Accurate Education – Reward Deficiency Syndrome

Reward Deficiency Syndrome

The Neurobiology of Addiction

 

“Reward Deficiency Syndrome,” a term first coined by Ken Blum in 1995, can be defined as:

 

“A brain reward genetic dissatisfaction or impairment that results in aberrant pleasure seeking behavior that includes drugs, excessive food, sex, gaming/gambling and other behaviors.”

 

These other behaviors include an array of disorders, such as PTSD,  ADHD, Tics, Tourette Syndrome, autism, Asperger Syndrome, OCD, “compulsive” sexual practices, binge eating and others. The relationships of these disorders becomes apparent with the understanding of the common genetic factors underlying them.

 

See also:

AA/NA and 12-Step Programs

Addiction Recovery

Complementary & Alternative Addiction Recovery

Synaptamine

Dopamine Diet

Dopamine Enhancement

  

Definitions and Terms Related to Pain

Key to Links:

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the brain

Enormous possibilities for health and creativity are held captive by your likes and dislikes. Inspecting your desires and attachments to food and making choices intuitively with discrimination will make your spiritual practice and every other relationship more rewarding.

– Leonard Perlmutter

Reward Deficiency Syndrome (RDS)

 

The Underlying Basis for Drug Addiction

Why do some people become addicted to drugs, while others do not? Importantly, at first, people may perceive what seem to be positive effects from drug use. They also may believe that they can control their use; however, when addiction takes over, a person’s ability to maintain self-control can become seriously impaired. Brain imaging studies from drug-addicted subjects show physical changes in areas of the brain that are critical to judgment, decision-making, learning, memory and behavior control.

 

At the heart of understanding the neurobiology of addiction is to understand the neurophysiologic correlates of perceiving the reward of feeling good, experiencing pleasure and the sense of well-being. Currently, neuroscience literature
 regarding addiction centers on dopamine and considers dopamine to be both a “pleasure molecule” and 
an “anti-stress molecule.”

 

The Neurobiology of Reward and Addiction

Initially, person may use substances for several reasons, such as to experience the euphoric effects, to relieve stress, to overcome anxiety or depression (or both), or to blunt pain, physical or psychological. A person may continue a number of behaviors, such as gambling, sex, computer gaming or other activities for the same motivations. But with repeated exposure, however, substance use or behaviors in some people can become uncontrollable and the person begins to lose the ability to stop the behavior or substance use even when continuing becomes harmful or disruptive to their lives. When away from the substance or behavior they develop compulsive desires and cravings to resume the behavior or substance use. This loss of control and compulsive drive to continue are the defining characteristics of addiction.

 

It is believed that this addictive process represents a chronic disease that is manifested by changes in the brain that are influenced by genetic and environmental factors. The essence of addiction revolves around a reward response, in which behaviors and chemicals trigger a sense of reward associated with pleasure and perception of well-being. The understanding of reward systems and behavior begins with recognizing the basic drives that sustain life and survival of both the individual and the species, including eating and sexual behavior.

 

The primary rewarding effects of addictive substances and behaviors occur in several brain structures that link basic emotions and connect them to memories, which drive behavior. These behaviors produce sensations of pleasure in response to actions that support survival (e.g., eating, sex) but also sensations of fear in response to potential dangers. These sensations in turn trigger the endocrine (hormone) and autonomic nervous systems, stimulating bodily responses. The brain’s reward and stress systems can be seen to reinforce life-sustaining behaviors.

 

Several areas of the brain are involved in the perception of reward, pleasure and well-being and in turn they play roles in the formation of addictions. The prefrontal cortex modifies pleasure and pain signals from other brain areas. Feelings of reward are focused in the core of the limbic system where neurons in the ventral tegmental area (VTA) release the neurotransmitter dopamine into the nucleus accumbens (NAc). Nerve activity within this VTA–NAc circuit is necessary to experience reward, although other areas and brain reward circuit also exert strong influences. For example, the hippocampus contributes memories relevant to an experience that modifies the reward experience positively or negatively. The amygdala adds important emotional information about a reward stimulus that contributes to the motivational impact of the experience. In addition, parts of the prefrontal cortex (i.e., anterior cingulate and orbitofrontal cortices) modify pleasure and pain signals to help integrate all the information and allow the individual to decide whether to initiate 
or suppress a particular behavior in response to the stimulus.

 

The use of most addictive substances increase the levels of dopamine in the brain reward centers well beyond what occurs in naturally rewarding situations (e.g., sex, food). Some drugs (e.g., marijuana, heroin) produce dopamine effects indirectly. Amphetamines cause some brain areas to release more dopamine, and cocaine prevents its reuptake of dopamine after its release, thus prolonging its effects. These excessive dopamine effects disrupt normal nerve signaling in the brain.

 

The brain adjusts to excess dopamine levels by producing less dopamine and by reducing the number of receptors that respond to it in the receiving (postsynaptic) neuron. As a result, the pleasurable effects of
 a drug become diminished with continued use. Worse, the pleasurable effects of normal activities also are blunted, creating a state called anhedonia (a reduced ability to experience pleasure), a hallmark of prolonged addiction.

 

The prolonged impairment of the dopamine balance and pleasure circuits in the brain lead to changes in the neurochemical pathways and structures in the reward-related areas of the brain. These changes drive the intense cravings and compulsive behaviors for substances that increase dopamine levels. Furthermore, these neurochemical and structural changes persist even after use of the addictive substances stop or the addictive behaviors cease. Current research indicates that it may take as long as three years or more for many of these changes resolve.

 

The challenge in treating addiction is to learn means of facilitating a return to neurochemical and structural normalcy as a means of preventing relapse. Use of medications and nutritional supplements directed at increasing dopamine production in the brain has been a common focus of recommended treatments. Targets for treatment also include addressing genetic variants that contribute to addiction susceptibility as a consequence of suboptimal dopamine production and maintenance as well as reduced numbers of dopamine receptors.

 

More About Dopamine

It is theorized that increased levels of dopamine
 were part of a general physiological adaptation related to survival around two million years
 ago by primitive human species and later (beginning approximately 
80,000 years ago) further evolved as a result of dietary changes and other environmental and social factors. High species dopamine levels are thought to characterized by higher intelligence, a sense of personal destiny, religious/cosmic preoccupation and an obsession with achieving goals and conquests. According to theory, dopaminergic drive is extremely goal-oriented, fast-paced, and even manic sometimes, given that dopamine is known to increase activity levels, speed up our internal clocks and create a preference for new experiences.

 

Dopamine is manufactured from L-tyrosine, an amino acid found in meat, in several areas of the brain, especially in the nucleus accumbens (Nac), considered to be the center of reward experience. Activities,  behaviors and chemicals or medications that contribute to higher dopamine levels in the Nac correlate with greater sensations of pleasure and well-being.

 

Dopamine functions in the brain as a neurotransmitter that activates receptors in the brain, known as dopamine receptors D1 through D5. Research indicates that one receptor in particular, the D2, receptor, is of particular importance in achieving pleasure and reward and the relative abundance of D2 levels of in the Nac influences the capacity of dopamine to trigger pleasure and sustain a sense of well-being. Furthermore, there are genetic (DNA) variants that determine whether an individual is born with a fewer or greater number of D2 receptors. Those who have fewer D2 receptors require more dopamine to achieve a sense of reward, pleasure and perception of well-being. Thus, there is a genetic influence, or drive, towards behaviors that increase dopamine levels, including ingestion of medications and chemicals that increase dopamine levels in the reward and pleasure center of the brain. Medications and chemicals that are known to increase dopamine levels include the addictive drugs cocaine, opioids, marijuana, alcohol, amphetamines, methamphetamines and also sugar. Obviously, this not a complete list.

 

“Reward Deficiency Syndrome”

It is believed that those individuals with inadequate levels of dopamine in the reward center of their brain (the Nac) due to genetic or environmental circumstances, experience an innate drive to respond to chemicals and activities that increase their low or inadequate dopamine levels. This is the basis of the “Reward Deficiency Syndrome,” the condition of sub-optimal dopamine levels in the Nac and related brain areas. It is further recognized that a variety of activities increase dopamine levels, including behaviors such as sex, binge eating, gambling, thrill-seeking, computer gaming and even expressing strong anger. The dopamine drive inherent in these behaviors is believed to contribute to their addictive potential, especially in those people who may have genetic or environmental circumstance that predispose them to low dopamine levels and/or low amounts of D2 receptors.

 

As such, it is believed that “Reward Deficiency Syndrome” is the common denominator underlying both chemical and behavioral addictions and also contributes to compulsive disorders such a obsessive compulsive disorder (OCD) as well as PTSD, ADD and certain anger disorders.

 

Evaluating Addiction Risk and Management

Vulnerability to addiction differs from person to person and is influenced by both environmental factors (home, family, nutrition, availability of drugs, stress, and peer pressure in school, early use and method of administration) and genetic risk factors. Researchers estimate that genetic factors account for between 40% to 60% of a person’s vulnerability to addiction, (especially alcoholism) including the effects of environment on gene expression (epigenetics) and function. It is also significant that individuals with comorbid mental disorders are at greater risk of drug abuse and addiction than the general population.

 

Understanding how genetic variants, stress and other environmental factors contribute to dopamine levels provides opportunities for alternative approaches to treating addiction and other manifestations of RDS.

(Return to this page in the near future for more information on genetic testing.)

 

 

The Brain Reward Cascade

 Neurotransmitters within the mesolimbic reward system

The brain reward cascade starts in the hypothalamus of the brain sitting in the midbrain called the mesolimbic system where serotonin acts as the neurotransmitter activating the enkephalins (one type of brain endorphin); the enkephalins are released in the hypothalamus and stimulate mu receptors in another part of the brain called substania nigra that contains the neurotransmitter GABA (an inhibitory neurotransmitter) that stimulates GABA-B receptors that projects to the ventral tegmental area (VTA) brain region where dopamine neurons are inhibited to allow for just the right amount of dopamine to be released at the nucleus accumbens (reward site of brain).

 

Reward Deficiency Syndrome (RDS)

Associated with the new definition and understanding of addiction as related to reward deficiency is a major paradigm shift in our  approaches to treatment.  The following articles are available to provide further understanding of the nature of Reward Deficiency Syndrome and how to treat it.

 

 

RDS – Overview

  1. The Addictive Brain – All Roads Lead to Dopamine – 2012
  2. Hatching the behavioral addiction egg – Reward Deficiency Solution System – 2014
  3. Sex, Drugs, and Rock ‘N’ Roll – Hypothesizing Common Mesolimbic Activation as a Function of Reward Gene Polymorphisms – 2012

 

RDS – ADD

  1. Attention-deficit-hyperactivity disorder and reward deficiency syndrome – 2008
  2. Reward Deficiency Syndrome – Attentional Arousal Subtypes, Limitations of Current Diagnostic Nosology, and Future Research – 2015

 

RDS – Gaming

  1. linking-online-gaming-and-addictive-behavior-converging-evidence-for-a-general-reward-deficiency-in-frequent-online-gamers-2014

 

RDS – Genetics

  1. Multilocus Genetic Composite Reflecting Dopamine Signaling Capacity Predicts Reward Circuitry Responsivity 2012
  2. Genetic Addiction Risk Score (GARS) – Testing For Polygenetic Predisposition and Risk to Reward Deficiency Syndrome (RDS) – 2011
  3. Neurogenetic Impairments of Brain Reward Circuitry Links to Reward Deficiency Syndrome (RDS) – Potential Nutrigenomic Induced Dopaminergic Activation

 

RDS – Obesity

  1. Reward Deficiency Syndrome Studies of KB220 Variants
  2. Mood, food, and obesity
  3. Dopamine and glucose, obesity, and reward deficiency syndrome – 2014
  4. Dopamine for “wanting” and opioids for “liking”: a comparison of obese adults with and without binge eating. – PubMed – NCBI
  5. “Liking” and “Wanting” Linked to Reward Deficiency Syndrome (RDS) – Hypothesizing Differential Responsivity in Brain Reward Circuitry – 2012
  6. Neuro-Genetics of Reward Deficiency Syndrome (RDS) as the Root Cause of “Addiction Transfer”- 2011

 

RDS – Chronic Pain

  1. Hypothesizing that brain reward circuitry genes are genetic antecedents of pain sensitivity and critical diagnostic and pharmacogenomic – 2009
  2. A Multi-Locus Approach to Treating Fibromyalgia by Boosting Dopaminergic Activity in the Meso-Limbic System of the Brain – 2014

 

RDS – PTSD

  1. Neuro-psychopharmacogenetics and Neurological Antecedents of Posttraumatic Stress Disorder – Unlocking the Mysteries of Resilience and Vulnerability – 2010
  2. Diagnosis and Healing In Veterans Suspected of Suffering from Post-Traumatic Stress Disorder (PTSD) Using Reward Gene Testing and RewardCircuitry Natural Dopaminergic Activation-2012
  3. Putative dopamine agonist (KB220Z) attenuates lucid nightmares in PTSD patients – Role of enhanced brain reward functional connectivity and homeostasis redeeming joy – 2015

 

RDS – Sleep

  1. Dopaminergic Neurogenetics of Sleep Disorders in Reward Deficiency Syndrome (RDS) – 2014

 

RDS – Treatment

RDS Treatment Overview

  1. Clinically Combating Reward Deficiency Syndrome (RDS) with Dopamine Agonist Therapy as a Paradigm Shift – Dopamine for Dinner? 2015
  2. Neurogenetics and Nutrigenomics of Neuro-Nutrient Therapy for Reward Deficiency Syndrome (RDS)

 

RDS Treatment – Meditation

  1. Increased dopamine tone during meditation-induced change of conscio… – PubMed – NCBI

 

RDS Treatment – Music Therapy

  1. Do dopaminergic gene polymorphisms affect mesolimbic reward activat… – PubMed – NCBI

 

RDS TreatmentSynaptamine

Synaptamine – Overviews

  1. Synaptamine – brief summary

 

Synaptamine – Buptrenorphine

  1. Withdrawal from Buprenorphine:Naloxone and Maintenance with a Natural Dopaminergic Agonist – A Cautionary Note

 

Synaptamine – Fibromyalgia

  1. A Multi-Locus Approach to Treating Fibromyalgia by Boosting Dopaminergic Activity in the Meso-Limbic System of the Brain

 

Synaptamine – Lucid Nightmares

  1. Putative dopamine agonist (KB220Z) attenuates lucid nightmares in PTSD patients – Role of enhanced brain reward functional connectivity and homeostasis redeeming joy – 2015
  2. Using the Neuroadaptagen KB200zTM to Ameliorate Terrifying, Lucid Nightmares in RDS Patients – the Role of Enhanced, Brain- Reward, Functional Connectivity and Dopaminergic Homeostasis – 2015

 

Synaptamine – PTSD

  1. Putative dopamine agonist (KB220Z) attenuates lucid nightmares in PTSD patients – Role of enhanced brain reward functional connectivity and homeostasis redeeming joy – 2015
  2. Diagnosis and Healing In Veterans Suspected of Suffering from Post-Traumatic Stress Disorder (PTSD) Using Reward Gene Testing and RewardCircuitry Natural Dopaminergic Activation-2012

 

Synaptamine – Sleep

  1. hypothesizing-that-putative-dopaminergic-melatonin-benzodiazepine-reward-circuitry-receptors – 2013

Emphasis on Education

 

Accurate Clinic promotes patient education as the foundation of it’s medical care. In Dr. Ehlenberger’s integrative approach to patient care, including conventional and complementary and alternative medical (CAM) treatments, he may encourage or provide advice about the use of supplements. However, the specifics of choice of supplement, dosing and duration of treatment should be individualized through discussion with Dr. Ehlenberger. The following information and reference articles are presented to provide the reader with some of the latest research to facilitate evidence-based, informed decisions regarding the use of conventional as well as CAM treatments.

 

For medical-legal reasons, access to these links is limited to patients enrolled in an Accurate Clinic medical program.

 

Should you wish more information regarding any of the subjects listed – or not listed –  here, please contact Dr. Ehlenberger. He has literally thousands of published articles to share on hundreds of topics associated with pain management, weight loss, nutrition, addiction recovery and emergency medicine. It would take years for you to read them, as it did him.

 

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