Lyme and Dopaminergic Function: Hypothesizing Reduced Reward Deficiency Symptomatology by Regulating Dopamine Transmission

doi:10.15761/JSIN.1000163

. 2017 May;3(3):10.15761/JSIN.1000163.

doi: 10.15761/JSIN.1000163. Epub 2017 May 11.

Lyme and Dopaminergic Function: Hypothesizing Reduced Reward Deficiency Symptomatology by Regulating Dopamine Transmission

Kenneth Blum^{1

2

3

4

5

6

7}, Edward J Modestino⁸, Marcelo Febo¹, Bruce Steinberg⁸, Thomas McLaughlin⁹, Lyle Fried², David Baron⁵, David Siwicki⁷, Rajendra D Badgaiyan⁶

Affiliations

¹ Department of Psychiatry, McKnight Brain Institute, University of Florida School of Medicine, Gainesville, FL., USA.
² Division of Neuroscience Research & Addiction Therapy, Shores Treatment & Recovery Center, Port Saint Lucie, FL., USA.
³ Department of Clinical Psychology and Addiction, Institute of Psychology, Eötvös Loránd University, Budapest, Hungary.
⁴ Division of Addiction Services, Dominion Diagnostics, LLC., North Kingstown, RI, USA.
⁵ Department of Psychiatry and Behavioral Sciences, Keck School of Medicine, University of Southern California, Los Angeles, CA., USA.
⁶ Department of Psychiatry, Wright State University, Dayton, Oh., USA.
⁷ Department of Precision Medicine, Geneus Health LLC, San Antonia, TX, USA.
⁸ Department of Psychology, Curry College, Milton, MA, USA.
⁹ Center for Psychiatric Medicine North Andover, MA, USA.

PMID: 28736624
PMCID: PMC5521197
DOI: 10.15761/JSIN.1000163

Lyme and Dopaminergic Function: Hypothesizing Reduced Reward Deficiency Symptomatology by Regulating Dopamine Transmission

Kenneth Blum et al. J Syst Integr Neurosci. 2017 May.

. 2017 May;3(3):10.15761/JSIN.1000163.

doi: 10.15761/JSIN.1000163. Epub 2017 May 11.

Authors

Kenneth Blum^{1

2

3

4

5

6

7}, Edward J Modestino⁸, Marcelo Febo¹, Bruce Steinberg⁸, Thomas McLaughlin⁹, Lyle Fried², David Baron⁵, David Siwicki⁷, Rajendra D Badgaiyan⁶

Affiliations

¹ Department of Psychiatry, McKnight Brain Institute, University of Florida School of Medicine, Gainesville, FL., USA.
² Division of Neuroscience Research & Addiction Therapy, Shores Treatment & Recovery Center, Port Saint Lucie, FL., USA.
³ Department of Clinical Psychology and Addiction, Institute of Psychology, Eötvös Loránd University, Budapest, Hungary.
⁴ Division of Addiction Services, Dominion Diagnostics, LLC., North Kingstown, RI, USA.
⁵ Department of Psychiatry and Behavioral Sciences, Keck School of Medicine, University of Southern California, Los Angeles, CA., USA.
⁶ Department of Psychiatry, Wright State University, Dayton, Oh., USA.
⁷ Department of Precision Medicine, Geneus Health LLC, San Antonia, TX, USA.
⁸ Department of Psychology, Curry College, Milton, MA, USA.
⁹ Center for Psychiatric Medicine North Andover, MA, USA.

PMID: 28736624
PMCID: PMC5521197
DOI: 10.15761/JSIN.1000163

Abstract

The principal vector of Lyme disease in the United States is Ixodes scapularis: black legged or deer ticks. There is increased evidence that those infected may be plagued by anxiety or depression as well. Researchers have identified transcripts coding for two putative cytosolic sulfotransferases in these ticks, which recognized phenolic monoamines as their substrates. It is hypothesized that protracted Lyme disease sequelae may be due to impairment of dopaminergic function of the brain reward circuitry. The subsequent recombinant proteins exhibited sulfotransferase function against two neurotransmitters: dopamine and octopamine. This, in itself, can reduce dopamine function leading to many Reward Deficiency Syndrome behaviors, including depression and possibly, anxiety. In fact, it was shown that activity of Ixosc Sult 1 and Sult 2 in the Ixodid tick salivary glands might contain inactivation of the salivation signal through sulfonation of either dopamine or octopamine. This infraction results in a number of clinically observed mood changes, such as anxiety and depression. In fact, there are common symptoms observed for both Parkinson and Lyme diseases. The importance of understanding the mechanistic and neurobiological effects of Lyme on the central nervous system (CNS) provides the basis for pro-dopamine regulation as a treatment. WC 195.

Keywords: Borrelia burgdorferi; dopamine; lyme disease; reward deficiency syndrome.

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Conflict of interest statement

Conflict of interest Kenneth Blum, PhD, is the holder of a number of U.S. and foreign patents issued and pending related to Nutrigenomics and Nutraceuticals. Through IGENE LLC., Dr. Blum licensed the Genetic Addiction Risk Score (GARS™) to Dominion Diagnostics, LLC as a sales organization in the addiction space. He is a paid consultant of Dominion Diagnostics, LLC. The Shores Treatment & Recovery Center; Dr. Blum is a member of the scientific advisory board of Dominion Diagnostics, LLC., and is Chief Scientific Advisor of Dominion Diagnostics, LLC. There are no other author conflicts of interest.

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References

1. White DJ, Chang HG, Benach JL, Bosler EM, Meldrum SC, et al. The geographic spread and temporal increase of the Lyme disease epidemic. JAMA. 1991;266:1230–1236. - PubMed
1. Burgdorfer W. Lyme Borreliosis: ten years after the discovery of the etiologic agent, Borrelia burgdorferi. Infection. 1991;4:257–262. - PubMed
1. Lukehart SA, Marra C. A comparison of syphilis and Lyme disease: central nervous system involvement. In: Schutzer SE, editor. In Lyme Disease: Molecular and Immunologic Approaches. Cold Spring Harbor, NY: Cold Spring Harbor Laboratory Press; 1992.
1. Burgdorfer W, Barbour AG, Hayes SF, Benach JL, Grunwaldt E, et al. Lyme disease-a tick-borne spirochetosis? Science. 1982;216:1317–1319. - PubMed
1. Steere AC, Malawista SE, Hardin JA, Ruddy S, Askenase PW, et al. Erythema chronicum migrans and Lyme arthritis: the enlarging clinical spectrum. Ann Intern Med. 1977;86:685–698. - PubMed

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[1] White DJ, Chang HG, Benach JL, Bosler EM, Meldrum SC, et al. The geographic spread and temporal increase of the Lyme disease epidemic. JAMA. 1991;266:1230–1236. - PubMed

[2] White DJ, Chang HG, Benach JL, Bosler EM, Meldrum SC, et al. The geographic spread and temporal increase of the Lyme disease epidemic. JAMA. 1991;266:1230–1236. - PubMed

[3] Burgdorfer W. Lyme Borreliosis: ten years after the discovery of the etiologic agent, Borrelia burgdorferi. Infection. 1991;4:257–262. - PubMed

[4] Burgdorfer W. Lyme Borreliosis: ten years after the discovery of the etiologic agent, Borrelia burgdorferi. Infection. 1991;4:257–262. - PubMed

[5] Lukehart SA, Marra C. A comparison of syphilis and Lyme disease: central nervous system involvement. In: Schutzer SE, editor. In Lyme Disease: Molecular and Immunologic Approaches. Cold Spring Harbor, NY: Cold Spring Harbor Laboratory Press; 1992.

[6] Lukehart SA, Marra C. A comparison of syphilis and Lyme disease: central nervous system involvement. In: Schutzer SE, editor. In Lyme Disease: Molecular and Immunologic Approaches. Cold Spring Harbor, NY: Cold Spring Harbor Laboratory Press; 1992.

[7] Burgdorfer W, Barbour AG, Hayes SF, Benach JL, Grunwaldt E, et al. Lyme disease-a tick-borne spirochetosis? Science. 1982;216:1317–1319. - PubMed

[8] Burgdorfer W, Barbour AG, Hayes SF, Benach JL, Grunwaldt E, et al. Lyme disease-a tick-borne spirochetosis? Science. 1982;216:1317–1319. - PubMed

[9] Steere AC, Malawista SE, Hardin JA, Ruddy S, Askenase PW, et al. Erythema chronicum migrans and Lyme arthritis: the enlarging clinical spectrum. Ann Intern Med. 1977;86:685–698. - PubMed

[10] Steere AC, Malawista SE, Hardin JA, Ruddy S, Askenase PW, et al. Erythema chronicum migrans and Lyme arthritis: the enlarging clinical spectrum. Ann Intern Med. 1977;86:685–698. - PubMed

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Lyme and Dopaminergic Function: Hypothesizing Reduced Reward Deficiency Symptomatology by Regulating Dopamine Transmission

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Lyme and Dopaminergic Function: Hypothesizing Reduced Reward Deficiency Symptomatology by Regulating Dopamine Transmission

Authors

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Abstract

Conflict of interest statement

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