Probing the Mysteries of Recovery through Nutrigenomics and Holistic Medicine: Science Meets Recovery

Can you imagine jumping out of a plane without a para­chute? In spite of all the effort and progress made by the addiction community, as a whole, it has failed to both comprehend and willingly incorporate well-established, evidence-based medical modalities into treatment, especially as it relates to relapse prevention. The patient who carries certain high-risk genetic deficits, such as low dopamine function (“dopamine resistance”) in the reward site of the brain, is at a high risk of relapse. Following treatment—residential or non-residential, where no attempt is made to enhance the function of brain dopamine—the patient who is released back into society is doomed to fail. Are we approaching the time when, along with tender loving care, providers can supply that needed parachute?

Researchers have identified a linkage between neurotransmitters, individual behavioral traits and underlying genes, leading to a new understanding of the science of human nature and more specifically, the so-called state of “happiness.” With this knowledge, treatment for chemical dependency can be enhanced to focus not only on achieving sobriety, but on finding a quality of life in recovery, that approaches happiness.

Translational research in the addiction/behavioral health field has led to an opportunity for more comprehensive treatment based on better understanding of neuro-genetics, brain cell metabolism and brain healing (Blum et al., 1977; Blum et al. 1996; Blum et al., 2000). In conjunction with talk therapy, life skills and support through follow-up, they encompass a holistic approach to recovery, which should become the basis of guidelines for a new “standard of care” (Blum et al., 1981).

While intensive research must continue, this article reviews the latest research related to nutrigenomics, hyperbaric oxygen therapy, music therapy and neuro-feedback; and ­suggests how they can be used together to heal neurological deficits associated with both substance use disorder (SUD) and other impulsive and compulsive disorders that result from genetic defects in the dopaminergic pathways especially in the nucleus accumbens (NAc), the reward site of the brain.

Neuropsychiatric genetics

Drug seeking behavior is related to the brain reward circuitry, particularly in the dopaminergic system (Blum & Wallace, 1974). When dopamine is released, it stimulates receptors (D1-D5) that reduce stress, thereby creating a sense of well-being (Blum et al., 2009a). Dopamine release is the normal reward for satisfying an individual’s most basic drives for food, reproduction and safety.

In food- and drug-addicted individuals, dopamine deficiency is usually due to an association with the dopamine D2 receptor gene (DRD2) gene A1 allele and other polymorphisms (gene variations) involved in the reward cascade (Blum et al., 1990a; Stice et al., 2008; Volkow et al., 2009). This reduced dopamine release and/or receptivity has been described as reward deficiency syndrome (RDS)[Blum et al,1996]. Individuals with these genetic polymorphisms crave substances that will increase dopamine release at the “reward site” in the mesolimbic region of the brain, just to feel normal. Repeated episodes of substance abuse also can result in reduced dopamine receptivity and craving, even in ­people with normal dopamine genetics.

Evidence is emerging that supporting stimulation of the dopaminergic system with a specialized natural, non-addictive D2 agonist may have a place in recovery from addiction to psychoactive chemicals. Neuroimaging tools (qEEG , PET and fMRI) are being used to demonstrate the impact of Synaptamine Complex Variant [KB220 IV and KB220Z oral]™ (patented, patent pending and evidence-based) as an activator of the mesolimbic ­system in drug abuse.

After administration of intravenous KB220 (LifeStream Inc. Prescott, Arizona, Protocol*), aberrant electrophysiological parameters were significantly reduced or “normalized” at the reward circuitry site (Miller et al., 2010). The important point here, is that using qEEG analysis, we found that one acute dose of KB220 regulated the dysfunction of the brain reward area by increasing alpha activity and increasing low beta activity. This brings about two important features: anti-craving and calmness.

This research provides support for an older study of 600 outpatient poly-substance abusers who received intravenous KB220 for 10 treatment sessions, in addition to repeated doses of oral KB220Z twice daily for 14 days [see figure 1].

In a recent study, researchers at G &G Holistic Addiction Treatment Center found significant evidence that one acute oral dose of SYNAPTOSE™ [KB220Z] was able to induce the same effect as is observed after 10 training sessions using the Peniston biofeedback protocol to treat ­alcoholics. These effects were not observed in a matched group of individuals who were given a placebo in a triple blind controlled study. Similar to the IV treatment, one oral dose resulted in regulation of the brain dysfunction in protracted abstinent psychostimulant abusers, including increased alpha activity and increased low beta activity. (Blum et al., 2010a).

Similar and even more robust findings have been obtained using KB220Z oral (Synaptose™) in long-term heroin addicts using fMRI. In preliminary experiments, KB220Z activated the mesolimbic system of the brain (Caudate-Accumbens), compared to matched group of individuals who were given a placebo. In heroin addicts from China (Medical Image Processing Group, Institute of Automation, Chinese Academy of sciences, Beijing), during protracted abstinence, the reward site of the brain (the Caudate-Accumbens), when viewed by fMRI, looks like a dead blue-black sea (no activity). In contrast, after KB220Z the reward site significantly lights up in bright yellow coloration (meaning that dopamine sites are being activated by KB220Z). Furthermore, KB220Z, at least temporarily, reverses abnormalities observed in protracted abstinent heroin addicts at the Putamen loci. Prior to the administration of the KB220, that area of the brain shows dysfunction due to low Dopamine D2 receptors; but after KB220 administration, it approaches normal electro-activity. This research is in progress and awaiting outcome data [Blum et al., 2009b].

Numerous clinical trials support the idea that long-term activation of dopaminergic receptors with KB220 and KB220Z, will result in the proliferation of D2 receptors leading to enhanced “dopamine sensitivity,” and thus, an increased sense of happiness, particularly in carriers of the genetic variant in DRD2 A1 allele. While beneficial results have been demonstrated in previous studies, the actual “mechanism of benefit” in the brain has yet to be defined. The DRD2 gene is responsible for the production of dopamine D2 receptors in the brain. Carriers of the A1 form produce 30 to 40 percent less Dopamine D2 receptors (Blum et al., 2008). We await research that promises to directly illustrate, via PET scanning, the effects of continuous use of KB220Z on D2 receptor numbers.

Hyperbaric Oxygen therapy (HBOT)

There is growing interest in the use of HBOT to treat the neurotoxicity induced by long-term alcohol and psychostimulant abuse. Even in the absence of double-blind studies, there is enough positive anecdotal information and case studies to warrant intensive investigation in residential treatment. An example is the case of a 19-year-old serious drug abuser with a preliminary brain SPECT scan that looked as bad as the scan of a demented 74-year-old man. The scan of the drug abuser showed a marked improvement in blood flow after just one HBOT session (Harch, 2007). It is conjectured that the ‘mechanism of benefit’ involves supplying additional oxygen to hasten the combustion of neurotoxins that accumulate in the brain from the excess intake of alcohol. Previous research from our laboratory showed that raising endorphin levels in the brain increases blood flow in the reward site of the brain (Blum et al., 1985). Synaptose raises brain levels of endorphins by preventing their breakdown. Coupled with an enhanced oxygenation by HBOT, the synergy should translate to improving brain health in addicts. Brain healing is necessary in order to overcome neurological deficits that result from SUD. HBOT has been used to successfully treat a myriad of other neurologically-based disorders including: traumatic brain injuries, cardiovascular accidents, post-traumatic stress disorder, dementia and Parkinson’s Disease.

Neurofeedback

Electroencephalographic (EEG) bio­feedback has been employed in SUD over the last three decades, and in conjunction with other therapies, may be useful in enhancing outcomes. Based on published clinical studies and employing efficacy criteria (adapted by the Association for Applied Psychophysiology and Bio­feedback and the International Society for Neurofeedback and Research) alpha theta training either for alcoholism alone, or in combination with beta training for stimulant and mixed substance abuse, combined with residential treatment programs, is probably efficacious. One experiment in which alcoholics with depressive syndrome were treated with neurofeedback, demonstrated sharp reductions in self-assessed depression (Saxby & Peniston, 1995). On the Millon Clinical Multiaxial Inventory, these subjects showed significant de­creases in schizoid, avoidant, dependent, ­his­trionic, passive-aggression, schizotypal, borderline, anxiety, somatoform, hypomanic, dysthymic, alcohol abuse, drug abuse, psychotic thinking and psychotic depression. Follow-up after 21 months indicated sustained prevention of relapse in alcoholics who completed alpha-theta brainwave neurofeedback training.

Neurofeedback is also showing promise as a treatment modality for adolescents, especially those with stimulant abuse, attention and conduct problems. It is attractive as a medi­cation-free, neurophysiologic and self-actualizing treatment for a substance-based, brain-impaired and self-defeating disorder. This technique is used to exercise the brain to achieve a feeling of well-being through its impact on neurotransmitter re­balancing. Thus, a combination of KB220Z and biofeedback also may be synergistic, especially when one considers the genetics, personality and environmental predictors of drug use in adolescents (Conner et al., 2010; Blum et al., 2010b).

Music/sound therapy

Listening to music strongly modulates activity in a network of mesolimbic structures involved in reward processing (Menon & Levitan, 2005). These areas are thought to be in­volved in regulating autonomic and physiological responses to rewarding and emotional stimuli. Music is one of the most rewarding and pleasurable of human experiences. However, little is known about why some people have a more or less powerful mesolimbic experience when they are listening to music. It is conjectured that adequate dopamine release and subsequent activation of reward circuitry by listening to music might also be affected by an individual’s D2 receptor density in the reward site (Blum et al., 2010c; Kirsch et al., 2006).

Music may induce an endorphinergic (opioid like natural neurotransmitter) response in the NAc and is associated with dopamine release in the reward site of the brain (Goldstein, 1980). Indeed, some researchers have found that music therapy can be used as a motivational tool in sample of severely impaired inpatient patients with co-occurring mental illness and addiction (Ross et al., 2008).

Talk therapy

The efficacy of incorporating talk therapy as an adjunct to treatment for SUD is well documented. In particular, the use of talk therapy and appropriate interviewing prior to any inpatient or outpatient therapeutic modality is paramount to future success and ultimate outcome. For example, many adolescents use alcohol and other drugs (AODs); however, most of these adolescents do not seek help because of peer pressure and anxieties about stigma and confidentiality concerns. A pilot test for high-risk adolescents (age 12-18 years) in a ­primary care setting employed a brief motivational intervention (MI) that included conducting small feedback sessions with adolescents, parents and clinic staff. The feedback sessions revealed the following: clinic staff thought teens would not talk about AOD use, while adolescents reported that they would talk about their AOD use, but were afraid of being judged. Parents were also concerned that the service provider might be judgmental. ­Feedback from the MI pilot indicated that teens were willing to talk about their AOD use and indicated readiness to change. Findings suggest that providing a brief MI in a personal care setting is a viable approach for working with high-risk youth (Stern et al.,2007).

Evidence from a series of studies—including a randomized double-blind placebo controlled inpatient investigation using neuroadaptogen therapeutic agent to reduce stress/especially in a residential setting prior to entering group session on day seven of treatment, resulted in a pronounced decrease of stress (Blum et al., 2009a). Thus, it is proposed that the coupling of MI and neuro-nutrient rebalancing may have important therapeutic benefits.

Brain health

There are some problems regarding assessment and restoration of brain health. Most treatment programs do not attempt to determine the state of peripheral markers for associated disorders, such as evaluating adrenal function, thyroid function, tissue levels of heavy metals like mercury and hormonal imbalances. Moreover, objectivity in diagnosis could im­prove by incorporating genotyping for a number of important well-characterized gene polymorphisms associated with RDS (Blum et al., 2007b).

Additionally, the chronic administration of powerful pharmaceuticals, results in down regulation of receptors and reduced dopamine function. An alternative would be to treat the chemically-dependent person with natural dopaminergic agonists which will up-regulate neurotransmitter receptor density and increase dopamine release at the NAc. This would affect genetic predisposition, and assist in reducing craving behavior. In addition it would induce a sense of well-being during and especially after residential treatment, to prevent relapse (Blum et al. 2009c; Lawford et al., 1995).

Achieving happiness

Up until the present time there have been 18 clinical trials that show benefits of using KB220 and KB220Z in recovery from RDS behaviors. However, prior to brain imaging studies, the neurophysiologic effect and mechanism of action has been elusive. The results of these imaging studies support an interaction of variants of KB220 and KB220Z with mesolimbic activation leading to “normalization” of abnormal dopa­minergic function in patients carrying gene polymorphisms related to dopamine deficiency. In terms of happiness, the authors propose that a reduction in stress will impact one’s state of happiness. Thus, agents that induce stress reduction should have important benefits with regard to craving reduction and achieving a state of well-being or happiness (Blum et al., 2009d).

When these new techniques and concepts, which have emerged from scientific research, even the genes involved in spirituality ( Hamer , 2005; Comings , 2008; Charlton, 2008; Zimmer , 2004) are incorporated into treat­ment they will bridge the gap, enhance self-help group compliance, so that for the first time in many decades “science will meet recovery.”

* Note: KB220 and KB 220Z and is a patented Neuroadaptagen, utilizing among others, precursor amino-acid-enkephalinergic degradation inhibition
—synaptic-inhibition of catecholamine degrad­ation including the Genetic Addiction Risk Score (GARS) and exclusively distributed by Reward Deficiency Solutions, LLC., San Diego, Calif.

Conflict of Interest: Both Kenneth Blum and John Giordano are involved in the distribution of products manufactured by Reward Deficiency Solutions, LLC, San Diego, Calif.

Acknowledgements: The authors want to thank David Miller, Merlene Miller, Mathew and Debra Manka , LifeStream Inc., Prescott, Ariz.; and Stan Stokes and Charles Gant of Bridging the Gap, Winchester, Va., for providing the preliminary scans of the qEEG IV of KB220. The authors would also like to thank both Cameron Allen (Synaptic Connections Research Institute and Welcome Home Vets, Charleston, SC); and James Thompson (Brain Enhancement Solutions & Technologies, Orlando, Fla., and New York, NY) for qEEG analysis. We are indebted to the editorial assistance of Margaret Madigan (Reward Deficiency Syndrome Solutions, LLC, San Diego, Calif.) and Siohban Morse (G & G Holistic Addiction Treatment Center, North Miami Beach, Fla.). The authors appreciate the editorial comments by B. William Downs and Roger L. Waite of Reward Deficiency Solutions, LLC, San Diego, Calif.; and a special thanks to our publicist Joe Ullrich at Omni Publicity, Inc. 

Resources  

The following Web site links are suggested for additional information:www.addictionsearch.com;www.drugstrategies.org;www.RewardDeficiencySyndrome.com, andwww.lifestreamsolutions.com.

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