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“Dopamine For Dinner” To Prevent Relapse: Paving The Road To “Dopamine Homeostasis”

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“Dopamine For Dinner” To Prevent Relapse: Paving The Road To “Dopamine Homeostasis”

What is the best policy to provide evidence-based medical treatment to both people undergoing treatment and those in recovery?

This is a huge question in the addiction treatment arena. How social media has emerged as a way for users to interface with entities such as SoberGrid (boasting 36,000) and Incredible Marketing (boasting 121,000) is interesting to note. I find this an important link for the millions caught up in Reward Deficiency Syndrome (RDS) (all addictive drug and non-drug related behaviors) across the United States. Similarly, I applaud the significant efforts of filmmakers like Michael DeLeon and Gregory Smith, and those involved in “Recovery Unplugged” and health tracking apps from KnKt’d.

For the first time, the federal agency responsible for most public funding of drug addiction treatment, Substance Abuse and Mental Health Services Administration (SAMHSA), has added language to its grant applications designed to steer the treatment industry away from the abstinence model. From the early days of Alcoholics Anonymous (AA) in 1935 to current thinking, there are those that subscribe to the AA treatment model for RDS in the United States, an abstinence model that promotes abstaining from all drugs, including medications prescribed specifically for addiction, as the only acceptable route to recovery.

SAMHSA is now encouraging all states to reject the status quo and to require the option of medication-assisted treatment (MAT) in clinical settings. This new initiative appears in SAMHSA’s block grant application for fiscal years 2016–2017 ($1.8 billion being awarded by this organization in fiscal year 2015).

While it is generally agreed that FDA-approved MAT—including burprenorphine/naloxone combinations for opioid addicts—may be useful for the short-term treatment (not long-term because of dopamine blockade), in spite of its 100-patient restriction, the vast majority rehabilitation facilities in the U.S. do not offer such care. And although the FDA has approved MAT for alcoholism, opioid dependence, and even nicotine abuse, there are no such approvals for cocaine and marijuana abuse.

America is in the throws of a serious heroin and opioid epidemic killing our kids (see, for example, Deleon’s film “Kids Are Dying”). The Centers for Disease Control and Prevention (CDC) reported that heroin-related overdose deaths almost quadrupled between 2002 and 2013.

In fact, federal drug czar Michael Botticelli, sworn in February 11, 2015, stated that the U.S. government would make drug court funding conditional on states being guided by the science on treatment, rather than ideology.

Certainly moving in this direction paves the way for even better long-term, less aversive treatments, since all the current FDA-approved drugs favor blocking dopamine. We do know that long-term utilization of burprenorphine/naloxone combinations, for example, can lead to typical withdrawal symptoms and in some cases even suicide. There is some evidence that comparative analysis of long-term treatment with burprenorphine/naloxone combinations with short-term utilization revealed no significant benefit in treatment (long term vs. short term) of probands and their resultant clinical outcomes.

Over many decades, my associates and I, and even Nora D. Volkow (Director of NIDA), have argued that “Dopamine Function” is an important cornerstone for a healthy and happy life. If we accept this tenant, it makes little sense to block dopamine’s activity in the long term. In fact, we have shown that long-term utilization of burprenorphine/naloxone combinations induce a reduction in one’s normal affect.

While there is no magic bullet, in the mid-80s Mark Gold and associates were on the right track when they proposed the use of Bromocyrptine, a powerful D2 agonist, to treat cocaine addiction. However, this treatment did not hold up because when Bromocyrptine was utilized on a chronic basis it resulted in D2 receptor down regulation. More importantly, this concept, along with earlier work from my laboratory, suggested that “dopamine agonist therapy” and not “dopamine antagonist therapy” should be embraced in the long-term treatment of addicts.

So while it is important to embrace short-term dopamine antagonist therapy as espoused by FDA approval of MAT drugs, it is not recommended for the long-term. Understandably, while many of the proponents of current MAT would argue against this premise, our scientific challenge would be to find ways to boost dopamine without concomitant D2 down regulation.

Can you imagine if we could harness our brains to provide a regulation or “normalization” of dopaminergic function, leading to what has been termed “dopamine homeostasis”?

In fact, only a very small percentage of treatment centers currently embrace this concept and offer dopamine boosting modalities such as yoga meditation, yoga exercise, brain spotting, cognitive behavioral therapy (CBT), trauma therapy, sound therapy, music therapy, and serving foods prepared using “dopamine for diner” cooking recipes, to name a few.

The literature indicates that some practices such as yoga meditation actually show a marked increase in neuronal dopamine. Moreover, certain healthy low glycemic foods (part of low calorie, low fat, and low carbohydrate diets) are known to boost dopamine function (e.g., fish oil, etc.). However, little direct evidence for dopamine boost has been linked to other holistic approaches, including hyperoxygenation.

It is important to be aware that a number of studies have shown that low dopamine function can lead to reduced cognition (164 studies); reduced memory (199); reduced decision making abilities (45); reduced energy (95); impaired exercise (73); excessive cravings (241); performance (291); aging (218); stress (374); sadness (257); poor relationships (36); lack of well-being (984); and overeating (162). Individuals displaying RDS (addictive) behaviors have been shown to possess low dopaminergic function due to gene polymorphisms (e.g., DRD1-4, DAT1, COMT, MAO, etc.), and as such victims of RDS, or even so-called healthy people, have varying degrees of the above listed endophenotypes.

Admitting to bias, along these lines it has been consistently shown that a well-researched (27 clinical trials) “Neuroadaptagen Amino-Acid –Enkephalinase Inhibition Therapy,” known as KB220, provides gentle activation of dopamine across the brain reward circuitry shown in abstinent human heroin addicts and abstinent psychostimulant addicts. Additionally, significant increases in resting state functional connectivity has been shown in animal models using state of the art resting state fMRI measurements. Continued required research may show that long-term dopamine agonist therapy (similar to KB220) leads to needed “dopamine homeostasis,” the missing link to all RDS addictive behaviors, both substance and non-substance related.

I am proposing “Reward Deficiency System Solution” that includes (1) Genetic Addiction Risk Score Testing; (2) Medical Monitoring for both Compliance to MAT and Abstinence from psychoactive drugs; (3) long-term development of dopamine agonist therapy “to induce dopamine homeostasis”; and (4) Polymorphic DNA directed mRNA genetic expression profiling.

In summary, I encourage our greatest minds in the addiction space to at least acknowledge that for the betterment of humankind, finding ways to boost (regulate), not block, dopamine function in the long term could prevent relapse and provide a quality of life in recovery by redeeming joy. While we might not be there yet my challenge to the scientific and clinical community is to at least admit that our current treatment in America is broken and needs to be fixed. This admission in no way negates the enormous efforts of countless people who have unselfishly given so much to the field.

Lastly, our concern about “An American Epidemic” is underscored by the recent announcement that the FDA has approved OxyContin for severely sick children eleven years old. The potential abuse in prescribing OxyContin for severely sick children, in spite of good attentions, could be catastrophic!

Further Reading

Badgaiyan, R. D., Sinha, S., & Blum, K. (2015) Do We Really Need to Continue Pharmacotherapy for Opioid Use Disorder (OUD) Indefinitely? Journal of Reward Deficiency Syndrome 1(1):16–19.

Blum, K., Chen, A. L., Chen, T. J., Braverman, E. R., Reinking, J., Blum, S. H., … Oscar-Berman, M. (2008). Activation Instead of Blocking Mesolimbic Dopaminergic Reward Circuitry Is a Preferred Modality in the Long Term Treatment of Reward Deficiency Syndrome (RDS): A Commentary.  Theoretical Biology & Medical Modeling 5:24.

Blum, K., Femino, J., Teitelbaum, S., Giordano, J., Oscar-Berman, M., & Gold, M. (2013) Springer Briefs in Neuroscience: Molecular Neurobiology of Recovery: The 12 Step Program & Fellowship. New York, Heidelberg, London: Springer.

Blum, K., Liu, Y., Wang, W., Wang, Y., Zhang, Y., Oscar-Berman, M., … Gold, M. S. (2015). rsfMRI effects of KB220Z™ on Neural Pathways in Reward Circuitry of Abstinent Genotyped Heroin Addicts. Postgraduate Medicine 127(2):232–41.

Borstein, J. (2015). Malibu Beach Recovery Diet Cookbook. Malibu, CA: Vidov Publishing Inc.

Dackis, C. A., & Gold, M. S. (1985) New concepts in cocaine addiction: the dopamine depletion hypothesis. Neuroscience and Biobehavioral Reviews 9(3):469–77.

Fight RDS,

Hill, E., Han, D., Dumouchle, P., Dehak, N., Quatieri, T., Moehs, C., … Blum, K. (2013). Long Term Suboxone™ Emotional Reactivity as Measured by Automatic Detection in Speech. PLoS One 9;8(7):e69043.

Kjaer, T. W., Bertelsen, C., Piccini, P., Brooks, D., Alving, J., & Lou, H. C. (2002). Increased Dopamine Tone During Meditation-Induced Change of Consciousness. Brain Research: Cognitive Brain Research 13(2):255–9.

SAMHSA. (2015). Medication-Assisted Treatment (MAT). Retrieved from

Volkow, N. D., Frieden, T. R., Hyde, P. S., & Cha, S. S. (2014). Medication-Assisted Therapies—Tackling the Opioid-Overdose Epidemic. New England Journal of Medicine 370(22): 2063–6.

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