate any medical history she provided. This is typical of how Lyme disease and its sufferers are mischaracterized and in a high percentage of cases, misdiagnosed and inappropriately treated, if treatment is provided at all.
The climate for Lyme diagnosis and treatment appears to be slowly improving, but research funds are still a fraction of what is needed. So what can a Lyme patient do?
Health bloggers suggest everything from 'energy' treatments to completely ineffective compounds to potentially toxic ones. Many of these have little scientific data for any purpose at all, much less to treat a disease with such a wide variety of damaging effects. Turmeric, however, does have research to verify its mechanisms. Much of the research was done long before Lyme disease was widely recognized, and turmeric is not seen as specifically efficacious against Lyme in the medical community. This article was written to provide information about turmeric's benefits in Lyme in an easily read and scientifically accurate manner. It is not intended to suggest that turmeric will cure Lyme, nor to recommend it in place of other appropriate medical treatment, but only to provide information on how turmeric's well-known mechanisms may help with Lyme disease.
The following contains more detail than many people may wish, but it seemed important for this to be helpful to medical professionals as well as the general public. If you find the technical explanations boring, feel free to skip over them. The parts that you do understand will still be helpful.
The first section has to do with how Lyme disease is transmitted via ticks, and how the human body's immune response to it affects the progress of a Borrelia infection. The Borellia spirochete has no inherent toxicity of its own. It affects its host via its ability to elicit an exaggerated response from the victim's own immune system, causing cardiac damage, arthritis and neurological deficits, amongst others. Its purpose is not to kill its host but to replicate itself in the host in sufficient numbers to be passed on to subsequent hosts. The fact that a human is usually a dead end host does not reduce the degree of damage incurred from the organism, unfortunately.
The second section describes the symptoms that appear after the pathogen has moved out of the bloodstream and into the tissues and extra-cellular matrix. This is the point at which the inflammation triggered by Borrelia begins to produce noticeable neurological and arthritic symptoms. Cardiac symptoms may take longer to appear, though that is not the case for everyone. The third section lists some ways in which turmeric can help what is sometimes called chronic Lyme (or more often dismissed as "Post Treatment Lyme Disease Syndrome"). Unfortunately, many people have already come to this point before they are correctly diagnosed. However, this is also the point at which potent anti-inflammatories like turmeric may provide the most striking help. I admit to a certain amount of personal bias in the reference to PTLDS, but nothing in the following discussion depends on one's opinion of that argument.
Some definitions are important. Turmeric is a spice with a four-thousand-year written history of use. It is a whole food, not a dietary supplement. It is not the same thing as curcumin. Turmeric contains a small percentage of the three curcuminoids (curcumin, demethoxycurcumin and bisdemethoxycurcumin), in addition to multiple other active and supporting compounds in its 200-plus constituents. The curcuminoids are hydrophobic and lipophilic, meaning that they are insoluble in water or water-based compounds, and soluble in fats (lipids). They are also soluble in alcohol, but for obvious reasons turmeric has been traditionally consumed with a fat.
In the regional cuisines of India, turmeric is included in a cooked dish that contains a fat and also a compound to slow its rapid clearance from the body. In India, that compound has most often been the capsaicin in chilli peppers and to some extent also, the cumin that is present in many Indian recipes. Interestingly, the ubiquitous 'curry powder' contains both turmeric and cumin, and both spices are present in many Indian recipes. However, the piperine in black pepper (Piper nigra) or long pepper (Piper longa) is more potent than either capsaicin or cumin, allowing the use of smaller amounts and making it more palatable to most westerners.
Despite the widespread claims, neither piperine nor any other similar compound has a significant direct effect on the absorption of curcumin in the small intestine. The single trial which made the oft-repeated claim of '2000% improvement' in absorption was poorly designed and has never been replicated. The 2000% figure just keeps getting passed around and repeated. What piperine does is to slow the metabolism of curcumin in the small intestine. Thus, intact curcumin is available for a longer period of time to be absorbed if a lipid is present, and of course, in that case, more is indeed absorbed. But it is not solely because of a direct effect of piperine on the intestine. What piperine does affect, however, is the 'brush border' of the intestinal lining, causing it to expand and provide more surface area for absorption. This will certainly result in increased absorption if a fat is present to allow significant absorption at all. But without the fat, absorption is dependent on the minimal amounts of short-chain fatty acids produced by intestinal bacterial, which is not a significant source of fat for monogastric species (those with only one stomach).
A now common turmeric preparation is 'golden paste,' made popular by Dr. Doug English, an Australian veterinarian. Golden paste is formulated by cooking whole turmeric powder in water and then adding a healthy fat and a small amount of freshly ground black pepper. This is analogous to the way turmeric is used in India, with similar results to those seen in the consumption of turmeric in India.
What are those results, particularly in regard to Lyme disease? Turmeric is best known for its anti-inflammatory benefits, but paradoxically, an anti-inflammatory response may not be the best initial reaction to Lyme. The research in Lyme arthritis and Lyme neuroborreliosis strongly indicates that anti-inflammatories can reduce both the bacterial burden and the physical damage. But these conditions are present only after a well-entrenched infection. The claim for benefit from an anti-inflammatory compound in the first hours and days of infection rests on less firm ground. After studying many research papers and communicating with some of the papers' authors, my conclusion is that potent anti-inflammatories such as turmeric are not appropriate during the initial phase of an infection. Of course, that presumes that the infected person is aware of the tick bite immediately. That is often not the case and the early infection progresses to disseminated Lyme before symptoms are noticed. When that happens, an effective use of whole turmeric can be beneficial.
The Initiation and Progression of Lyme Disease
The first step in a Lyme infection takes place in the gut of the tick, before the spirochetes ever come in contact with the new host. Ticks are often thought of as mere vessels, or carriers, for the pathogens. But the spirochetes actually change the expression of some of a tick's own genes, to facilitate survival in the tick prior to infection of the next host [2]. When tick larvae feed from an infected host, Borrelia spirochetes migrate to and remain in the ticks' midgut. They change how several of the ticks' genes are transcribed. For example, Borrelia upregulates a gene that encodes a particular protein called PIXR. One function of PIXR in the tick gut is to prevent gram-positive bacteria such as Staphylococcus aureus from forming protective biofilms. These biofilms also provoke an immune response against the bacteria. By upregulating PIXR and inhibiting the growth of other bacterial populations, it appears that Borrelia benefits both from decreased demand upon energy resources and decreased immune response from the tick host. [3,4]. Other tick genes are affected, but those details are beyond the scope of this discussion. The intention was simply to make the point that the Borrelia spirochete is not a passive organism being transported by ticks, but an active player with its own defense and survival mechanisms.
Ticks progress from larval stage to nymphs to adults, with a blood meal and a molt in between each stage. The Borrelia spirochetes are actively involved at each stage, changing their gene expression to meet the changing environments, and changing that of the ticks as well. To mention another one of those changes, a protein on the outer membrane of the spirochete, OspC (outer surface protein C), increases in levels at the time of the blood meal preceding the molt from larva to nymph. This facilitates the spirochetes' migration to the tick's salivary glands, where it can transfer at the next feeding into a new host [5]. Conversely, however, after the post infection period in a new mammalian host, the expression of OspC is greatly reduced. Mammals have a strong antibody response to OspC, so reducing its expression helps Borrelia evade attack from the new host's immune system.
Once in the bloodstream, Borrelia is able to attach itself to the walls of the blood vessels, allowing it to progress toward specific targets. This was described in an illuminating article in the online Open Access journal, Cell Reports [1]. (Use of the image below licensed by CC BY-NC-ND 4.0.)
Biomechanics of Borrelia burgdorferi Vascular Interactions
If the thought of bugs "crawling" along the insides of your blood vessels gives you a shiver of distaste, you're not alone. It's bad enough to think of them being swept throughout the body via the bloodstream's ebb and flow. The idea of them being in any sense self-directed is emphatically unpleasant. The spirochetes are not even remotely sentient, of course--they respond to chemical signals in their environment in a manner pre-determined by their DNA.
Borrelia moves through the blood vessels in the capillary bed and into the tissues. The spirochetes are small enough to fit between the endothelial cells that line the blood vessels and move throughout the extracellular spaces into the organs and other tissues. Their structure, a spiral shape with flagella located inside their outer membrane, allows them to move through the viscous environment outside the organs and the structural elements of the body. The collagen around our joints and the connective tissues that hold organs in place are examples of the "extracellular matrix' in which rod-shaped or spherical bacteria are unable to move easily, but which spirochetes can readily navigate [21]. In addition, in most bacteria with flagella, the flagella themselves provoke an immune response. Because Borrelia's flagella are wholly contained between the outer and inner cell membranes, they're hidden from the host's immune system.
Typical symptoms in the first days after a bite are the rash called erythema migrans (or 'bullseye' rash) and also symptoms that are often interpreted as flu, though not everyone experiences both of these and some experience neither one. The rash is unlikely to be visible on the skin of furred animals, and may also be difficult to distinguish in dark skinned humans. Its usefulness is thus limited, though it does provide a definitive diagnosis for Lyme when present and visible.
Up to this point, the prior consumption of turmeric may not be significant in terms of resisting or fighting the Borrelia spirochete. But now the new host has some (probably small) number of invaders at the site of the tick bite. Within about 48-72 hours, they will begin to disseminate out into the new host's tissues. Different strains of the Borrelia spirochete favor different organ systems, though they can all attack any part of the body. But B. burgdorferi sensu lato strictu, the strain most often found in the United States, typically causes arthritis, neurological damage and cardiac damage. B. afzelii, the strain found in some parts of Europe often exhibits cutaneous symptoms such as lichen sclerosus and Acrodermatitis Chronica Atrophicans [6]. B. garinii often presents with Bannwarth Syndrome in Europe, though that has been found in the US as well with B. burgdorferi, as far back as 1983 [7,8,9].
This is the point at which the use of turmeric (or any anti-inflammatory) has to be considered carefully. Trials have shown that mice deficient in a compound called Toll-like receptor 2 (TLR2) had a greater burden of spirochetes than those who were not deficient. TLR2 is one of a group of Pattern Recognition Receptors (PRR's) that enable the innate immune system to recognize pathogens and dispatch macrophages and other members of the body's defenses to fight them off. As it happens, turmeric is a TLR2 inhibitor. That's one of the ways it reduces chronic inflammation. The sixty four thousand dollar question is whether its anti-inflammatory mechanism also inhibits the human body's immune system response to the Borrelia spirochete.
Papers on Lyme disease and inflammation have focused mostly on the chronic inflammation present in Lyme's neurological symptoms and arthritis. But those are symptoms of an established Lyme infection, at least two weeks beyond the point of the original tick bite. An acute inflammatory response to initial infection may be desirable, to rally the body's innate immune system.
Borrelia protects itself with an anti-inflammatory strategy, in fact. One anti-inflammatory cytokine, IL-10, is upregulated by Borrelia in mice in the first hours of an infection, which results in a decreased immune system response [10,17]. Human immune system responses to Borrelia have been demonstrated to be very similar to that of the mouse, and it seems reasonable to assume that human IL-10 production has the same effect on the early Borrelia infection in humans. Turmeric, unfortunately, is a strong stimulator of IL-10 production [18]. IL-10 deregulation is known to play a role in many inflammatory diseases (osteoarthritis and rheumatoid arthritis, for example, as well as inflammatory bowel disease), which may explain why turmeric has been found so beneficial with them [19]. But its ability to stimulate IL-10 production may work against the new Borrelia human or animal host, by inhibiting the immune system's immediate attack on the spirochetes.
So a very important question is "How to deal with a suspected new infection?"
One obvious response would be an immediate course of an appropriate antibiotic, but many family practitioners will not agree to prophylactic antibiotics. In addition, there is considerable controversy over whether the typical small dosage of prophylactic antibiotics is even helpful.
A 2014 study of Borrelia identified a roughly three-day period during which there is a population "bottleneck" for proliferation of the spirochetes [12]. It is not clear that this is significant after a tick bite, however. The "bottleneck" was identified when very large numbers of spirochetes were injected into mice, a different situation from the several hundred that are typically found at the site of an actual tick bite. But the roughly three-day period before significant dissemination takes place apparently does also occur after a tick bite as well as after spirochete inoculation. During this period, the spirochetes do not move beyond the initial site of infection. It seems likely that this brief time of vulnerability to antibiotics may account, at least in part, for the persistent claim that Lyme can be "cured" with a two-week course of doxycycline or tetracycline. As many know from unhappy experience, however, that time frame is often well in the past when symptoms begin to be noticed. But assuming that one sees a tick in situ and wants to take prophylactic action, what might be effective? The beginning of the answer requires that we look at how our immune systems react to the presence of Borrelia.
The Immune System Response to Borellia
Mammals have two immune systems. One develops as the fetus grows in the uterus, the innate immune system. This immune response is not dependent on prior infection or vaccines or any of the responses that people typically think of when the immune system is mentioned. It "knows" what doesn't belong in the body without requiring prior exposure to it. This basic information is inherited along with all the other mammalian characteristics, though there are variants between species and between ethnic populations in humans. Pattern Recognition Receptors were mentioned in an earlier paragraph; those are part of the innate immune system. They identify things which are inimitable to our bodies, and send out cells, called phagocytes, to destroy them (there are multiple types of phagocytes, depending on what part of the body they arise from and are typically located in). Other parts of the innate immune system may participate in the response to Borellia, but phagocytes appear to play the most significant role.
The process of pathogen destruction by phagocytes is called phagocytosis. The phagocytes engulf the pathogens-in this case the Borrelia spirochetes-and break them down into fragments. This process has actually been visualized with high power microscopy and is known to be very effective. Why then don't the phagocytes destroy all the spirochetes? Multiple mechanisms appear to be at work in the innate immune system's response to Borrelia.
The first is the response to "outer surface proteins," as mentioned earlier. The protein OspC is present, as the name implies, on the outer surface of the spirochetes' membranes, where it is thus "visible" to innate immune system components. Research on mice established that mutant spirochetes which do not express OspC are quickly cleared at the site of infection by the murine (mouse) immune system. The mutant spirochetes are not able to infect the mice with Lyme disease. [11]. In fact, tests showed a 70% greater uptake of the mutant spirochetes by macrophages (a type of phagocyte) than 'wild type' spirochetes. In other words, the absence of OspC renders the Borrelia spirochetes more vulnerable to attack and destruction by the individual's innate immune system.
At first reading, this would seem to contradict the earlier statement that Borellia downregulates the expression of OspC to evade a new host's immune response to it. However, in the immediate hours after infection (possibly even the first few days), OspC expression remains high. It drops after that point, when the acquired immune system begins to take over.
OspC has an anti-phagocytic property that interferes with phagcytosis. Research has not established the specific method of protection provided to the spirochetes, but theorized that it might change the phagocytic receptor profiles so the phagocytes no longer recognized the spirochetes [11]. Alternately, the authors suggested, OspC may shield compounds in the spirochetes from interacting with phagocytes. Once the immediate infective period has passed, OspC is strongly down-regulated, because it induces a potent response from the adaptive immune system (more on that in the next paragraphs). But during the immediate hours or even days after infection it is part of the spirochetes' defense arsenal.
An additional response to Borrelia occurs when spirochetes are ingested by phagocytes. One surprising discovery (with a particular type of mononuclear phagocyte called a monocyte) is that Borrelia spirochetes are able to invoke the death (apoptosis) of the monocytes that ingest them [13,15,16]. In most diseases, the pathogen is broken down within the phagocyte and its degraded elements are used as nutrients for the phagocyte itself, which is then able to go on and ingest additional pathogens. In the case of Borrelia, however, the internalization and fragmentation of the spirochete appears to enable signaling events that result in local inflammation and the eventual death of the phagocyte.
If one wanted to be fanciful, this might be represented as the dying spirochete sending out an SOS that results in the death of its killer. In fact, however, previously heat-killed Borrelia taken up by monocytes were also able to induce these signaling events, though at a much lower level. This seems to fly in the face of the common assumption that dead is, well--dead. We know, of course, that some cellular activity continues after the official death of multicellular organisms. But biological signaling from the remnants of killed cells seems like something out of science fiction (as it turns out, though, it is not so unusual after all [14]).
These two protective mechanisms--the ability to avoid phagocytosis to begin with and the subsequent death of phagocytes that have consumed and killed spirochetes--may help to explain why phagocytes are not able to completely destroy all the spirochetes at the site of an infection. The anti-inflammatory effect of IL-10 upregulation further dampens the innate immune system's response (though IL-10's role in disseminated Lyme infection is a positive one) [20].
Very early in the infective process, the adaptive, or "acquired," immune system comes into play. This response does depend on the innate immune system's exposure to a pathogen, along with a "learned" response to compounds on the outer surface of the pathogens.
A typical progression from innate to adaptive immune system response begins with phagocytosis. The engulfed pathogen is enveloped in a membrane called a phagosome, within the phagocyte. Other cell bodies, called lysosomes, contain enzymes which can break down molecular bonds. When the lysosome's membrane contacts a phagosome membrane, the lysosome's enzyme contents are ejected into the phagosome, and break down the pathogen contained inside it. In several types of phagocytes, molecules called "major histocompatibility complex-II," or MHC-II, acquire fragments of the pathogen and "present" them on the surface of the cell. Here they are visible (in the chemical sense of visibility) to cells from the adaptive immune system such as T cells and B cells. When those cells encounter the antigens again, they "recognize" them from the previous exposure and are able to mount an immediate response to them.
(Anyone who has studied the immune system knows what a minimal explanation this is, but the intention was only to present the fundamentals before going on to how the adaptive immune system deals with Lyme disease, and how turmeric can be involved in amelioration of symptoms.)
Again, this is the typical progression from the rapid-response innate immune system to the long-lived adaptive immune system. The human body mounts a robust immune response to Borrelia, though it is not sufficient in itself to clear a Borrelia infection. However, this is not fundamentally different from the response to other pathogens. The value of the innate immune system is its very rapid reaction to the presence of pathogens. The adaptive immune system then normally takes over and manages the long term response.
But as in almost every other aspect, Borrelia is not typical. As mentioned earlier, the degradation of spirochetes triggers a sequence of signaling events [22]. Phagosomal signaling provokes the production of inflammatory cytokines, which then activate adaptive immune system members (T and B cells). For example, interleukin-6 (IL-6), one of these cytokines, activates T helper cells and induces Th17 differentiation. But IL-6 participates in many other immune system regulatory functions, and chronic excessive levels can lead to increased vascular permeability, a phenomenon seen in the synovial tissues of rheumatoid arthritis (RA), and which may explain in part the frequent misdiagnosis of Lyme infection as RA.
Phagocytosis also results in the production of interleukin-10 (IL-10), an anti-inflammatory cytokine which is able to inhibit the immune system's inflammatory response, and thus reduce its ability to clear the spirochetes at the site of the tick bite [22].
Dendritic cells (DC's) found in the skin are another type of innate immune system cell, and these are normally the first ones to encounter Borrelia at the time of a tick bite. Phagosomal signaling activates DC's, setting into motion a sequence of pro-inflammatory cytokines which recruit other immune system cells. But again, Borrelia-activated DC's also express IL-10, which down-regulates the immune system response.
Once adaptive immune system cells are activated, more abnormalities are found. For example, in uninfected individuals, lymph nodes typically contain roughly equal numbers of T and B cells in clearly defined and organized zones. In Borrelia-infected mice, lymph nodes downstream from the bite location contained exceptionally high numbers of naïve B cells, accompanied by destruction of the typical T and B cell zones [23]. This is characteristic of the lymphadenopathy seen in many new cases of Lyme disease. T cells were still present, but further research showed that the high population of B cells was independent of T cell presence. The significance of this is that while B cells can be activated directly by bacterial antigens, their specificity and versatility depends in part on being activated indirectly by helper T cells. If those cells are present in far lower numbers than the B cells, then the B cells' response to the pathogen is muted and delayed.
Another feature of normal lymph nodes is the presence of germinal centers. These distinct sites within a lymph node hold mature B cells as they reproduce and specialize into several types. Germinal-center B cells were detected in Borrelia-infected mice at 8-10 days after infection. Their numbers increased to a peak at day 15, although their frequencies (corresponding to how extensively they were specialized) increased for about another week. Beyond that time, germinal center B cells rapidly decreased. The germinal centers themselves were detectable until about day 28. Examination of the lymph nodes on day 28 found them appearing "empty" and "exhausted" [23]. One study showed that B. burgdorferi infection induced type I IFN signaling that increased the proliferation of B cells and disrupted lymph node architecture [33].Without the strong T-dependent germinal centers, mice infected with Borrelia lacked the long-lived "plasma" type of B cell with its permanent memory for pathogen antibodies.
The bottom line is that while the mammalian host is able to mount a strong immune system response to Borrelia, the spirochete employs a wide variety of mechanisms to evade, dilute and fight off that response. Anything that would slow or dampen the immune system response may be unhelpful, and unfortunately that would include any effective form of turmeric. In the three to four week period prior to widespread dissemination of the bacteria, potent and specific antibiotics would seem to be the most effective weapons.
However, since most people are not aware of the infection until after dissemination occurs, turmeric's anti-inflammatory benefits definitely should be employed (as long as there are no adverse interactions from medications in use).
Symptoms of Lyme Disease
The range of complications from untreated or inadequately treated Lyme disease is so wide that it has been dismissed as "all in the patients' minds" by otherwise well meaning and sincere doctors. But there is well-documented research to support each of the major symptom classes, and the underlying mechanisms have all been well-characterized. One factor that confuses diagnoses is the fact that each person tends to exhibit only a small range of the potential symptoms at any given time, so two patients reporting suspected Lyme disease may have an apparently different group of symptoms. Likewise, one patient may exhibit one or two of the symptom classes at one time, and a different group at another time.
Pain, particularly joint pain: This can vary from one individual to another, and may even vary in the same person from one time to another. But the most noticeable symptom is pain in the large joints, often the knees. For some people, the pain may manifest in one joint, resolve in that location, and flare up again in another joint. Muscle pain is regularly reported as well, which has led to diagnoses of fibromyalgia rather than Lyme disease.
Cardiac damage: Cardiac arrhythmias are frequently reported, resulting from spirochete infection of heart tissue. The literature commonly reports arrhythmias only as a symptom of Lyme carditis. However, arrhythmias may be present without diagnostic confirmation of an atrioventricular block.
Although it is not widely reported, some people have experienced coronary artery vasospasm, resulting in angina with its concomitant risk for myocardial ischemia (heart attack). Elevated troponin levels have been seen in some cases, but not all. Nor does every patient show an atrioventricular block. One thing I have not seen mentioned at all is whether vasospasm-induced atrial or ventricular fibrillation may be the culprit in some arrhythmias. Coronary artery spasm is a well-documented factor in ventricular arrhythmias, but I have found no mention in the Lyme disease literature to its possible connection with Lyme. I suspect that is the case, but have no data to confirm it.
Neurological symptoms: Neurological problems include memory loss, difficulty with balance, tinnitus, muscle twitching (especially in facial muscles), difficulty making decisions and other aspects of confusion, trouble learning new educational material, and others. These are sometimes grouped under a general reference to brain fog." But they may be individually present to a lesser or greater degree as well. Bell's Palsy, a type of facial paralysis, may cause facial muscle and eyelid drooping, or may make it impossible to completely close the eye on one side, and may interfere with eating and even speaking.
Fatigue: Other than pain, one of the most debilitating symptoms is the severe fatigue suffered by many Lyme patients. Because Lyme patients usually can not provide any specific cause for the fatigue, it is common for them to be accused of laziness, lack of motivation and other failures. This is especially true for pediatric Lyme patients, where such accusations may result in behavioral problems that would not have been present otherwise.
Ocular involvement: A frequently overlooked group of Lyme symptoms is visual problems. These may be as benign as an increased number of 'floaters,' or more serious, such as 'dry eye' (caused when Bell's Palsy keeps the eyes from closing completely), retinal separation, optical nerve inflammation or uveitis. Many people with Lyme disease are much more sensitive to light than others. One case report stated that Borrelia spirochetes were found in the eye even though the patient tested negative for Lyme [28].
Psychiatric reactions: One of the most troubling aspects of Lyme disease is the extent to which patients have been prescribed psychotropic medications with diagnoses of various kinds of mental illness. The simple fact of being unable to find help with the pain and other symptoms of Lyme disease is depressing in and of itself, of course. But psychotropic medications don't address the symptoms of Lyme disease themselves, only a symptom of those symptoms, so to speak. Even if they were a valid long term response to the emotions provoked by Lyme symptoms, the fact of their prescription often confirms the claims heard by too many Lyme patients--that their symptoms are all in their heads. Even worse, however, is the assumption that emotional and behavioral changes warrant no further action than to write a prescription for an antidepressant or antipsychotic. A Lyme sufferer may thus go for years on a progression of ever more potent medications and combinations of them before learning that their problems stem primarily from an infection that could have been treated with antibiotics. At that point, weaning off the unnecessary medications becomes just one more obstacle to healing from the Lyme itself. This is a particularly distressing situation for children and young adults whose Lyme symptoms may be diagnosed as mental aberrations. They face not only the accusation of mental illness but the physiological burden of psychotropic medications that do little to help their symptoms and nothing to address the underlying infection. It is regrettable that the Lyme community appears to have largely accepted the suggestion that Lyme "causes mental disease." No, it may cause some of the symptoms of mental disease, just as it may trigger the appearance of rheumatoid arthrits, fibromyalgia, multiple sclerosis and any of the other conditions that Lyme can mimic. That is an important distinction.
The foregoing is only a summary. It does not list every symptom a Lyme patient may experience.
How can turmeric affect symptoms of Lyme disease?
1. The presence of Borrelia spirochetes in the major joints (most often the knees, but others as well) triggers infiltration of mononuclear cells (one type of phagocytes) into the synovial tissue of the joints and also provokes the production of inflammatory cytokines. In its effects on cartilage and synovial tissues, Lyme-induced damage resembles that of osteoarthritis. Osteoarthritis was at one time thought to be due simply to mechanical wear and tear on joints, but more recent research has pinpointed the damage caused specifically by inflammatory processes [24]. These are the same processes encountered in the chronic inflammation provoked by the Borrelia spirochetes.
One cytokine found in both osteoarthritis and Lyme arthritis is Tumor Necrosis Factor alpha (TNF-α), a protein that is widely expressed throughout the body. Many trials have shown that the curcumin in turmeric inhibits TNF-α [25]. TNF itself is far more complex than the usual statements about it would suggest, but its basic function is to participate in cell signaling. TNF is produced by the macrophages recruited by Borrelia, but also (indirectly via TLR-2 stimulation) by lipoproteins on the cell surface of the spirochetes themselves. Curcumin inhibits TNF-α, and also the inflammatory products that are provoked by its presence (interkeukin-1ß, interleukin-6, NF-κB and others). In the effective form of golden paste, turmeric has reduced the pain of arthritis both from Lyme infection and from osteoarthritis.
One interesting discovery is that curcumin's anti-inflammatory, antioxidant and neuroprotective mechanisms in the brain depend at least in part on the presence of the TNFR2 receptor for TNF-α. Knockout mice lacking this receptor were not helped by administration of curcumin [26]. Humans, fortunately, do posses the TNFR2 receptor. But the fact that its lack suppressed the benefits of curcumin suggests that curcumin's enhancement of TNFR2 signalling may play a larger role in its benefits for Lyme neuroborrelosis than simple anti-inflammatory effects. This is borne out by research conducted by Wua et al and Gupta et al [29,30].
2. Because the Borrelia spirochetes are small enough to pass through the blood-brain barrier into the brain itself, Borrelia is able to provoke inflammation in the brain and cause cognitive defects (Lyme neuroborreliosis). Curcumin, a small molecule, also can pass through the blood-brain barrier, and thus can address the effects of Borrelia in the brain. TNF-α is also involved in pro-inflammatory processes in the brain.
Another way in which turmeric helps in neuroborrelosis is to inhibit the production of quinolinic acid. Quinolinic acid is produced by the brain's own immune system cells (microglia) and also by other macrophages in the brain as a response to Borrelia. It is an excitotoxin, which interferes with neuron function and can even lead to cell death. One of its effects is to interfere with short term memory, a symptom frequently mentioned in lyme neuroborrelosis. Quinolinic acid is normally present in the brain at nanomolar levels, but in the presence of inflammatory stimuli, l-tryptophan is converted directly to quinolinic acid, significantly increasing its levels. Turmeric's ability to reduce its synthesis may be a significant factor in improvement of the 'brain fog' reported by so many Lyme patients.
3. Turmeric's ability to modulate immune system responses may help with the autoimmune diseases often found along with Lyme disease. One reason Lyme is often misdiagnosed as fibromyalgia and other immune system dysfunctions may be that an over-reactive immune system, repeatedly stimulated by the spirochetes, can invoke symptoms typical of those conditions. Psoriasis and lichen sclerosus are two autoimmune conditions identified with Lyme disease, for example. Anecdotal reports from a 270,000 member turmeric group on Facebook is positive for the effective use of turmeric in both of these conditions.
4. Cardiac damage is likely a primary cause of death from Lyme disease, though it was not recognized as such until recently. Lyme patients who consumed golden paste reported improvement in the frequency of cardiac arrhythmias (or even their elimination). Like beta blockers, which are frequently prescribed in Lyme disease, turmeric is a vasodilator, which can help lower blood pressure and thus the burden on the heart. Its effect as a vasodilator may also explain why it helps with cardiac arrhythmias, if my supposition about vasospasm-induced atrial fibrillation is correct.
5. Lyme disease has been associated with a greater risk of lymphoma, both non-Hodgkin lymphoma and one of its subtypes, mantle cell lymphoma. The association with all non-Hodgkin lymphomas is less certain than with mantle cell lymphoma. A Danish-Swedish [31] case report study found that overall risk of non-Hodgkin lymphoma was not associated with self-reported tick bites or a seropositive status for Borrelia infection. However, when subtypes of non-Hodgkin lymphoma were examined, a greater risk for mantle cell lymphoma was found even in people who did not recall a tick bite, yet tested positive for Borrelia. The curcumin in turmeric has been shown to inhibit all the specific pathways involved in mantle cell proliferation (NF-kappaB and its downstream products COX-2, TNF-α, IL-6 and others)[32].
6. Facial muscle twitching is widely reported in Lyme, sometimes as the specific condition 'hemifacial spasms.' Turmeric, consumed as golden paste, has been able to greatly reduce or even eliminate this non-painful but very irritating condition. It can interfere with speaking, with eating and even make it difficult to open the eye on the affected side. Its presence can make the patient reluctant to socialize or even be in public at all.
Bell's Palsy is often reported when it is hemifacial spasms that are actually present. But Bell's Palsy is a regular symptom of Lyme as well, and can contribute to eye problems by making it difficult to close one eye.
This is only a summary of the many ways in which turmeric, consumed in an effective form such as golden paste, can reduce symptoms and improve quality of life for Lyme patients. Additional factors are involved in many cases, such as co-infections with other tick-borne pathogens and existing co-morbidities like diabetes, obesity and cardiovascular disease. Depending on interactions with medications in use, golden paste may not be advisable for every Lyme patient. But where its use is appropriate, the combination of cooked turmeric, a healthy lipid and freshly ground black pepper has made a significant difference to many people. Additional information on the preparation and use of golden paste is available here. Additional information about Lyme disease and the current research into treatment is available on the LymeDisease.org website.
Sources:
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