Biophoton Therapy for Lyme Disease

Increased Immune System Function
Lyme disease (LD), caused by Borrelia burgdorferi sensu lato complex spirochete, is the most prevalent vector-borne illness in the US. Unfortunately, not enough people receive proper diagnosis or treatment of Lyme infection resulting in persistent symptoms for approximately 30% of patients that can last months or even years after antibiotic therapy has been completed.
Even after decades of research, much remains unknown about the causes and progression of Lyme disease (LD), including why some antibiotics fail in certain patients and what leads to post-treatment Lyme disease syndrome (PTLDS) sometimes known as chronic Lyme.
Researchers have several hypotheses as to why some individuals experience persistent symptoms after receiving antibiotics. One possibility is that some spirochetes survive antibiotic treatment but remain inactive, not stimulating an effective host response. Another theory states that many LD patients lack enough immune activation due to factors like having difficulty detecting infectious agents and lacking suitable inflammatory triggers that would trigger proper immune activation responses.
An additional potential mechanism of PTLD involves B cells’ production of autoantibodies to self-antigens through molecular mimicry, epitope spreading or posttranslational or enzymatic modification of themselves; molecular mimicry appears to be most commonly studied among these mechanisms regarding PTLD; however other antigen-independent ones could also play a part.
Linden Hu and colleagues plan to conduct several large multi-institutional studies that will test these hypotheses. One such investigation, for example, involves following individuals diagnosed with LD for at least a year to understand better what happens at a molecular level that allows some individuals to recover while others continue suffering symptoms for extended periods.
Improved Circulation
Biophoton Therapy (also referred to as Biphotonic blood therapy) uses ultraviolet light therapy to assist with circulation and increase oxygen utilization by the body, thus strengthening immunity against germs, viruses, and bacteria while providing more energy to cells that need it.
Borrelia burgdorferi is the cause of Lyme disease, an infection resulting in Lyme neuroborreliosis (LNB). LNB symptoms may include cognitive dysfunction and fatigue that do not go away with standard antibiotic treatments; this may be a result of mitochondrial dysfunction impairing energy production leading to cortical function impairment and subsequent neurological dysfunction.
Non-invasive interventions that use ultra-weak photons to strengthen mitochondrial function and restore cellular energy balance have been found to successfully address neurocognitive deficits associated with chronic Lyme disease. In this case study, one patient with chronic Lyme disease underwent biophoton therapy for four weeks; neurophysiological outcomes were measured via quantitative EEG and event related potentials, lung function measured via spirometry, as well as quality-of-life assessed with the Short Form-36 Health Survey (SF-36) results.
Brain network function was significantly enhanced during biophoton therapy treatment compared to placebo conditions, as demonstrated by normalized posterior alpha peak frequency, decreased attentional dysregulation as measured by the theta/beta ratio and frontal alpha asymmetry scores, faster reaction times on visual/auditory processing ERP tasks, increased EC/EO alpha ratios and improvements in Brodmann area z-scores across sensorimotor and frontal regions.
Pulmonary function saw significant improvement with biophoton therapy and was associated with bioenergetic normalization. Biophoton therapy appears promising for treating persistent neurocognitive and fatigue-related symptoms of post-infectious neurological dysfunctions and warrants further controlled clinical studies.
Biophoton therapy sessions also provided live blood analysis over twelve days that showed biophotons could reverse tissue glycation and reduce cholesterol accumulation in the blood, suggesting that combined ozone and biophoton therapy sessions may increase energy in cells and the entire body, providing more strength to combat against viruses, bacteria and germs that cause chronic Lyme disease symptoms.
Reduced Inflammation
Red light therapy’s near-infrared wavelengths promote cell activity and toxin clearance, helping reduce inflammation in the body. Red light therapy also strengthens immunity, increases energy, and improves sleep quality; its near-infrared wavelengths may even boost immunity against viruses like Lyme disease; ask your Lyme Literate Medical Doctor (LLMD) about the best approach for you!
Lyme Disease (LD), caused by Borrelia burgdorferi bacteria transmitted via tick bites, can produce symptoms that affect both central and peripheral nervous systems. Although most individuals recover with early diagnosis and antibiotic treatment, 10-20% may continue experiencing persistent symptoms months or even years post-therapy – an effect known as Post-Treatment Lyme Disease Syndrome or PTLD.
Studies indicate that PTLD occurs when Borrelia burgdorferi bacteria remain in tissues like joints and nervous system following antibiotic treatment, leading to persistence. While various autoimmune mechanisms have been proposed as possible explanations, molecular mimicry seems most plausible due to the similarities between Borrelia antigens and self-antigens.
However, it has become clear that more complex pathologies exist which may involve host immune response and persistence of the spirochete. Research has also demonstrated that the spirochete can alter their biofilm formation and pathogenicity during antibiotic treatment; for instance, those growing as microcolony (MC) forms or stationary phase (SP) forms with round bodies are more resistant than log phase spirochetes to antibiotic treatment while possessing more of a proinflammatory phenotype than log phase forms.
Inflammation in the CNS has been linked with various symptoms of PTLD, including memory problems and fatigue. A number of proinflammatory cytokines and chemokines, including Interferon-gamma (IFN-) and nitric oxide have been implicated in its development; researchers have proposed a correlation between IFN- production and duration of PTLD; Treg cells have been demonstrated to decrease in patients living with PTLD; therefore combination therapy targeting IFN- and nitric oxide pathways may be required in order to effectively treat PTLD patients.







