PROPOSED LINK BETWEEN LYME DISEASE AND CFS*

[Guest guest]

PROPOSED LINK BETWEEN LYME DISEASE AND CFS*

Rich Van Konynenburg, Ph.D.

Independent Researcher and Consultant

_http://www.lymeinfo.net/methylationblock.html_

(http://www.lymeinfo.net/methylationblock.html)

 

[LYMEINFO NOTE: Dr. Van Konynenburg is a proponent of the Glutathione

Depletion--Methylation Cycle Block hypothesis for the pathogenesis of CFS. To

read

more about this theory and treatment, see the links to the left of this

page.]

Review of the Glutathione Depletion-Methylation Cycle Block (GD-MCB)

Hypothesis for CFS [1]

 

1. The person inherits a genetic predisposition (polymorphisms in several of

certain genes) toward developing CFS. (This genetic factor is more important

for the sporadic cases than for the cluster cases of CFS.)

2. The person then experiences some combination of a variety of possible

stressors (physical, chemical, biological, psychological/emotional) that place

demands on glutathione.

3. Glutathione levels drop, producing oxidative stress, removing protection

from B12, allowing toxins to accumulate, and shifting the immune response to

Th2.

4. Toxins react with B12, lowering the rate of formation of methylcobalamin.

Lack of sufficient methylcobalamin inhibits methionine synthase, placing a

partial block in the methylation cycle.

5. Sulfur metabolites drain through the transsulfuration pathway

excessively, pass through sulfoxidation, and are excreted.

6. A vicious circle is established between the methylation cycle block and

glutathione depletion, and the disorder becomes chronic.

Depletion of glutathione by Borrelia burgdorferi

 

1. Bb requires cysteine for its metabolism [2].

2. Cysteine diffuses passively into Bb from its host, i.e. there is no

active transporter protein [2].

3. Bb uses cysteine in the synthesis of several of its essential enzymes:

Osp A, Osp B, CoASH, a hemolysin, and others [2,3].

4. Bb does not use glutathione for its redox control. Instead, it uses

reduced Coenzyme A (CoASH) [4].

5. Cysteine is the rate-limiting amino acid for the synthesis of glutathione

in humans, so that depletion of cysteine will produce depletion of

glutathione [5].

6. Bb lowers the cysteine and glutathione levels in its human host, and

inhibits the activity of glutathione peroxidase [6].

7. Low glutathione and low activity of glutathione peroxidase allow a rise

in hydrogen peroxide concentration and oxidative stress [7].

8. Elevation of hydrogen peroxide causes Bb to assume its cyst form [8], in

which it is less vulnerable to antibiotics [9].

New hypothesis for a link between Lyme disease and chronic fatigue syndrome

 

 

1. Borrelia burgdorferi (Bb) deplete glutathione in the host.

2. For a person who is genetically susceptible to developing CFS, this

provides a link to the GD-MCB hypothesis for CFS and is one of the possible

routes

into this disorder.

3. If Bb and its biotoxin were not eliminated, Lyme disease and CFS would

coexist in the host, and this would constitute " chronic Lyme disease. "

4. If Bb and its biotoxin [10] were eliminated, but the methylation cycle

block continued, the person would continue to be ill with CFS. This would

constitute " post-Lyme disease syndrome, " which would be analogous to the other

post-infective fatigue syndromes [11].

5. If Bb and its biotoxin were eliminated, and the methylation cycle block

was lifted, I believe it is likely that the person would become well.

In addition,

 

6. Perhaps the Borrelia burgdorferi toxin is one of the toxins that will

react with vitamin B12. Mold toxins have been implicated in such reactions, but

no data were cited [12,13].

References

 

1. Van Konynenburg, R.A., " Glutathione Depletion.Methylation Cycle Block, A

Hypothesis for the Pathogenesis of Chronic Fatigue Syndrome, " poster paper,

8th Intl. IACFS Conf. on CFS, Fibromyalgia, and Other Related Illnesses, Fort

Lauderdale, FL, January 10-14, 2007 _LINK_

(http://phoenix-cfs.org/GSHMethylationVanKonynenburg.htm) .

2. Sambri, V., and Cevenini, R., Incorporation of cysteine by Borrelia

burgdorferi and Borrelia hersii, Can. J. Microbiol. 38: 1016-1021 (1992).

3. Williams, L.R., and Austin, F.E., Hemolytic activity of Borrelia

burgdorferi, Infection and Immunity 60(8): 3224-3230 (1992).

4. Boylan, J.A., Hummel, C.S., Benoit, S., Garcia-Lara, J., Treglown-Downey,

J., Crane, E.J., III, and Gherardini, F.C., Borrelia burgdorferia bb0728

encodes a coenzyme A disulphide reductase whose function suggests a role in

intracellular redox and the oxidative stress response, Molecular Microbiol.

59(2), 475-486 (2006).

5. Griffith, O.W., Biologic and pharmacologic regulation of mammalian

glutathione synthesis, Free Radic Biol Med. 1999 Nov;27(9-10):922-35.

6. Pancewicz, S.A., Skrzydleweska, E., Hermanowska-Szpakowicz, T.,

Zajkowska, J., and Kondrusik, M., Role of reactive oxygen species (ROS) in

patients

with erythema migrans, an early manifestation of Lyme borreliosis, Med. Sci.

Monit. 7(6), 1230-1235

7. Levine, S.A., and Kidd, P.M., Antioxidant Adaptation, Its Role in Free

Radical Pathology, Allergy Research Group, San Leandro, CA (1985).

8. Murgia, R., and Cinco, M., Induction of cystic forms by different stress

conditions in Borrelia burgdorferi, APMIS 112, 57-62 (2004).

9. Kersten, A., Poitschek, C., Rauch, S., and Aberer, E., Effects of

penicillin, ceftriaxone and doxycycline on morphology of Borrelia burgdorferi,

Antimicrob. Agents Chemother. 39(5), 1127-1133 (1995).

10. Shoemaker, R., Schaller, J., and Schmidt, P., Mold Warriors, Gateway

Press, Baltimore (2005).

11. Hickie, I. Davenport, T., Wakefield, D, Vollmer-Conna, U., Cameron, B.,

Vernon, S.D., Reeves, W.C., Lloyd, A., Dubbo Infection Outcomes Study Group,

Post-infective and chronic fatigue syndromes precipitated by viral and

non-viral pathogens: prospective cohort study, BMJ. 2006 Sep 16;333(7568):575.

Epub

2006 Sep 1.

12. Anyanwu, E.C., Morad, M., and Campbell, A.W., Metabolism of mycotoxins,

intracellular functions of vitamin B12, and neurological manifestations in

patients with chronic toxigenic mold exposures. A review,

ScientificWorldJournal 4, 736-745 (2004).

13. Anyanwu, E.C., and Kanu, I., Biochemical impedance on intracellular

functions of vitamin B12 in chronic toxigenic mold exposures,

ScientificWorldJournal 7:1649-57 (2007).

*The author has kindly given his permission to reprint this article at

LymeInfo.