Amyotrophic Lateral Sclerosis (ALS), also known as Lou Gehrig’s disease, is one of the most devastating diseases of our modern era, but new research is showing that the disease may have a trigger that was not realized before, Borrelia burgdorferi, the bacterium responsible for Lyme disease.
ALS causes gradual motor neuron death, hence its classification as a neurodegenerative disease. It is estimated that at least 20,000 people in the U.S. suffer from this condition and the average life expectancy only is 2-5 years following a diagnosis, although about 25% of patients live longer than 5 years. Thanks to funds raised from the Ice Bucket Challenge in 2014, researchers have discovered a new genetic contributor – a gene called NEK1. While identifying genetic contributors may help lead to more effective treatments, it is only one piece of the puzzle. As the saying goes, “genes load the gun, environment pulls the trigger.” Ignoring the “triggers” limits treatment options, hinders preventative measures from being explored, and over-simplifies the complexity of chronic disease. One of the triggers that have been implicated in ALS is chronic infection with various pathogens, one example being B. burgdorferi – the bacterium responsible for causing Lyme disease.
Although this finding and its clinical implications are controversial, it deserves attention for a couple of reasons. For one, misdiagnosis is serious business, especially when recovery rates are higher for the disease being overlooked than for the one being given (Lyme disease is more treatable than ALS). There have been thousands of case reports of patients with ALS that end up having Lyme disease and subsequently improved following antibiotic treatment. Left untreated, Lyme disease can infect and cause damage to the central nervous system. CNS infection with B. burgdorferi is known as neuroborreliosis. Symptoms of Lyme disease and ALS can be overlapping, particularly in the early stages of ALS. These include muscle pain or weakness, muscle twitching or cramps, loss of coordination, poor concentration or other cognitive changes, and behavioral changes such as irritability. Alternatively, the Lyme infection works epigenetically to turn on genes that cause ALS and/or turn off genes that suppress it.
Another reason the link between Lyme disease and ALS should not be ignored is that there are multiple studies documenting the presence of certain bacterial, viral, and fungal infections in ALS patients. It is not just speculation. A review article published just this year in Current Topics in Medicinal Chemistry mentions the Halperin study, which found that 50% of ALS patients tested positive for B. burgdorferi compared with 10.5% of controls. On the other hand, a larger-scale study published this year in the European Journal of Neurology found no association between borrelia antibodies and ALS. However, one of the main problems with this study (and others that seek to disprove a possible link), employ testing methods (antibody testing) that are not used for the diagnosis but rather for the use of prevalent studies. This two-tier test has been shown to miss up to 80% of Borrelia burgdorferi. Accuracy is largely dependent on the patient mounting a proper antibody response and yet chronically ill patients often have immune dysregulation that results in antibody responses that do not follow the normal pattern. There are also other concerns with this type of testing, which goes beyond the scope of this article. DNA-based testing, such as polymerase chain reaction (PCR) methods are specific (if positive, it is a true positive result) but not very sensitive (as it misses a high percentage). This same review article includes a case study of a patient with an ALS-like illness who tested positive for Lyme disease using PCR.
It is worth noting that other infections have been linked to not only ALS but also to other neurodegenerative diseases such as Multiple Sclerosis and Alzheimer’s disease. It is well-established that pathogens can cause neurodegeneration via the deposition of misfolded protein aggregates, oxidative stress, deficient autophagic processes, synaptopathy, and neuronal death. The authors of the review article postulate that these mechanisms combine with things like aging, metabolic disease, toxins, EMF’s, and genetics to trigger neurodegenerative disease. Even if these infections are more opportunistic than they are causative, they are still linked to morbidity and the progression of disease and therefore should be addressed.
Layperson analyses, case reports, and anecdotal stories have brought to light other fascinating arguments regarding the relationship between geographical patterns of the occurrence of Lyme disease being similar to that of ALS and stories of recovery from ALS when treated for Lyme. Meanwhile, the research is still trying to catch up. Many government agencies and physicians have been quick to dismiss the link between ALS and Lyme disease. This is unfortunate since the best researchers and clinicians are those who keep an open mind and thoroughly investigate all avenues. If ALS is essentially a death sentence, don’t we owe it to those suffering to spend research dollars investigating all the proposed mechanisms and the possible interplay between them? We think so!
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