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.
Highlights
Lyme disease (Lyme borreliosis) is an infectious disease caused by Borrelia bacteria
We suggest the use of the term “dopamine agonist therapy” for long-term and concur the short-term use of “dopamine antagonistic therapy” with warning
The addicted brain, DRD2 A1 carriers, favors NeuroadaptagenAmino-Acid therapy [38] due to an increased sensitivity to promote dopaminergic activity. This occurs as a result of dopamine synthesis: DRD2 A1 allele carriers display augmented striatal activity of L-amino acid decarboxylase
Summary
Lyme disease (Lyme borreliosis) is an infectious disease caused by Borrelia bacteria. It is our position that Lyme induction antagonizes the function of dopamine by inactivation and enhancement of pro-inflammatory cytokines, bringing about a deficiency of Toll–Receptors (i.e., TLR3) This will have profound effects and can induce unwanted anxiety and depression. There is no current research showing the possibility of reduction of anxiety or depression induced by Lyme, the rationale seems sound In this regard, Willuhn et al [37] found that as dopaminergic function decreases, cocaine consumption and other addictive behaviors increase, including the behaviors that are irrelevant of substance abuse. Even if the resultant RDS behaviors (i.e., anxiety and depression) could lead to subsequent substance and non-substance addiction seeking as induced by Lyme, mimicking either genetic or epigenetic insults, our proposal of utilizing KB220z seems parsimonious. Our proposal is extended to the fact that the hospitalization and perhaps mortality due to enhanced relapse of RDS seeking should consider prevention tactics such as the Neuroadaptagen–AminoAcid therapeutic (KB220), referred to as the Natural Assisted TreatmentTM [38]
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