Diet & Dopamine
A Dietary Approach to the Management of Chronic Pain and Reward Deficiency Syndrome
“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.”
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Dopamine Diet in the Management of Chronic Pain and the Reward Deficiency Syndrome (RDS)
As a quick overview of dopamine and the Reward Deficiency Syndrome (RDS), it is believed that the underlying basis for a number of medical conditions is associated with a deficiency of the neurotransmitter, dopamine, in the pleasure center of the brain, the nucleus accumbens (NAc). This deficiency may be based in genetic predisposition or by the environmental/experiential history of the individual or, frequently, a combination of both.
RDS and Chronic Pain
RDS is believed to play a contributing role in chronic pain. The control and sensitivity to pain is believed to reside in different locations in the brain, especially in the mesolimbic system of the brain, including the NAc. A number of genes and their genetic variants impact pain tolerance and/or sensitivity, including those related to dopamine receptors in the NAc that influence levels of dopamine. It is theorized that these genetic variants are associated with a predisposition to intolerance or tolerance to pain.
Recent studies have evaluated diet and depletion of dopamine precursors including tyrosine and phenylalanine. These studies indicate that depletion of dopamine appears not to increase the actual measure of severity perception of pain but rather increases the “unpleasantness” of pain. Increasing the “unpleasantness” of pain would function as a greater drive to reduce pain. Furthermore, these studies also identified a reduced mood associated with dopamine depletion, potentiating depression.
For those with either genetic variants or other circumstances predisposing to reduced dopamine levels, there may be an advantage to emphasizing dietary and other behavioral activities that would support maintaining higher dopamine levels.
Dopamine, Stress and Chronic Pain
While acute stress, including psychological stress, may actually serve to reduce awareness of pain and is associated with increased release of dopamine in the NAc, chronic stress, including chronic pain, has the opposite effect, increasing pain by inducing a hyperalgesic state. Studies indicate that stress-induced hyperalgesia which includes both thermal and chemical sensitivity, persists up to nine days after stress exposure.
Moreover, other neurotransmitters are also involved as well as dopamine. Disruption of the serotonin system in this part of the brain related to repeated stress produces a long-lasting increase in pain sensitivity. In fact, there is a disruption of both serotonergic and dopaminergic functions that occur within the NAc following chronic stress. This may account for some of the pain benefits that are obtained from some antidepressant medications that increase serotonin levels. It also underscores the intimate relationship between pain and depression. These mechanisms are well represented in fibromyalgia, a chronic pain condition markedly worsened by, and associated with, chronic stress.
Due to the impaired sense of well being associated with chronic stress, especially chronic pain, anad the potential role of dopamine depletion in aggravating chronie pain, maintaining optimal levels of dopamine in the NAc is believed to be beneficial in the management of chronic pain. Early research directed at enhancing dopamine levels through the supplementation of a medical food, Synaptamine, suggests a therapeutic role in the management of chronic pain. Other dietary interventions directed at increasing or maintaining dopamine leves are also thought to be beneficial.
RDS and Addiction
RDS is believed to be the underlying, fundamental basis for addiction, chemical or behavioral, which develops when a susceptible individual with insufficient dopamine levels experiences a drug or behavior that raises dopamine levels in the NAc. This experience of elevated dopamine levels triggers a strong sense of reward that fuels the drive to continue the behavior which evolves into an addiction.
As long as the addictive chemical or behavior is maintained, the reward drive is met and a sense of well being is maintained. But upon cessation of the addictive chemical or behavior, the dopamine levels drop, leading to withdrawal and craving. Furthermore, while in the withdrawal state, which may be prolonged, a re-exposure to the addictive agent (relapse) is accompanied by a hypersensitive reward response, in other words a magnified pleasure response, to the dopamine release triggered by the relapse. This magnified response results in a strong drive to maintain continued use (continued relapse). This re-experienced dopamine drive is strong and may overcome an addictive individual’s drive to stay sober.
RDS and Impulsive & Compulsive Disorders
In addition to the above, RDS is also believed to be an underlying factor in various impulsive and compulsive disorders including obsessive compulsive disorder (OCD), ADD, and Intermittent Explosive Disorder as well as PTSD.
Foods and Dopamine
Foods That May Contribute to Increased Dopamine
Dopamine doesn’t come in food, our body manufactures it from the dietary ingestion of the amino acid tyrosine . Researchers have looked at specific dietary modifications as a means to increase dopamine levels in the brain. By eating foods rich in tyrosine one may theoretically increase dopamine levels but of course it is not that simple. Also, feasting on tyrosine rich foods may have a transient effect on increasing dopamine levels but this surge in dopamine may lead to a subsequent crash in levels which would be counterproductive. It is likely wiser to simply assure adequate, frequent ingestion of tyrosine rich foods to support your potential needs for production.
Meat, Poultry and Fish
Tyrosine deficient diets are highly unlikely in industrialized countries. Since tyrosine is an amino acid, the building blocks of protein, foods rich in protein will be rich in tyrosine, especially meat. Other good sources of protein includes eggs, cheese, chicken, turkey and fish. Fatty fish such as salmon, halibut, striped bass, rainbow trout, tuna, and sardines are also good sources of omega-3 fatty acids which have been shown to increase brain dopamine levels. Eggs also contain choline, a substance believed to help optimize neurotransmission and elevate dopamine levels.
While vegetables are not a particulary good source of tyrosine, many vegetables are excellent source of folate (Vitamin B9) which is necessary for the manufacturing of dopamine as well as serotonin, adrenaline and noradrenaline. Folate-rich vegetables include: artichokes, avocados, black beans, broccoli, cauliflower, chickpeas, kale, lentils, spinach and red beets. Red beets also contain tyrosine as well as “betaine” which is believed to regulate levels of serotonin and dopamine which may help improve mood.
Many fruits contain tyrosine although not at concentrations as high as meat, poultry and fish. Some fruit that contain tyrosine include apples, bananas (the “riper” the banana, the greater the tyrosine content), blueberries, papaya, prunes, strawberries and watermelons. Fruits (and vegetables) also contain many antioxidants that also may contribute to higher levels of dopamine, though somewhat indirectly (see below).
Many fruits, especially cherries, blueberries, blackberries and raspberries, contain quercetin, a substance that inhibits COMT, an enzyme that breaks down dopamine, which may lead to increased dopamine levels.
Other foods associated with increasing dopamine include certain beverages, oils, nuts and herbal supplements.
Chocolate contains phenylethylamine (PEA), a precursor (building block) to the body’s manufacturing of dopamine which may trigger a release of dopamine. Many chocolates also contain another amino acid, tyramine which is associated with dopamine increases.
Coffee appears to increase levels of dopamine in the short-term because of it’s stimulatory effect. The increased cognitive function associated with drinking coffee is in part a result of inceased dopamine. Over time it is believed, however, that tolerance builds up to the effect of caffeine.
Gingko biloba may function to improve cognitive function which is thought to possibly be a result of increasing levels of dopamine.
There is some evidence that panax ginseng acts on the brain’s dopaminergic system
Green tea contains polyphenols and L-theanine thought to be associated with increasing dopamine. In addition, green tea contains antioxidants and NRF2 activators, thought to indirectly increase dopamine levels.
Nuts & Seeds:
Almonds, sesame seeds and pumpkin seeds have been suggested to help maintain sufficient dopamine levels.
Oregano oil contains carvacrol – a substance believe to help maintain sufficient levels of dopamine in the bra
Spirolina, an aquaculture food dietary supplement, is a rich sources of tyrosine.
The active ingredient in the spice turmeric is “curcumin,” a powerful antioxidant and NRF2 activator that is known to cross the blood-brain barrier and increase levels of dopamine.
Wheat contains phenylalanine, an amino acid that gets converted into tyrosine and then dopamine. If you’re sensitive to the effects of gluten, avoid wheat products.
Diet and Dopamine
Sugars and Carbohydrates
Diet can affect dopamine levels in the NAc which can play a role in chronic pain, and impact predisposition to addiction relapse or exacerbation of behavioral disorders. It has been well established that eating sugar and sweets and other carbohydrates reacts with the same opioid receptors in the brain that opioids do, thus triggering a dopamine response that mimics that of exposure to an addictive drug or behavior. This is the basis for sugar cravings and the potentially addictive nature of eating sweets, including binge eating, and why sweets taste so good. Because cating sweets and carbohydrates triggers a dopamine surge that is followed by a rapid drop in dopamine levels, it is believed that this may contribute to a relapse into addictive behavior. In addition, patients in early remission from one addiction often transfer their addiction to another manifestation of RDS, including another chemical addiction, a behavioral addiction or trigger or exacerbate an impulsive or compulsive disorder. The most frequent addiction transfer with opioid addiction is to magnify a craving for sweets.
Different carbohydrates offer a range of potential risks and is believed to be related to the “glycemic index” of the carbohydrate. The glycemic index of a carbohydrate refers to the impact of carbohydrate-rich foods and fluids on changes in glucose and insulin. In this respect, the glycemic index ranks foods from 0 to 100 with values less than 30 to 40 being considered ‘low glycemic’, 40 to 70 ‘moderate glycemic’ and those greater than 70 considered ‘high glycemic’. Low glycemic index foods raise blood glucose and insulin levels more slowly than higher glycemic index foods and are also considered to have less impact on dopamine levels compared with higher glycemic foods.
Research suggest that the magnitude of increase of glucose levels, the rate at which this increase in glucose occurs and the overall insulin response to food ingestion, also increase the risk for obesity, cardiovascular disease and high blood pressure.
It is recommended that patients with chronic pain or conditions associated with RDS, especially chemical addictions, maintain a low glycemic diet.
Ways to Fight Sugar Cravings
1. Substitute whole fruit for sweets.
Fruit contains fructose, which is metabolized differently than sucrose or glucose — and it still provides satisfaction for the urge for sweet. Be careful to restrict fruit intake to a few servings a day. But, at all costs, avoid high fructose corn syrup (HCFS), a particularly unhealthy sweetener added to most sodas and many unlikely foods including salad dressings.
2. Avoid artificial sweeteners.
Artificial sweeteners seem to offer a healthier option to sugar but research indicates this is not true. Eliminate aspartame, sucralose, saccharine — even stevia in large amounts — since they can trigger a desire for sweet food and create the need for more and more to feel satisfied. One study has identified a link between increased consumption of artificial sweeteners and weight gain.
3. Clean out the kitchen.
Get rid of any sugary snacks and foods at home and work and reduce temptation.
4. Create a backup plan for confronting sugar cravings.
If sugar cravings feel uncontrollable, think proactively and create a plan or distraction that will help you overcome them. Eat a piece of fruit. Go for a walk. Listen to some music. Call or text a friend. Engaging a predetermined plan can make all the difference in avoiding undesired behaviors.
Use of alcohol, like other potentially addictive drugs, triggers a dopamine response although by different receptors than opioids and sweets. The same arguments against it’s use as a means of reducing risk for relapse apply as noted above. However, in addition to the dopamine argument, alcohol affects the prefrontal cortex area of the brain that suppresses normal inhibition of impulsive behavior. One of the significant changes in the neurochemical circuitry that occurs in addiction results in a predisposition to impulsive behavior. The use of alcohol, even in relatively low amounts can contribute to an impulsive behavior culminating in relapse. As many patients with addiction will relate, sometimes relapse occurs so quickly as an impulse, that “I didn’t even think about it, I just found myself using again.”
For this reason, absolute abstinence of alcohol should be engaged, especially in early stages of remission to both chemical and behavioral addictions. Current research on neurocircuitry changes associated with addiction suggest that it may take up to 3 years of remission to reverse.
Stress has been long recognized as a contributor to the severity of chronic pain and both the initiation of addiction and other reward deficiency conditions but also addiction relapse and exacerbation of reward deficiency syndromes. Different mechanisms have been proposed as to how stress contributes to these conditions.
Emotional and physical stress, including chronic pain, trigger physiologic changes that result in increased levels of free radicals, also known as reactive oxygen species (ROS) and reactive nitrogen species (RNS). The increase levels of these chemical species is know as “oxidative stress.” Increased oxidative stress is believed to accompany addiction and reward deficiency syndromes. It is also believed that increased oxidative stress results in increassed risk for cardiovascular diseas and cancer.
One proposed mechanism in which oxidative stress impacts neurochemistry and physiology is through epigenetic mechanisms. Epigenetics, an emerging area in the neuroscience field, has provided important clues about how drugs of abuse interact with DNA, RNA and genes, modulate genetic functions and regulate different manifestations of pain and addiction. Epigenetics explains how environmental and psychological factors regulate the activity of our genome without inducing changes in the DNA sequence. It has been proposed that epigenetics mediates our behavior, in part, and has long- term effects on the regulation of the genetic function.
Different foods in our diets contribute to varying degrees of oxidative stress and therefore may contribute to the severity of symptoms related to chronic pain and addiction, including pain severity, anxiety, depression and risk for relapse. For this reason, an anti-inflammatory diet is recommended as part of the dopamine diet, both as a means of maintaining dopamine levels as well as providing synergistic benefits.
The Mediterranean diet along with the Paleo diet are two of the diets currently proposed that emphasize anti-inflammatory foods. Fish and other foods rich in omega-3 fatty acids along with vegetables high in antioxidants contribute to reducing oxidative stress. Of course, avoidance of foods high in omega-6 fatty acids, high glycemic index carbohydrates and high calorie, low nutritional value foods (highly processed and fast foods) is key to an anti-inflammatory diet.
While not technically part of the diet, supplements including medical foods, vitamins, nutraceuticals and natural supplements that provide added nutritional value and enhanced anti-inflammator and antioxidant benefits are recommended. Of particular value are the NRF2 activators, antioxidants that stimulate cellular production of the body’s own antioxidants.
L-tyrosine and L-phenyalanine
There is some evidence that supplementing with the amino acids L-tyrosine and L-phenyalanine which are building blocks for the production of dopamine can stimulate the manufacture of dopamine and, at least transiently, increase levels of dopamine. Studies that have investigated diets that are depleted of L-tyrosine and L-phenyalanine result in a greater perception of the “unpleasantness” of pain and to lower mood.
This is an herbal supplement that inhibits the enzyme monoamine oxidase (MAO) that breaks down serotonin and dopamine, thus increasing their levels.
See Rhodiola Rosea
The singularly most effective supplement for raising and maintaining dopamine is Synaptamine, a medical food supplement. Synaptamine contains a number of natural ingredients including tyrosine, rhodiola rosea that promote increased levels of dopamine and has been shown to be effective in the management of chronic pain as well as reducing withdrawal symptoms and facilitating addiction remission and the reduction of nightmares associated with PTSD. Developed by the researcher that first discovered and defined RDS, Synaptamine has a huge, and still growing body of research evidence that confirms benefit in managing multiple RDS conditions.
Synaptamine is available online or through Accurate Clinic.
Synaptamine is a Patented Formula is made of a proprietary blend containing:
Pyridoxal-5-Phos USP, L-Tyrosine, L-Glutamine, Rhodiola Rosea Root SE, Rosavins, Griffonia Seed Extract 5-HTP, L Phenylalanine, Chromium GTF Plus, Passion Flower SE Isovitexin, N-Acetyl-L-Cysteine USP, Glucosamine N-Acetyl, Arabinogalactan FiberAid AG99, Aloe Vera FD Powder 200X, White Birch Bark 4:1 Extract, Bosellia Serrata Gum Extract, Spirulina Algae.
Behavioral Alternatives to Increase Dopamine
ould be incomplete to not mention other means of increasing levels of dopamine other than by increasing dopamine production. Studies support that certain activities also are associated with increasing dopamine levels including fasting, meditation, physical exercise, massage and obtaining adequate sleep. Dopamine is particularly associated with reward. Activities that provides one with pleasure or a sense of accomplishment such as achieving a goal have been shown to help maintain or increase brain dopamine levels, especially in the nucleus accumbens, the reward center of the brain.
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 the primitive human species and later (beginning approximately
80,000 years ago) it 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. Dopamine is known to increase activity levels, speed up our internal clocks and create a preference for new experiences.
Dopamine is found in abundance in several areas of the brain, especially in the nucleus accumbens (NAc), 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 experiencing pleasure and reward. 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 (NAc). Medications and chemicals that are known to increase dopamine levels include the addictive drugs cocaine, opioids, marijuana, alcohol, amphetamines, methamphetamines and also sugar (not a complete list).
RDS – Overview
- The Addictive Brain – All Roads Lead to Dopamine – 2012
- Hatching the behavioral addiction egg – Reward Deficiency Solution System – 2014
- Sex, Drugs, and Rock ‘N’ Roll – Hypothesizing Common Mesolimbic Activation as a Function of Reward Gene Polymorphisms – 2012
- Increased Dopamine Receptor Activity in the Nucleus Accumbens Shell Ameliorates Anxiety during Drug Withdrawal – 2012
- Dopamine and glucose, obesity, and reward deficiency syndrome – 2014
RDS – Chronic Pain
- Hypothesizing that brain reward circuitry genes are genetic antecedents of pain sensitivity and critical diagnostic and pharmacogenomic – 2009
- A Multi-Locus Approach to Treating Fibromyalgia by Boosting Dopaminergic Activity in the Meso-Limbic System of the Brain – 2014
- The indirect pathway of the nucleus accumbens shell amplifies neuropathic pain – 2016
- Four Cases of Chronic Pain That Improved Dramatically Following Low-Dose Aripiprazole Administration – 2011
- The Neurobiology of Time Processing – 2016 Positive emotions and brain reward circuits in chronic pain – 2016
- Positive emotions and brain reward circuits in chronic pain – 2016
- Chronic Back Pain Is Associated with Alterations in Dopamine Neurotransmission in the Ventral Striat
um – 2015
RDS – Dopamine & Diet
- Dopamine Precursor Depletion Influences Pain Affect Rather than Pain Sensation – 2014
- Dopamine and Pain Sensitivity – Neither Sulpiride nor Acute Phenylalanine and Tyrosine Depletion Have Effects on Thermal Pain Sensations in Healthy Volunteers – 2013
- Acute Phenylalanine Tyrosine Depletion – A New Method to Study the Role of Catecholamines in Psychiatric Disorders – 2004
- Effects on Mood of Acute Phenylalanine Tyrosine Depletion in Healthy Women – 2000
- Caffeine increases striatal dopamine D2:D3 receptor availability in the human brain – 2015
- Complexity of dopamine metabolism – 2013
- Specific behavioral and cellular adaptations induced by chronic morphine are reduced by dietary omega-3 polyunsaturated fatty acids – 2017
RDS – Oxidative Stress
RDS – Treatment
RDS Treatment – Overview
- Clinically Combating Reward Deficiency Syndrome (RDS) with Dopamine Agonist Therapy as a Paradigm Shift – Dopamine for Dinner? 2015
- Neurogenetics and Nutrigenomics of Neuro-Nutrient Therapy for Reward Deficiency Syndrome (RDS)
RDS Treatment – Synaptamine
Synaptamine – Overviews
Synaptamine – Fibromyalgia
- A Multi-Locus Approach to Treating Fibromyalgia by Boosting Dopaminergic Activity in the Meso-Limbic System of the Brain – 2014
Emphasis on Education
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