Can HBOT or plasmapheresis truly eliminate Lyme disease without antibiotics? While both therapies have intriguing mechanisms, their effectiveness as standalone treatments remains unproven. This in-depth analysis reviews their strengths, limitations, and role in Lyme care.
Introduction
Lyme disease, caused by the spirochete Borrelia burgdorferi, often poses challenges in treatment due to the pathogen’s ability to persist in the host. Even after antibiotic therapy, a subset of patients experience ongoing symptoms (sometimes termed chronic or persistent Lyme disease). A proposed explanation for persistence is that Borrelia can evade immune clearance by sequestering in immune-privileged or low-perfusion tissues. Electron microscopy studies have shown that B. burgdorferi may literally “hide” within collagen fibers of connective tissue or inside host cells. In such niches – e.g., collagen-rich joint cartilage, ligaments, brain or nerve tissues behind the blood-brain barrier – the bacteria are less accessible to immune cells and systemic antibiotics.
This biological context has spurred interest in unconventional treatments like hyperbaric oxygen therapy (HBOT) and plasmapheresis (therapeutic plasma exchange) as standalone approaches, on the premise that they might reach or affect Borrelia in these protected reservoirs. This report critically examines the scientific rationale and available evidence for HBOT and blood filtration (plasmapheresis) as independent treatments for Lyme disease. We focus on the biological plausibility of these methods in eradicating or suppressing B. burgdorferi dwelling in connective tissues, central nervous system, joints, and other immune-privileged sites. We also distinguish realistic potential benefits from speculative claims, scrutinizing the depth and quality of supporting literature (ranging from in vitro studies and animal data to clinical trials and case reports). Importantly, we assess whether these therapies show evidence of efficacy on their own (without concurrent antibiotics), and maintain a critical, evidence-based tone throughout.
Borrelia Persistence in Immune-Privileged Tissues
B. burgdorferi has evolved multiple strategies to evade host defenses and persist. One key mechanism is physical sequestration in locations where immune surveillance and drug penetration are limited. Researchers have observed that Lyme spirochetes can bind to and burrow within extracellular matrix components like collagen and decorin in connective tissue. By lodging in collagen-rich matrices (e.g., cartilage, tendons) or even inside host cells (such as synovial lining cells in joints), the bacteria become less accessible to antibodies, phagocytes, and complement. These tissues often have lower blood flow and oxygen tension, creating a relatively protected microenvironment. Indeed, connective tissue is considered a “privileged site” for Borrelia, where the organism may persist despite an otherwise competent immune response.
Similarly, when Borrelia invades the central nervous system, it resides behind the blood-brain barrier, further shielding it from immune attack and many antibiotics. This propensity to inhabit immune-evasive niches contributes to treatment difficulties. It has been suggested that joint tissues can serve as a long-term reservoir for B. burgdorferi in infected hosts. Notably, spirochetes have been visualized nestled between collagen fibrils in connective tissue, effectively hiding from immune recognition. Such localization also correlates with areas of low oxygen tension – for example, deep within avascular collagenous tissue – which may favor Borrelia survival since the spirochete is microaerophilic.
This biological insight underpins the hypotheses behind hyperbaric oxygen therapy and plasmapheresis: HBOT aims to flood tissues with oxygen to kill or inhibit the microbe, and plasmapheresis aims to remove circulating inflammatory factors or microbial products that the immune system cannot reach in tissues. In the following sections, we dissect how plausible these approaches are in targeting Borrelia in its strongholds, and review what evidence exists for their efficacy as standalone treatments.
Hyperbaric Oxygen Therapy (HBOT) for Lyme Disease
Mechanistic Rationale and Biological Plausibility
Hyperbaric oxygen therapy involves breathing nearly 100% oxygen at elevated atmospheric pressure (typically 2 to 3 ATA) inside a pressurized chamber. These conditions greatly increase the amount of oxygen dissolved in blood plasma and drive oxygen deeper into tissues than under normal conditions.
The rationale for applying HBOT to Lyme disease stems from Borrelia’s sensitivity to high oxygen levels and the hypothesis that pressurized oxygen can penetrate into low-perfusion tissues where the bacteria reside. Laboratory observations support this mechanism: in vitro, B. burgdorferi loses infectivity when exposed to ambient atmospheric oxygen (~21% O₂, ~160 mmHg), whereas it remains viable under low oxygen (4% O₂, ~30 mmHg). Notably, ~30 mmHg is about the normal oxygen tension in peripheral tissues, suggesting that Borrelia may thrive in the low-O₂ niches of the host. By contrast, during HBOT a patient breathing pure O₂ at 2.36 ATA can achieve tissue oxygen levels around 300 mmHg – an order of magnitude higher than usual.
This super-oxygenation could directly harm B. burgdorferi, which appears to be vulnerable to elevated O₂ concentrations. Crucially, hyperbaric oxygen can diffuse into areas with limited blood flow. Unlike oxygen carried bound to hemoglobin (which is constrained by perfusion), dissolved oxygen in plasma under high pressure can permeate into edema, biofilms, and avascular tissues to some extent. Researchers have posited that hyperbaric treatment might succeed where antibiotics falter: for example, fibroblasts in connective tissue can shelter spirochetes from antibiotics, but oxygen under pressure will still saturate these tissues (even crossing the blood-brain barrier).
Thus, HBOT could potentially reach Borrelia in collagen matrices, joint cartilage, or CNS locales that antibiotics have trouble penetrating. The biological plausibility is that sustained hyperoxia might either kill the bacteria outright or enhance the host immune response in those regions (oxygen can boost phagocyte activity and tissue healing). Additionally, anecdotal reports note Herxheimer reactions (an inflammatory response to microbial die-off) during HBOT, hinting that bacterial killing may be occurring. Taken together, the mechanistic reasoning for HBOT in Lyme is moderately sound: B. burgdorferi is a microaerophile, and raising tissue oxygen to supraphysiologic levels could suppress or eliminate it in places it normally hides.
Clinical Evidence from Trials and Case Studies
Despite the theoretical rationale, scientific evidence for HBOT in Lyme disease is limited and not yet conclusive. No large randomized controlled trials have been published, but several case series and reports suggest potential benefits. The most oft-cited data come from an observational trial at Texas A&M University in the 1990s led by Dr. William Fife. In that series, 91 patients with chronic Lyme disease underwent a course of HBOT (between 10 and 133 sessions per patient at ~2.4 ATA for 60–90 minutes each). Many of these patients had longstanding symptoms despite standard antibiotic treatments. The reported outcomes were promising: approximately 84.8% of treated patients showed a significant improvement or resolution of symptoms, as measured by symptom score reductions. Symptom severity scores fell dramatically (average score dropping from 114 pre-HBOT to 49 post-HBOT on a standardized scale). Patients experienced improvements in cognitive function, pain, fatigue, and neurological symptoms, with about 70% maintaining lasting benefit at follow-up. Such results, albeit uncontrolled, indicate that HBOT can produce measurable clinical gains in a majority of patients.
Notably, nearly all patients in Fife’s cohort experienced a Jarisch-Herxheimer reaction early in the HBOT course (within the first week), consistent with a spirochetal die-off effect. This lends credence to the idea that HBOT was impacting the bacteria. However, it must be emphasized that in this trial, most patients also continued on antibiotics during HBOT, so HBOT was not strictly a standalone treatment in all cases. A subset (about one-third) were off antibiotics, and at least one patient who had been antibiotic-free for years still improved on HBOT alone, but the lack of a control group makes it hard to discern HBOT’s independent effect. Moreover, this study was not published in a peer-reviewed journal at the time (it is described in conference proceedings and white papers), so the data should be viewed with caution.
Additional evidence comes from small-scale reports. A 2014 case report from Taiwan documented a patient with chronic Lyme symptoms (persistent joint pain, neuropathy, memory issues despite prior antibiotic therapy) who underwent thirty 90-minute HBOT sessions. The patient experienced notable relief: after HBOT, his joint pain, muscle twitching, sleep disorder, extremity numbness, and short-term memory problems had all resolved. This improvement was attributed to HBOT, suggesting it can ameliorate chronic Lyme symptoms in at least some cases. Importantly, the report lacked long-term follow-up, so it is unknown if the benefits were sustained.
Another published case series in 1998 (by Freeman et al., as referenced in Lyme disease conference literature) similarly found that a majority of chronic Lyme patients improved with HBOT, especially in neurologic symptoms like confusion and fatigue. However, that too was an open-label series without a control.
On the flip side, more recent patient-reported data paints a mixed picture. In the MyLymeData project (a large Lyme patient registry), 347 patients who tried HBOT reported only a 22% perceived effectiveness rate. Some patients noted moderate to severe side effects from the therapy as well. This suggests that in broader practice, HBOT might not be as universally impactful as early small studies implied – or that only a subset of patients respond dramatically, while many see little change. It underscores the need for controlled trials to truly quantify HBOT’s benefit in Lyme.
In summary, the evidence base for HBOT in Lyme consists of encouraging but preliminary findings. Mechanistically, it makes sense that high-pressure oxygen could reach and stress Borrelia in hypoxic niches. Clinically, case reports and series document symptom improvements, and the occurrence of Herxheimer reactions under HBOT suggests a genuine antimicrobial effect. Yet the lack of randomized trials or long-term follow-ups means we must be careful: these results could be influenced by placebo effect, concomitant treatments, or publication bias toward positive outcomes.
At present, HBOT remains an investigational adjunct therapy for Lyme disease – it is not FDA-approved for this indication, and mainstream guidelines consider the evidence insufficient. The realistic potential is that HBOT might alleviate symptoms and perhaps reduce bacterial load in certain tissue compartments, but it is unproven that HBOT alone can reliably eradicate B. burgdorferi from a human host.
Blood Purification via Plasmapheresis for Lyme Disease
Mechanistic Rationale
Plasmapheresis, or therapeutic plasma exchange (TPE), is a procedure that filters a patient’s blood to remove and replace the plasma component. In practice, blood is drawn, the plasma (which contains antibodies, immune complexes, cytokines, and other soluble factors) is separated and discarded (or purified), and then the cellular blood components are returned with replacement fluids. The conceptual rationale for plasmapheresis in Lyme disease is fundamentally different from HBOT. Rather than targeting the bacteria through a direct toxic effect, plasmapheresis aims to remove inflammatory or pathogenic factors from the circulation.
In severe or persistent Lyme—especially post-treatment Lyme disease syndrome—some hypotheses suggest that symptoms may be driven by immune dysregulation, such as autoantibodies, persistent immune complexes, or residual bacterial antigens that continue to provoke inflammation. By filtering the plasma, plasmapheresis can eliminate these circulating elements and potentially reduce inflammation or break immune feedback loops. This immunomodulatory approach is standard in certain autoimmune and neuroinflammatory diseases (e.g., Guillain-Barré syndrome, myasthenia gravis).
However, Borrelia burgdorferi resides predominantly in tissues, not in blood, especially in late-stage disease. Therefore, plasmapheresis is not expected to remove substantial amounts of live bacteria. Its plausible benefit would instead come from modifying the immune response: (1) clearing excess cytokines or antibodies contributing to neuropathy, arthritis, or fatigue; and (2) possibly alleviating autoimmune mechanisms triggered by infection. The therapy is not bactericidal, and thus not aimed at eradicating Borrelia directly.
Evidence from Clinical Cases and Studies
The use of plasmapheresis in Lyme disease is limited to case reports, with no clinical trials or large studies. The most compelling evidence arises from cases of neurological Lyme disease with autoimmune features. For instance, Çelik et al. (2015) described a 15-year-old with Lyme neuroborreliosis who developed acute cerebellar ataxia and motor weakness unresponsive to IV antibiotics and IVIG; after several rounds of plasmapheresis, the patient achieved full neurological recovery. Similarly, Elleuch et al. (2023) reported a 4-year-old boy misdiagnosed with Guillain-Barré who had Lyme-associated paralysis; his symptoms improved significantly only after plasmapheresis was initiated.
In both cases, the rationale for plasmapheresis was the likely presence of autoimmune or inflammatory mediators, not persistent infection per se. These patients also received appropriate antibiotics; plasmapheresis served as an adjunct to treat immune complications that persisted after bacterial clearance.
For plasmapheresis, speculative claims are also a risk. Some alternative and integrative medicine providers promote “blood cleansing” or apheresis-based detox therapies for chronic Lyme disease, implying that filtering the blood can remove toxins or even the infection itself. Scientifically, this is an overstatement. Borrelia burgdorferi primarily resides in tissues—not circulating freely in blood—and there is no clinical evidence that plasmapheresis can eradicate the infection from these reservoirs. The existing peer-reviewed reports where plasmapheresis yielded clinical benefit (e.g., Çelik et al., 2015; Elleuch et al., 2023) involved patients with post-infectious, immune-mediated neurological complications, such as acute demyelinating polyneuropathy resembling Guillain-Barré syndrome. In those cases, plasmapheresis likely helped by removing circulating autoantibodies or inflammatory cytokines—not by acting directly on Borrelia itself. No controlled trials or case series suggest that plasmapheresis alone can cure an active Lyme infection. Therefore, while it may have value in specific immune-mediated complications, it should not be portrayed as a standalone antimicrobial treatment.
Beyond neurology, data on plasmapheresis in other Lyme manifestations (e.g. chronic fatigue, joint pain, cognitive dysfunction) is anecdotal at best. Some medical tourism clinics advertise apheresis for “chronic Lyme detox,” but such claims lack peer-reviewed support and often accompany unproven adjuncts like UV blood irradiation or ozone therapy. Without rigorous studies, the role of plasmapheresis in chronic Lyme remains speculative and potentially misleading when marketed as a curative standalone option.
Evidence from Clinical Cases and Studies
The use of plasmapheresis specifically for Lyme disease has been documented only in a handful of reports, mostly involving severe neurological manifestations. There have been no large trials evaluating plasmapheresis as a primary Lyme therapy, and the available evidence is limited to case reports or small case series.
One recurring scenario in the literature is Lyme neuroborreliosis mimicking Guillain-Barré syndrome (GBS), where patients develop acute nerve paralysis due to Lyme infection. In GBS, which is often autoimmune, plasmapheresis is a standard therapy. Several pediatric Lyme cases have followed a similar approach.
For instance, a 15-year-old patient with confirmed Lyme neuroborreliosis developed acute cerebellar ataxia and motor weakness that did not improve despite four weeks of IV ceftriaxone and intravenous immunoglobulin (IVIG) treatment. This suggested an immune-mediated process not resolved by clearing the infection. Plasmapheresis was then performed, resulting in a complete resolution of the patient’s neurological symptoms. Celik et al. (2015) reported this case and concluded that plasmapheresis can be a useful therapeutic alternative in pediatric neuroborreliosis, likely because it removes the offending antibodies or inflammatory mediators causing neural damage.
In another report, a 4-year-old boy with Lyme-related neuropathy and respiratory failure—initially misdiagnosed as GBS—showed no improvement with IVIG and only partial improvement of limb weakness with antibiotics. After undergoing plasmapheresis, the child’s breathing function recovered, and he was successfully extubated, with overall good neurological recovery. The authors noted that plasmapheresis was effective in this severe pediatric Lyme case and recommended considering it when standard immune therapies fail.
These cases illustrate a pattern: plasmapheresis has been life-saving or symptom-resolving in certain acute neuroborreliosis situations, presumably by halting an autoimmune attack on nerves. Crucially, in all reported cases, the patients also received appropriate antibiotics to treat the infection; plasmapheresis was implemented as an adjunct to address residual neuro-immune damage. While the outcomes were excellent (complete or significant recovery), plasmapheresis was not used in isolation—it was part of a combined strategy for complex cases.
Beyond acute neuropathies, one might ask if plasmapheresis has any role in chronic Lyme or Lyme arthritis. There is scant published data. Lyme arthritis that persists after antibiotics is thought to be due to immune dysregulation (e.g., inflammatory debris or autoimmunity in the joints), but treatment usually involves anti-inflammatory medications rather than plasmapheresis.
There are anecdotal accounts of chronic Lyme patients seeking plasmapheresis at specialized clinics—for example, patients traveling to Germany or Mexico for “blood cleaning” therapies. Some of these centers report improvement in fatigue, cognition, or psychiatric symptoms following a series of apheresis treatments, which they attribute to the removal of cytokines and toxins. However, these claims are not documented in the peer-reviewed literature and often accompany multiple other therapies (such as ozone, UV blood irradiation, or whole-body hyperthermia). Therefore, it is difficult to isolate the effect of plasmapheresis in those contexts.
The most plausible evidence for plasmapheresis in Lyme resides in the neurological cases discussed. A review of pediatric Lyme neuroborreliosis cases noted that plasmapheresis, especially when initiated early, shortened the course of illness and improved outcomes in patients with Lyme-associated paralysis who were not responding to antibiotics alone. Mechanistically, this makes sense because the neurological deficits in those cases were likely immune-driven (similar to GBS). Plasmapheresis in these instances acts just as it would in non-Lyme GBS—by removing pathological antibodies, it allows nerves to recover.
It is important to emphasize that in none of these reports is plasmapheresis suggested as a stand-alone cure for the infection. Rather, it is portrayed as a valuable adjunct or salvage therapy for complications of Lyme disease. For example, after antibiotic treatment of the infection, if severe inflammation persists, plasmapheresis can “reset” the immune system by clearing the inflammatory milieu.
Overall, the evidence for plasmapheresis in Lyme is extremely limited and situation-specific. There is no indication from studies that plasmapheresis can eradicate Borrelia burgdorferi from connective tissue or dormant niches. What it can do, in realistic terms, is ameliorate the immune consequences of infection. In acute neuroborreliosis with autoimmune features, it has demonstrated clear benefits in case reports. In chronic Lyme disease with primarily subjective symptoms, the benefits are much more speculative—there is a lack of rigorous data, and any positive reports are anecdotal.
Given that plasmapheresis is an invasive, hospital-based procedure with potential risks (infection, electrolyte disturbances, etc.), its use for Lyme is generally reserved for only the most severe refractory cases. The scientific integrity of using plasmapheresis as a broad Lyme treatment is questionable; it should not be portrayed as a detox panacea or a direct antimicrobial therapy, as there is no evidence for that role.
Discussion: Realistic Potential vs. Speculative Claims
Considering the above, how realistic are HBOT and plasmapheresis as standalone Lyme interventions? Both approaches stem from sound theoretical principles – oxygen toxicity to microaerophilic spirochetes in the case of HBOT, and removal of pathogenic immune factors in the case of plasmapheresis. Mechanistically, HBOT appears more directly capable of affecting Borrelia in its hiding places: hyper-oxygenation can permeate tissues throughout the body, and laboratory evidence confirms B. burgdorferi cannot easily survive in high-O₂ conditions. This suggests HBOT at least has the potential to suppress bacterial activity even in collagenous or brain tissues.
Plasmapheresis, by contrast, does not act on bacteria in situ at all – its effect is systemic and indirect, mainly through immune modulation. Therefore, if the goal is to kill or clear Borrelia, HBOT is the more plausible standalone candidate of the two. It’s conceivable that a sufficiently long and intensive course of HBOT could reduce the bacterial burden in a patient (some proponents even argue HBOT might “cure” Lyme by eliminating remaining spirochetes). In fact, in the Fife HBOT series a number of patients went into long-term remission, raising the question of whether their infections were eradicated or at least put into deep dormancy. Still, this was in a context where many also took antibiotics, so drawing a firm conclusion that HBOT alone cured them would be speculative.
When scrutinizing scientific integrity, one must ask: are these therapies being promoted beyond what evidence justifies? There is concern that in the Lyme community (which often includes patients desperate for relief), HBOT and plasmapheresis have sometimes been touted in an overly optimistic manner. For example, hyperbaric oxygen is frequently advertised by private clinics as having “transformative power” or being able to dramatically improve neurological Lyme symptoms. While there is some truth to improved symptoms, the evidence is mostly Level 4 (case series and expert opinion) and not yet validated by controlled trials. The FDA has explicitly stated that HBOT devices are not proven to cure Lyme disease and warns against false claims of cures.
The realistic position is that HBOT may serve as a supportive therapy – possibly accelerating recovery or helping patients who remain symptomatic – but it is not a replacement for antibiotic therapy in treating the infection. Its true efficacy as a standalone is unconfirmed; it might substantially help some patients (especially with neurological manifestations), modestly help others, and have minimal effect in some, as the mixed patient reports indicate.
For plasmapheresis, speculative claims are also a risk. Some alternative medicine circles have promoted “blood cleansing” for chronic Lyme, implying that filtering blood can remove the disease or “toxins” and lead to cure. Scientifically, this is an exaggeration. Plasmapheresis does not remove bacteria from tissues, and there is zero clinical evidence that it can cure an active Lyme infection by itself. At best, it may alleviate symptoms related to immune dysregulation. The cases where it did resolve illness were those where the illness was largely immune-mediated (paralysis due to post-infectious autoimmune reaction). In chronic Lyme patients without such clear immunopathology, plasmapheresis outcomes are undocumented; any claims of general benefit are therefore speculative.
It is telling that no guidelines or Lyme specialists routinely recommend plasmapheresis except in extraordinary circumstances – this indicates the medical community sees insufficient rationale to use it broadly for Lyme. The real potential for plasmapheresis is likely confined to adjunctive use: for instance, a patient with suspected Lyme-triggered autoimmune encephalitis might improve with plasma exchange, but even then it would be done alongside antimicrobial treatment and other immunotherapies.
Another point to critically consider is that neither HBOT nor plasmapheresis addresses Borrelia’s ability to persist in a dormant or cystic form. B. burgdorferi can enter a slow-growing or non-replicating state (round-body forms, biofilm aggregates) under stress. Antibiotics often have difficulty in this scenario, and it’s unclear whether high oxygen levels can kill bacteria that are metabolically inactive. HBOT might be less effective if the spirochetes hunker down in low metabolism cysts – oxygen toxicity requires active metabolism for reactive oxygen species to damage organisms. This nuance isn’t fully studied, so some claims that HBOT “eradicates all forms of Lyme” are not backed by research.
Similarly, plasmapheresis obviously has no direct impact on persister forms; it neither wakes them up nor kills them. Thus any persistent infection would remain unless the immune system, once calmed or reset, can go find and destroy those last hiding spirochetes (a big assumption).
Safety and practicality also temper the enthusiasm for these standalone treatments. HBOT is generally safe but not without risk – pressure-related injuries (ear drums, sinuses), oxygen toxicity (seizures), and claustrophobia are considerations. Dozens of HBOT sessions are costly and time-consuming, and insurance typically does not cover off-label HBOT for Lyme. Plasmapheresis is an invasive hospital procedure, with risks like bleeding, allergic reactions to replacement fluids, and infections via central lines. It’s also very expensive and not FDA-approved for Lyme, meaning insurance won’t cover it in that context.
These factors mean that even if a patient wanted to use these as standalone treatments, access may be limited to those who can afford out-of-pocket experimental therapies or who enroll in research studies. This reality check further underscores that these approaches are not mainstream or validated cures, but experimental avenues.
In sum, a critical appraisal finds that HBOT has a tangible mechanistic basis and some encouraging (if preliminary) clinical evidence, whereas plasmapheresis is more of a niche intervention with a plausibly beneficial immune effect in certain cases. Neither can be considered a proven independent cure for Lyme disease at this time. Claims to the contrary should be met with healthy skepticism.
The most scientifically defensible stance is that HBOT and plasmapheresis might play supporting roles in a comprehensive treatment plan – for example, HBOT to enhance oxygen-dependent killing in conjunction with antibiotics, or plasmapheresis to manage an immune complication. Used in isolation, their ability to resolve an entrenched Borrelia infection is unsubstantiated.
Conclusion
Hyperbaric oxygen therapy (HBOT) and plasmapheresis represent innovative but still experimental strategies in the fight against Lyme disease. Their appeal lies in targeting aspects of Borrelia persistence that conventional antibiotic therapy struggles with – HBOT by flooding hard-to-reach tissues with bactericidal oxygen, and plasmapheresis by extracting deleterious immune factors from the blood. Scientifically, HBOT offers a plausible direct assault on the bacteria’s Achilles’ heel (oxygen sensitivity), supported by in vitro data and cases where patients improved and even herxed under high-oxygen treatment. Plasmapheresis provides an indirect assist by resetting the immune system, which has shown clear merit in Lyme-associated autoimmune neuropathies.
However, a careful evaluation of the evidence reveals that these therapies, used alone, have not been proven to eradicate Lyme disease. HBOT’s evidence is mostly anecdotal or from uncontrolled studies, and while symptom improvements are documented, we lack definitive proof of bacterial clearance or long-term cure without antibiotics. Plasmapheresis’s benefits in Lyme are documented only in narrow circumstances and always alongside antimicrobials, making it more of a rescue therapy than a standalone solution.
Biologically, Borrelia burgdorferi’s talent for burrowing into collagenous niches and evading immune attack means that any standalone treatment must truly reach those sanctuaries. HBOT likely penetrates better than plasmapheresis in that regard, yet even HBOT might not fully overcome the bacteria’s defensive strategies (dormancy, biofilms, etc.). The realistic outlook is that HBOT can complement Lyme treatment by improving oxygen-dependent bacterial killing and possibly aiding recovery in damaged tissues – some patients may feel markedly better, but others might see only mild changes, and a few might not tolerate or benefit from it. Plasmapheresis, realistically, can mitigate immune-driven symptoms; it may hasten recovery from Lyme-induced inflammation (as seen in acute neuroborreliosis cases) but is not a cure for the infection itself.
From a scientific integrity standpoint, it is important to distinguish hope from hype. There is a genuine need for further research – controlled trials to test HBOT in persistent Lyme, and systematic studies on whether any subset of chronic Lyme patients could gain sustained benefit from plasma exchange. Until such data are available, HBOT and plasmapheresis should be regarded as investigational adjuncts. Patients and providers considering them should do so with careful rationale: HBOT might be worth a trial in a patient with refractory neurological Lyme symptoms, whereas plasmapheresis might be considered in a severe, immune-mediated complication of Lyme. Both carry non-trivial costs and risks, and neither is guaranteed to work.
Importantly, neither therapy has robust evidence to supplant antibiotics in clearing an active B. burgdorferi infection – and this report specifically focused on their standalone use, which remains largely speculative. In conclusion, hyperbaric oxygen therapy and plasmapheresis each address intriguing aspects of Lyme disease persistence, but their roles as standalone treatments are not solidly supported by current science. HBOT shows some mechanistic and preliminary clinical promise in reaching Borrelia in oxygen-poor niches and improving patient symptoms, yet it should be viewed as a potentially helpful adjunct rather than a proven cure. Plasmapheresis can be lifesaving in special cases of Lyme-related autoimmunity, but it is not a general Lyme treatment and has no demonstrated ability to eliminate tissue-hidden spirochetes.
Moving forward, a critical, evidence-driven approach is warranted: these therapies should be further studied under rigorous protocols, and until then, any claims of miraculous cures should be met with caution. The real potential of HBOT and plasmapheresis in Lyme lies in a nuanced, adjunctive use targeting specific problems (persistent infection niches or immune aftermath), whereas claims extending beyond that venture into the speculative. As our understanding of Borrelia persistence deepens and more data emerge, we will be better able to define if and how these advanced therapies can fit into the Lyme disease treatment arsenal – with scientific integrity as the guiding principle.