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THE EVOLUTION OF ADDICTION TREATMENT: THE DISEASE IS RDS AND
ADDICTION IS ITS SYMPTOM
Elizabeth Gilley*
USA.
Article Received on 15/11/2017 Article Revised on 06/12/2017 Article Accepted on 27/12/2017
INTRODUCTION
Enlarged perspective garnered from many sciences,
contribute to the advancement of the evolving Bio-
Psycho-Social Model of addiction-treatment (Guillemin
& Barnard, 2015; Ghaemi, 2009; Borrell-Carrio,
Suchman & Epstein, 2004; Engel, 1981). However, still
there is no unified, comprehensive model of addiction
and/or psychological theory from the last century, which
comes close to explaining cocaine addiction
complexity and neurological impairment (Henriques,
2015; Hunt, 2014). Some sufferers have described it as
soul cancer.
In 2011, The American Society of Addiction Medicine
provided more clarify and established a more formal
definition of the disease, stating in press that
is a primary, chronic disease involving brain reward,
motivation, memory and related circuitry. Dysfunction in
these circuits leads to characteristic biological,
psychological, social, and spiritual manifestations
(Smith, 2011). Practitioners from many sciences have
attempted to define addiction, characterizing the disease
according its expression within the realm of their field of
interest. However, outward expression is symptomatic
not causative. For example, addiction is psychologically
characterized by disruptions in motivation to meet basic
needs, while increasing using behaviors. This description
negates the influence of neurogenetic processes which
precede psychological and behavioral expression.
DISCUSSION
In true reductionist fashion, neuroscientists have
explored genetic precedents and created explanation for
neurological response patterns of the disease process.
Decades of research from the field of neuro-genetics
(Alguacil & Gonzalez-Martin, 2015) have provided the
foundation for the theoretical suggestion of a new
phenotype of addiction, Reward Deficiency Syndrome,
which manifests in compulsive, impulsive, and addictive
behaviors (Blum, Braverman, Holder, et al, 2000; Blum,
Gold, Liu et al, 2011a).
As RDS, redirects focus away from older addiction
models, it ignites a plethora of new research in search of
RDS solutions. Having identified polymorphic variances
which contribute to predisposition, a gene panel map can
be used to determine risk. Genetic Addiction Risk Score
(GARS) prescreening is now available (Blum, Oscar-
Berman, Demetrovics et al, 2014; Blum, Braverman,
Chen et al, 2008; Blum, Cull and Sheridan, 1995).
Cocaine is a strong central nervous system stimulant that
increases levels of dopamine, associated with pleasure,
itry. Normally
dopamine is released by a neuron in response to a
pleasurable signal and then recycled back into the cell
that released it, thus shutting off the signal between
neurons. Cocaine acts by preventing the dopamine from
being recycled, causing excessive amounts of the
neurotransmitter to build up, amplifying the message and
effector protein response, ultimately disrupting normal
SJIF Impact Factor 4.382
Review Article
ejbps, 2018, Volume 5, Issue 1 161-166.
European Journal of Biomedical
AND Pharmaceutical sciences
http://www.ejbps.com
ISSN 2349-8870
Volume: 5
Issue: 1
161-166
Year: 2018
*Corresponding Author: Elizabeth Gilley
USA.
ABSTRACT
The science of neurogenetics offers a new theoretical model of addiction, defining Reward Deficiency Syndrome
(RDS) as the phenotype of addiction. This model appears to be a perfect fit for understanding cocaine use disorder
and the
support of RDS, which is now inspiring research of RDS solutions. A new science of relapse is exploring the
molecular, cellular and neurological processes of craving, drug seeking, and relapse in nonhuman samples. Results
inspire hope for the future of recovery through neurological intervention to reset brain imbalances and disrupt the
neurotransmission of relapse.
KEYWORDS: Molecular, cellular and neurological.
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162
communication (Blum, Chen, Giordano, 2012a).
With habituation, some develop sensitization, tolerance
and neuroadaptation as repetitive neural loops are
engrained by experience. These neural pathways can be
reactivated by cue inducement, operating beneath the
level of conscious, initiating relapse on the molecular
and cellular levels. Atypical patterns of brain wave
activity become embedded and encoded into neural
circuitry.
Dopaminergic dysregulation and imbalance created by
self-administration of cocaine are met
responsive attempt to regain stability and balance by
adjusting the dopaminergic set point, creating a new
below normal for dopamine neurotransmission (Blum,
Bowirrat, Carnes et al, 2012b). Early dopaminergic
system research established that deficits of the DRD(2)
receptor and the DRD(2) A1 Allele predispose
individuals to a high risk for multiple addictive,
impulsive and/or compulsive behaviors (Bowirrat, &
Oscar-Berman, 2005; Blum, Gardener, & Oscar-Berman,
2012b). Activation instead of blocking mesolimbic
dopaminergic reward circuitry is the preferred modality
in the long term treatment of RDS (Blum, Chen, Chen
et al, 2008).
In addition to dopaminergic systems, Cocaine, a triple
reuptake inhibitor, also disrupts serotonin and
norepinephrine reuptake inhibitors, confusing receptor
perception and effector protein response. Research has
determin
includes the differential expression of genes that regulate
(Bannon, Johnson Michelbaugh et al, 2014, p. 2191).
This type of research may one day identify a unique
neurological signature or biological marker of cocaine
addiction.
Cocaine self-administration shows remarkable resistance
to extinction (Weiss, 2001). Additionally, in the specific
case of cocaine, drug seeking behavior can actually
progressively increase in strength, incubating during
abstinence (Grimm, 2001). Cocaine reinstatement is a
product of molecular and cellular processes which
intensify craving and increase drug seeking on a
neurological level. It has been hypothesized that
increases in drug use are caused by decreases in
dopamine signaling within the Stratium, as such
researchers are exploring the possibility that restoring
dopamine signaling in the Stratium might therefore
reduce drug use (Willuhn, Burgeno, Groblewski, et al,
2014). Results found that L-DOPA increased dopamine
release in rat studies.
Polymorphism, or gene variance alone, does not cause
addiction. Hypo-dopaminergic trait genes combined with
the interaction of environmental influences determines
outcome of Reward Deficiency Syndrome, which can
manifest in addictive behavior, and contributes a
spectrum of dopaminergic disorder, such as depression,
.
The complex interactions between genetic material and
environmental influences (Enoch, 2012) induce
epigenetic pressure, which result in RNA recoding DNA
While science has not yet discovered the exact cause, it
has simplified the RDS process of neurological
dysregulation which plays out in addiction. The RDS
model works perfectly for cocaine addiction. Although
currently without a great deal of research support, it has
been suggested that other drug addictions and the process
behavioral addictions may also fit neatly under the RDS
umbrella. Blum would like to establish a common
neurogenetic diagnosis for all addictions under the RDS
rubric (Blum, Febo, Bafgaiyan, et al 2017), based upon
the presence of Meso-Limbic manipulation of
hypodopaminergic function. He has been marketing this
idea in publication for the past few years (Blum, Febo,
McLaughlin, et al, 2014).
Pharmacological and pharmacokinetic research
contribute enlarged perspective of addictive variables
which may induce neuro-adaptation. Pharmacokinetic
research has provided understanding of individual
metabolism rates and processes of biotransformation,
which effect bioavailability of dosage. Routes of
substance delivery, intensity of dosage, frequency,
intermittency and reinstatement patterns all effect
neurological consequence.
Meta-analysis suggests
Minogianis, Roberts, et al, 2015).
cocaine intake determines tolerance versus sensitization
Ferris, Zimmer et al, 2013, p. 2013). Animal studies may
lead to clinical human study. However, the design of
these studies does not accurately reproduce the range of
human administration patterns, so results should not be
interpreted as generalizable to human populations.
Repetitive exposure to cocaine dysregulates
dopaminergic, serotonergic and norepinephrine systems,
initiates neuroadaptations which increase craving and
reinstate relapse. Understanding the pharmacokinetics of
drug use, and the pharmacological consequences of
cocaine use in particular, will prove to be helpful in
developing molecular and cellular pharmacological
interventions to assist in dopamine restoration and
rebalance other neurotransmitters such as norepinephrine
which is known to help regulate withdrawal and assist in
abstinence and glutamate which is associated with
intense craving and cue-induced reinstatement.
To further understand structural and functional
neuroadaptations caused by repetitive self-administration
of cocaine, researchers studied norepinephrine systems in
nonhuman primates, conditioned for self-administration
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but now forced to abstain, to check for any changes in
the artificially induced increases in norepinephrine levels
seen after repeated exposure, to find that there was no
difference in norepinephrine levels of abstaining
populations and control animals (Smith, Beveridge,
Nader et al, 2016). This line of research may someday
lead to pharmacological intervention for humans.
Research study design neuroimaging nonhuman subjects
reviewed functional brain activity in response to cue
reinforcement to find that increased glucose levels before
self-administration, decrease after self-administration.
This increase is interpreted as being associated with
human addiction neuroadaptations (Porrino, Beveridge,
Smith et al, 2016).
Another study performed rat brain tissue analysis of the
role of Neurokinin-I receptors suggests it mediates
alcohol seeking in response to cue activation for addicted
rats but was not significant in mediating cocaine seeking.
Interesting results showed no effect upon non-addicted,
nongenetically predisposed populations. This study may
be helpful in future pharmacological studies which
explore NK1R antagonists utility in treating cocaine use
disorders (Schank, King, Cheng et al, 2014).
Building upon the correlation between increased
glutamate release in the NAc, upon cue presentation, and
the resulting increase in cocaine-seeking, researchers
designed a study which explored the mediating effect of
increasing mGluRi transmission, finding that mGluRi
-AMPAR
levels, and thereby reduced cue-induced cocaine
(Loweth, Scheyer, Milovanovic et al, 2014, p.
78), in rats. mGluRi
PAMS should be explored in future research design as
possible pharmacological intervention to reduce craving
in human subjects.
Perhaps one of the more anticipated future contributions
from pharmacological research is the creation of a new
line of antidepressants, which function as triple reuptake
inhibitors and mimic
dopaminergic, serotonergic and norepinephrine systems.
Results from European neuro-scientist
study of the
reu
Chenu, El Mansari, et al, 2011, p. 211) offer evidence-
base support for the similarity of pharmacological
process in synthetic substitutes for commonly abused
drugs like cocaine, in rat populations. By exploring
potential dopamine expression by synthetic cocaine
replacement therapy in rat populations, Guiard
anticipates gaining insight into human response,
hopefully resulting in human pharmacotherapy
interventions (Guiard, El Mansari, & Blier, 2009). He
al
effect upon monoaminergic lesions (Guiard, El Mansari,
Merali et al, 2008). He is building a foundation of
evidence base for future human clinical trial, one
research study at a time.
Other research study found results supporting
Vulnerability to cocaine relapse involves
neuroadaptation of glutamatergic synapses within the
2011, p. 623). This animal study may be useful to the
development of future research design involving
pharmacokinetic and pharmacological manipulations
which may modify accumbal glutamate to reduce
cocaine seeking drive. Prior research concluded
background may differentially alter the glutamatergic
and GABAergic transmission associated with
vulnerability to cocaine relapse in the NAcc, and
underline the importance of considering individual
genetic differences when designing anti-relapse
(Miguens, Botreau, Olias, et al, 2011, p. 630).
The same year, the Kenneth Blum team of research
associates developed similar research design exploration
of the Meso-Limbic system, in human populations who
might benefit from amino-acid therapy.
synergy between acupuncture / aurioculotherapy and
natural activation of mesolimbic dopaminergic
pathways they tested the application of putatuve natural
treatment modalities for the reduction of drug hunger and
with successful result. This protocol has not only been
researched, and replicated. It has been patented,
manufactured, marketed and brought to market.
Humanity owes a debt of gratitude to pioneering research
scientists for their patience, and endurance, in creating
animal study research design which contributes to future
development of human intervention protocol. The
Neurogenetic Research Foundation for RDS have
presented publication of new RDS theory, backed by its
substantial and growing evidence base in support. There
is therapeutic value in the RDS model (Diana, 2011).
Research of RDS solutions (RDSS) is presenting viable
alternatives to traditional modalities, which increase
therapeutic response options. Potential neurological
intervention, gleaned from pharmacological and
pharmacokinetic research study of the molecular and
cellular processes of relapse, will hopefully revolutionize
treatment protocol. . The sciences of RDS and new
science exploring neurological processes of craving, drug
seeking and relapse are changing the landscape of
recovery.
Accomplishing the ultimate goals of stopping the
generational cycle of addiction, and resetting
neurological imbalances of RDS remain unrealized. As
focus shifts in search of population which experience
significantly higher risk and/or complexity of addictive
expression, we note that gender and/or ethnic variances
are minimal. Research of African American variance was
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164
insignificant (Levran, Randes, Correa da Rosa, et al,
2015).
Lets focus upon what matters, rather than what others
demand of us. We find extreme variance with
populations dually diagnosed with mental illness and co-
occurring SUD, as well as significant variance in those
populations of survivors who endured adverse childhood
experiences such as physical, emotional and/or sexual
abuse. In fact Posttraumatic Stress Disorder predicts
development of addictive behavioral patterns (Wilsnack,
Vogeltanz, Klassen, et al, 1977). Compassion demands
that these populations be given research priority.
Excluding these populations from research study distorts
perspective (Moberg, & Humphreys, 2016) which may
result in negating the validity of our diagnostic criteria
(Reiger, Laelber, Rae et al, 1998).
The population of individuals inheriting a deficiency of
DRD2 Receptors and/or the DRD2 A1 Allele have
significantly higher risk for development of impulsive,
compulsive and addictive behavioral patterns.
Populations with polymorphic influence of the GABRA2
gene display a higher risk of addictive potential. Rather
than look across boundaries of gender, or ethnicity, lets
look for genetic predisposition. This is the population
upon which to focus attention.
If the family is to survive the devastation of RDS (Please
note that I purposely did not say addiction because of the
negativity and harmful preconceptions with which
society has victimized its sufferers), it needs to be
informed. Genetic screening is a must. RDS has many
manifestations, contributing to a spectrum of
dopaminergic disorders beyond impulsive, compulsive,
and addictive expression, including depression, Autism,
the many faces of RDS. Genetic Addiction Risk Scores
(GARS) and possibly outcomes such as asperger can be
identified.
Perhaps in commitment to manifesting a brighter
healthier future, we turn our focus from disease to
wellness, develop more accurate diagnostic criteria,
better measurements of wellbeing self-efficacy
(McKiernan, Cloud, Patterson, et al, 2011), and abandon
ourselves to practice of positive psychological
applications from existential, transpersonal and integral
perspectives of whole-ism and oneness.
science of addiction and the science of well-
(Gilley, 2017) will empower recovery. We, are
responsible for manifesting
(Gilley, 2012). WE can recreate wholeness, wellness,
thriving. First LET US thoroughly dismantle false hurtful
constructs which disempower rather than heal, expose
half truths for the lie they are, and claim powerfulness,
rather than powerlessness.
In an ideal world, future research design will align with
quantum physics, rather than the reductionist, separatist,
Newtonian tendency. Future research will hopefully
study energy signals which are one hundred times more
powerful than molecular signals. Future research will
explore the healing potential of bio and psycho-electro-
magnetic frequencies (Gilley, 2016), include exploration
of infrared spectroscopy to identify of recovery markers
(Dempsey, Harris, Shumway et al, 2015) and effect of
frequency unbalance in energy signaling (Balconi,
Finocchiaro & Canavesio, 2014). Hopefully future
research will focus more upon developing benefit of
healing frequency, rather than investing in the weapon-i-
zation of frequency. Undoubtedly, the future of RDS and
addiction research will provide accuracy of perception,
righting a wrong created by hurtful, ugly response
patterns of improper addiction perspectives of the past
century. Perception determines behavior, on the level of
receptor and effector proteins and on the level of the
collective population. Yes, just as the quantum field
determines the expression of the particle, perception
determines behavior. Allow me to set the proper tone.
WE are not victims of our heredity. Even epigenetic
change is based upon perspective. Cellular intelligence is
powerful enough to change genetic heritage. Imagine the
power of the collective, aligned with higher truth.
Imagine the possibilities. Dare to thrive!
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