Reward Deficiency Syndrome (RDS)
Reward Deficiency Syndrome (RDS)
Definition
Reward Deficiency Syndrome, or RDS, is related to a number of mental health disorders, rather than standing alone as a separate and distinct mental illness. The mental illnesses to which RDS is related include a wide range of addictions, compulsive behaviors, and impulsive behaviors. Reward Deficiency syndrome refers to the breakdown of the reward cascade, and resultant aberrant conduct, due to genetic and environmental influences. RDS is a DNA-related gene and chromosome type of syndrome that interferes with the usual achievement of human physiological drives such as food, water, and sexual reproduction. The A1 (minor) allele of the D2 dopamine receptor (DRD2) gene has been shown to be associated with alcoholism, particularly its severe form, as well as with smoking, obesity, and other addictive behaviors.
Addiction is a brain disorder that causes the compulsive and continued use of and cravings for substances, regardless of negative consequences. These behaviors are related to neurotransmitter dysregulation, notably that of dopamine and serotonin. Addiction, along with compulsion, affects the nucleus accumbens, the part of the brain that produces pleasure. Because of its biologic basis, these behaviors are chronic with a propensity toward relapse. Addiction/compulsion causes loss of control over alcohol, nicotine, and substance use, so that uncontrollable behaviors occur more quickly as this mental disorder progresses. The name for this particular pattern is Reward Deficiency Syndrome. Defined by pharmacology professor Kenneth Blum in the 1990s, RDS arises in the human genetic units labeled the D2 (dopamine) receptor and the A1 allele. RDS is also linked to such illnesses as attention deficit hyperactivity disorder and
Tourette’s syndrome, conduct disorder, obesity, gambling, post-traumatic stress disorder (PTSD), and premenstrual syndrome (PMS).
Description
In the 1950s, researchers experimented placing electrodes into a rat’s brain. They discovered that the rat chose pressing a lever attached to the electrodes to provide brain stimulation, even over the basic needs of food and water. This suggested that the implanted brain area is the “pleasure center” of the brain. It contains the nucleus accumbens, a brain structure related to addictions, but also interestingly relevant to processing the rewards of food, sex, and video games (a modern addiction in some individuals). Neurologic reward pathways are very important to human survival, because they provide the drives for pleasure that require eating, love/sex, and reproduction for species survival. These natural rewards facilitate the release of dopamines in both the brain’s nucleus accumbens and frontal lobes.
Pharmacologist Kenneth Blum found that individuals with RDS generally possess a specific chromosome sequence in their DNA. This sequence is most often the A1 allele, D2 dopamine receptor. People with this sequence have 20% to 30% fewer D2 reward receptors than in the general population. This makes it more difficult for the pleasure drives to be met, forcing the individuals into high-risk behaviors to gain that fulfillment. In addition, people with the A1 allele are 74% more likely to have one or more of several RDS-related mental illnesses. These illnesses are related to addictions, compulsive behaviors, and impulsive behaviors.
Listed in the 2000 edition of the Diagnostic and Statistical Manual (DSM-IV) of the American Psychiatric Association, disorders that stem from RDS include alcohol abuse, substance abuse, nicotine/tobacco use, compulsive disorder, attention deficit hyperactivity disorder, conduct disorder, antisocial personality disorder, obesity, PTSD, and PMS. Such individuals need to stimulate themselves in abundance simply to feel normal. Alcohol and drugs used for stimulation of the pleasure center injures a person’s dopamine and endorphin system even more. With each use of drugs or alcohol, the difference between feeling high or even “normal” and being sober becomes larger and larger. Staying sober becomes boring and results in an overarching anxiety and irritability. To alleviate these bad feelings, these individuals often turn back to alcohol and drugs, sometimes overdosing and accidentally or purposefully dying in the process.
Prevalence
It is difficult to estimate the prevalence of RDS among the American population of 300 million, because of its many manifestations. Not only alcohol and substance use disorders but also tobacco/nicotine use, schizoid/avoidant behavior, PTSD, ADHD, Tourette’s syndrome, aggression, obesity and aberrant weight gain, PMS, and perhaps other mental disorders all fall under the RDS umbrella.
Because the prevalence of co-occurring disorders has increased in the last 30 years, the overall prevalence of RDS has also increased, being related to co-occurring disorders (always including substance/alcohol abuse). Further, the co-occurrence of mental illness and substance abuse itself is found in 50% of all individuals suffering from any of the severe mental disorders (SMDs). Therefore, RDS is related to these 50% of cases, possibly a proportion of the other 50% of SMDs, and to the further problems associated with substance and alcohol abuse and impulsive and compulsive behaviors: higher rates of relapse and hospitalization, incarceration, violence, homelessness, suicide, and exposure to infections such as HIV and hepatitis. It is not known how many Americans with obesity and other above-mentioned disorders are RDS-connected, in the absence of genetic testing.
Demographics
Children of alcohol-addicted or substance-addicted individuals are more highly at risk for developing alcohol use and substance use disorders than the general population. Thus, they are more likely to suffer from RDS. There is also evidence of the hereditary nature of some other RDS-related illnesses, especially morbid obesity, attention deficit (ADD/ADHD), and PMS.
Disruptive behavior disorders such as conduct disorder in youth and antisocial personality disorder in adults are related to RDS. The youth-related disorders frequently coexist with substance abuse problems. Other groups that may be affected by RDS are older adults with mood/anxiety disorders who self-medicate in grieving the losses of old age, incarcerated populations, the homeless, and those with eating disorders. Because obesity includes growing proportions of Americans from all demographic classifications in recent decades, and RDS is related to some of these cases, then RDS may affect all demographic designations, but further research is needed to clarify this with certainty.
Assessment
A thorough multi-discipline assessment is used to establish an individualized treatment plan for alcohol and substance abuse clients and should be used with RDS-related disorders. In addition, it is becoming increasingly important to establish gene involvement via genetic testing. This process begins with a clinical interview of the patient and family, which is vital in recognizing behavior patterns. A number of substance abuse checklists can help determine the presence of a substance abuse disorder. Genetic testing can establish the physical basis for RDS-related disorders. Mental health tests can uncover psychiatric illnesses. These tests include the Minnesota Multiphasic Personality Inventory (MMPI), Rorschach inkblot, and other personality and projective tests.
Treatment
Kenneth Blum was awarded U.S. Patent Number 6955873 for Diagnosis and treatment system for reward deficiency syndrome (RDS) and related behaviors on October 18, 2005. The diagnostic technique includes four kits for obtaining buccal (inner cheek) swabs for the following primary clusters of disorders: 1) neuro-transmitter, tryptophan, and opiate related problems in RDS behaviors, 2) the same problems in relation to weight gain, 3) allele analysis for attention deficit hyperactivity disorder, and 4) substance use disorders (SUDs), obesity, smoking, Tourette’s syndrome, schizoid/avoidant behavior, aggression, post-traumatic stress disorder (PTSD), and PMS.
In addition to swabs, the diagnosis includes the RDS Inventory Scale test, patented under this patent number. Upon analysis of the results of the swab or swabs obtained from a single client, the physician may or may not administer the patented medication formula via injection or oral ingestion for each kit that suggests treatment. Other treatments include a range of psychiatric medications and talking therapies, as well as holistic multidisciplinary techniques traditionally used for RDS-related mental illnesses before genetic testing and Blum’s treatment process was established.
Prognosis
Education, prevention, and early diagnosis are all vital to the mental health of individuals who may be at risk for RDS-related disorders. In particular, the earlier that alcohol and substance use disorders can be diagnosed, the better are the chances for successful treatment. Genetic testing for the A1D2 sequence of RDS is available and can be used in early diagnosis in infants and youth.
KEY TERMS
A1 allele— An allele related to RDS.
A1 D2— A chromosome sequence related to RDS.
Allele— One member of a pair or a series of genes that occupy a specific position on a specific chromosome.
D2— A dopamine receptor.
Dopamine— The neurotransmitter responsible for desire.
Fontal lobes— The large lobes at the front of the brain responsible for reasoning, problem-solving, and logic.
Neurotransmitter— A chemical that relays and amplifies electric signals between brain and central nervous system cells (neurons).
Nucleus accumbens— A structure deep inside and near the center of the brain that makes up a major part of the pathway of pleasure and reward.
Serotonin— The neurotransmitter responsible for satisfaction and inhibition.
Resources
PERIODICALS
Baicy, Kate. “Can Food Be Addictive? Insights on Obesity from Neuroimaging and Substance Abuse Treatment and Research.” Nutrition Noteworthy 7.1 (2005): article 4.
Blum, K., et al. “Genotrimtrade Mark, a DNA- Customized Nutrigenomic Product, Targets Genetic Factors of Obesity: Hypothesizing a Doamine-Glucose Correlation Demonstrating Reward Deficiency Syndrome (RDS).” Medical Hypotheses 68.4 (2006): 844–52.
Blum K., et al. “Reward Deficiency Syndrome in Obesity: A Preliminary Cross-Sectional Trial with a Genotrim Variant.” Advances in Therapy 23.6 (2006):1040–51.
Blum K., et al. “Reward Deficiency Syndrome.” American Scientist 84.4 (1996): 132–45.
Bowirrat, A., and Oscar-Berman, M. “Relationship between Dopaminergic Neurotransmission, Alcoholism, and Reward Deficiency Syndrome.” American Journal Of Medical Genetics. Part B, Neuropsychiatric Genetics: the Official Publication of the International Society of Psychiatric Genetics 132.1 (2005): 29–37.
Cohen, J. D., and K. I. Blum. “Reward and Decision.” Neuron 36 (Oct. 2002): 193–98.
Comings, D. E., T. J. H. Chen, K. Blum, J. F. Mengucci, S. H. Blum, and B. Meshkin. “Neurogenetic Interactions and Aberrant Behavioral Co-morbidity of Attention Deficit Hyperactivity Disorder (ADHD): Dispelling Myths.” Theoretical Biology and Medical
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Dick, Danielle M., PhD, Richard J. Rose, PhD, and Jaakko Kaprio, MD, PhD. “The Next Challenge for Psychiatric Genetics: Characterizing the Risk Associated with Identified Genes.” Annals of Clinical Psychiatry 18.4 (2006): 223–31.
Eisenberg, D. J. MacKill, M. Modi, J. Beauchemin, D. Dang, S. Lisman, J. K. Lum, and D. Wilson. “Examining Impulsivity as an Endophenotype Using a Behavioral Approach: A DRD2 TaqI A and DRD4 48-bp VNTR Association Study.” Behavioral and Brain Functions 3.2 (2007): http://www.behavioralandbrainfunctions.com/content/pdf/1744-9081-3-2.pdf
Linazaroso, G., N. van Biercom, and A. Lasa. “Hypothesis: Parkinson’s Disease, Reward Deficiency Syndrome and Addictive Effects of Levodopa.” Neurlogia 19.3 (2004):117–27.
Ponce, G., M. A. Jimenez-Arriero, G. Rubio, J. Hoenicka, I. Ampuero, J. A. Ramos, T. Palomo. “The A1 Allele of the DRD2 Gene (TaqI A polymorphisms) is Associated with Antisocial Personality in a Sample of Alcohol-Dependent Patients.”European Psychiatry 18.7 (2003): 356–60.
Schultz, W. “Behavioral Theories and the Neurophysiology of Reward.”Annual Review of Psychology 57 (2006): 87–115.
Shaffer, H. J., PhD, CAS, D. A. LaPlante, PhD, R. A. LaBrie, EdD, R. C. Kidman, BA, N. A. Donato, MPP, and M. V. Stanton, BA. “Toward a Syndrome Model of Addiction: Multiple Expressions, Common Etiology.” Harvard Review Psychiatry. 12.6 (2004): 367–74.
Volkow, N. D., G. Wang, J. S. Fowler, P. K. Thanos, J. Logan, S. J. Gatley, A. Gifford, Y. Ding, C. Wong, and N. Pappas. “Rain DA D2 Receptors Predict Reinforcing Effects of Stimulants in Humans: Replication Study.” Synapse 46.2 (2002): 79–82.
Wang, G, N. D. Volkow, P. K. Thanos, and J. S. Fowler. “Similarity Between Obesity and Drug Addiction as Assessed by Neurofunctional Imaging: A Concept Review.” Journal of Addictive Diseases 23.3 (2004): 39–53.
ORGANIZATION
The American Psychiatric Association, 1000 Wilson Boulevard, Suite 1825, Arlington, VA 22209-3901. Telephone: (703) 907-7300. http://www.psych.org
Patty Inglish, MS