What Causes Lyme Brain (Part 3)

Welcome to What Causes Lyme Brain (Part 3).  In previous weeks we’ve discussed two of the underlying causes of Lyme Brain – the infections themselves; and the inflammatory response. Today we’ll talk about the third causes – neurotoxins. This is an excerpt taken from my upcoming book, Lyme Brain, which is due for release in the fall.

Neurotoxins

One of the ways that Borrelia burgdorferi may act to cause Lyme Brain is by releasing toxins in the brain and central nervous system. Neurotoxins are substances that enter nerve cells through the nerve endings, disrupting the function of the cell along the way. There are many sources of neurotoxins, both infectious and non-infectious in nature. Other examples are heavy metals, molds and Candida, as well as the chemicals that we are exposed to by the industrialized products and services we consume in modern society.

While the concept of a specific neurotoxin produced by Borrelia has been a controversial one, there is at least some research supporting it.

Researchers Cartwright, Martin and Donta presented an abstract at a conference in 1989, which identified DNA in the Borrelia bacterial genome that produces a neurotoxin. This was named BbTox1.[i]

This toxin is cited to be similar in structure to the botulinum toxin, belonging to a family of toxic proteins called zinc endoproteinases. Professors Bradford and Allen in their article in the Townsend Letter for Doctors and Patients (Feb/Mar 2006) claim that the Borrelia toxin works by disabling the neurotransmitter acetylcholine, which would then impact motor functions as well as psycho-emotional states.

In reality, there is fairly limited research in this area. A PubMed search of BbTox1 only revealed one match, a study from Poland citing the existence of BbTox1 but with no new information.[ii]

Another possible mechanism of neurotoxicity secondary to Lyme disease may be increased levels of ammonia. David Jernigan, DC, DNM, an integrative practitioner, founder of the Hansa Center for Optimal Health and developer of Jernigan Neutraceuticals, states that he discovered that the majority of Lyme patients have elevated levels of ammonia in their brain and potentially in other parts of their bodies, too, including the liver.

Here is an excerpt from Dr. Jernigan’s blog:

“It would seem that Bb releases ammonia, which is converted to glutamine by way of the glutamine synthetase pathways, leading to localized swelling of astrocytes (brain cells). This ammonia-induced glutamine accumulation may cause dysfunction of astrocytes, which leads to impairment of vascular reactivity (other than through a decrease in arginine availability for nitrous oxide) and increased production of nitric oxide…It has been reported that many neurological problems are caused by either congenital or acquired hyper-ammonemia.”[iii]

Dr. Dietrich Klinghardt, another well-known integrative doctor who works with many Lyme patients, also believes that ammonia in the brain may play a contributing role in Lyme Brain. He associates ammonia elevations with a condition called Kryptopyrroluria (KPU), aka Hemopyrrolactamuria (HPU). This is a metabolic disorder that impacts one’s ability to metabolize zinc, biotin, manganese, B6 and arachidonic acid.

Brain-related symptoms that may be associated with HPU include:

• Poor dream recall
• Nervousness/anxiety
• Pessimism
• Depression
• Paranoia/hallucinations
• Perpetual disorganization
• Mood swings/emotional lability
• Stress intolerance
• Poor short-term memory
• Substance abuse
• ADHD
• Autism
• Withdrawal

(List taken from reference below)

Dr. Klinghardt estimates the incidence of HPU in Lyme disease patients to be 80% or higher, in patients with heavy metal toxicity (lead, mercury, cadmium, and others) over 75%, and in children with autism over 80%.[iv]

He states that as HPU is treated, high levels of ammonia tend to normalize.

Clearly, biotoxins and neurotoxins seem compelling and may well be a significant and under-acknowledged cause of Lyme Brain. Much more research is needed in this area. In the later sections, which address the treatment of Lyme Brain, we’ll talk about the ways to minimize the effects of these neurotoxins.

[i] Cartwright, M J, S E Martin, and S T Donta. “More Evidence of Lyme Biotoxins: A Novel Toxin (Bb Tox 1) of Borrelia burgdorferi [Lyme disease].” James Schaller, MD, MAR 50 Books & Top Journal Articles. http://www.babesiabook.com/articles/morelymebiotoxinevidence.html (accessed 2015).

[ii] Zajkowska, J M, and T Hermanowska-Szpakowicz. “New aspects of the pathogenesis of lyme disease.” Przegl Epidemiol 56, no. Suppl 1 (2002): 57-67.

[iii] Jernigan, D. “The Alkaline Brain: Lyme Borrelia-induced Hyper ammonemia.” Jernigan Neutraceuticals. 2016. www.jnutra.com/Ammonia.html (accessed 2015).

[iv] Forsgren, S. “Kryptopyrroluria (aka Hemopyrrollactamuria): A Major Piece of the Puzzle in Overcoming Chronic Lyme Disease.” Explore 18, no. 6 (2009).