DNA Directed Pro-Dopamine Regulation Coupling Subluxation Repair, H-Wave® and Other Neurobiologically Based Modalities to Address Complexities of Chronic Pain in a Female Diagnosed with Reward Deficiency Syndrome (RDS): Emergence of Induction of "Dopamine Homeostasis" in the Face of the Opioid Crisis

Abstract

Addiction is a complex multifactorial condition. Established genetic factors can provide clear guidance in assessing the risk of addiction to substances and behaviors. Chronic stress can accumulate, forming difficult to recognize addiction patterns from both genetic and epigenetic (environmental) factors. Furthermore, psychological/physical/chemical stressors are typically categorized linearly, delaying identification and treatment. The patient in this case report is a Caucasian female, aged 36, who presented with chronic pain and partial disability following a surgically repaired trimalleolar fracture. The patient had a history of unresolved attention deficit disorder and an MRI scan of her brain revealed atrophy and functional asymmetry. In 2018, the patient entered the Bajaj Chiropractic Clinic, where initial treatment focused on re-establishing integrity of the spine and lower extremity biomechanics and graduated into cognitive behavior stabilization assisted by DNA pro-dopamine regulation guided by Genetic Addiction Risk Severity testing. During treatment (2018-2021), progress achieved included: improved cognitive clarity, focus, sleep, anxiety, and emotional stability in addition to pain reduction (75%); elimination of powerful analgesics; and reduced intake of previously unaddressed alcoholism. To help reduce hedonic addictive behaviors and pain, coupling of H-Wave with corrective chiropractic care seems prudent. We emphasize the importance of genetic assessment along with attempts at inducing required dopaminergic homeostasis via precision KB220PAM. It is hypothesized that from preventive care models, a new standard is emerging including self-awareness and accountability for reward deficiency as a function of hypodopaminergia. This case study documents the progression of a patient dealing with the complexities of an injury, pain management, cognitive impairment, anxiety, depression, and the application of universal health principles towards correction versus palliative care.

Keywords: Genetic Addiction Risk Severity (GARS); H-Wave; KB220PAM; Reward Deficiency Syndrome (RDS); cognitive behavioral therapy; dopamine; photobiomodulation; proprioception; resting state network; subluxation.

Figure 1

Illustration showing the interaction of at least seven major neurotransmitter pathways in the complex of the Brain Reward Cascade (BRC). In the hypothalamus, environmental stimulation springs the release of serotonin, which in succession via, for example, 5HT-2a receptors activate (equal green sign) the ensuing release of opioid peptides from opioid peptide neurons, also occurring in the hypothalamus. Afterwards, the opioid peptides have, potentially via two different opioid receptors, two distinct effects: one that inhibits (red hash sign) through the mu-opioid receptor (possibly via enkephalin) and projects to the Substantia Nigra to GABAA neurons; or the other, which stimulates (equal green sign) cannabinoid neurons (the Anandamide and 2-archydonoglcerol, for example) via Beta-Endorphin-linked delta receptors, which in turn inhibit GABAA neurons at the Substantia Nigra. Additionally, when activated, cannabinoids, largely 2-archydonoglcerol, may indirectly disinhibit (red hash sign) GABAA neurons through activation of G1/0 coupled to CB1 receptors in the Substantia Nigra. In the Dorsal Raphe Nuclei, glutamate neurons can indirectly disinhibit GABAA neurons in the Substantia Nigra through activation of GLU M3 receptors (red hash sign). GABAA neurons, when stimulated, will, in turn, intensely (red hash signs) inhibit VTA glutaminergic drive via GABAB 3 neurons. It is also feasible that stimulation of ACH neurons at the Nucleus Accumbens ACH will stimulate muscarinic (red hash) or Nicotinic receptors (green hash). Lastly, Glutamate neurons in the VTA will project to dopamine neurons by way of NMDA receptors (equal green sign) to preferentially release dopamine at the Nucleus Accumbens, depicted as a bullseye which indicates a euphoria or “wanting” response. The outcome is that when dopamine release is low (endorphin deficiency), unhappiness is experienced, while general (healthy) happiness is dependent on the dopamine homeostatic tonic set point. (With permission from Blum et al.) [20].

Figure 2

MRI showing atrophy, and functional asymmetry.

Figure 3

Coupling DNA, Subluxation Repair, H-Wave and Pro-Dopamine regulation in a diagnosed Reward Deficiency Syndrome female patient.