MAIN CAUSES OF ADDICTIONS
- High Histamine levels – Decreases Dopamine and Serotonin
- Having the DRD2 A1 gene – Reward Deficiency Syndrome
- Early life stress / Pyrrole Disorder
The word “addiction” is derived from a Latin term for “enslaved by” or “bound to.” Anyone who has struggled to overcome an addiction — or has tried to help someone else to do so — understands why.
If you struggle with alcoholism, opiate dependence, psychostimulant abuse (e.g., cocaine), nicotine dependence, glucose binging and overeating, inability to focus (ADHD and other spectrum disorders), pathological gambling, excessive Internet gaming, sex addiction, and obsessive-compulsive disorder, among other repetitive known behaviors and want to change Excel Well LLC is here to help.
Early life stress including developmental trauma can play a role in one’s inclination toward alcoholism and drug addiction. (1) Results from preclinical studies indicate that alterations of the early microbial composition by way of antibiotic exposure, lack of breastfeeding, birth by Caesarean section, infection, stress exposure, and other environmental influences – coupled with the influence of host genetics – can result in long-term modulation of stress-related physiology and behaviour.(2) Early life stress can alter the production of neurosteroids especially allopregnanolone which is the calming neurosteroid that works on the GABA receptors. Yale Stress Center used progesterone in a study to increase the allopregnanolone levels in cocaine addicts with great results on reducing cravings. (3)
All of the above causes low grade inflammation which affects the neurotransmitters in the brain and in the gut which causes the dysfunctional HPA Axis and can lead to addiction.(4) So addressing the causes of the inflammation is one area to pursue if one is trying to end addiction.
Measuring the glucocorticoid receptor sensitivity is highly recommended. Specific patterns of a dysregulation of the HPA axis and GR function are found in different stress-related psychiatric entities e.g. major depression, job-related exhaustion or posttraumatic stress disorder. GR challenge tests like the dexamethasone-suppression test (DST), the dexamethasone-corticotropin-releasing hormone (dex-CRH) test or most recently the analysis of the dexamethasone-induced gene expression are employed to sensitively measure HPA axis activity in these disorders. They provide information for a stratification of phenotypic similar but neurobiological diverse psychiatric disorder.
Getting the hormones to optimal levels (high normal or slightly above) not just normal levels is very important too. Pregnenolone, Cortisol and Progesterone levels should be checked.
There is always the psychosomatic (mind over matter) issues when it comes to addictions as well so seeing a mental health professional who specializes in addiction is highly recommended. You can read Tony Robbins techniques to Changing Behavior here.
Reward Deficiency Syndrome (RDS)
is a psychological theory first noted by Kenneth Blum PhD in 1996. It is characterized by reward-seeking behavior and/or addictions, stemming from genetic variations, most notably resulting from those carrying the D2A1 allele. People carrying the A1 allele tend to have insufficient numbers of D2 receptors in their brain, resulting in lack of pleasure and reward from activities that would provide others with pleasure.
This can result in addiction, mood disorders, compulsions, impulsivity, and other spectrum disorders. Since the normal “pleasure” neurotransmitters such as dopamine are lower among these individuals, they don’t feel as good as they should from normal activities. This leads them to seek out more extreme thrills such as addictive drugs or behaviors like gambling.
Due to the thrill seeking to feel the same level of reward as normal individuals, a person who is deficient in reward may finally feel some degree of pleasure from the addictive stimuli. Unfortunately, it is somewhat difficult to determine whether the reward-deficiency syndrome (RDS) was a result of genetic inheritance, or whether it was caused by stress or drug usage. Engaging in addictive behavior can inherently alter the pleasure center of the brain as well as neurotransmission.
It should be hypothesized that temporary cases of RDS can be caused by various drugs, stressors, or behaviors that can create changes within the brain. Therefore one could argue that the genetic D2 abnormalities could have been caused by drug usage or the addictive behavior in some cases. In other cases, it may be more likely that the genetics lead an individual to seek out an addictive substance due to lack of reward.
What causes reward deficiency syndrome? (Contributing factors)
In cases of reward-deficiency syndrome, researchers agree that there is usually a major genetic component. Throughout years of research, the goal has been to find a specific genetic variant that could be contributing to this condition. Early research regarding Reward Deficiency Syndrome discovered a link between carrying a certain allele (the “A1”) and alcoholism. Upon further investigation, this same allele was also associated with the development of other addictive, compulsive, and impulsive behaviors and disorders.
Examples of disorders influenced by this allele include (but are not limited to): ADHD, compulsive eating, obesity, pathological gambling, and Tourette’s syndrome. Although there may be multiple genetic factors that contribute, prominent researcher Kenneth Blum has determined that RDS is more likely among those with a specific A1 allele. Those carrying the A1 allele tend to have a significantly fewer number of D2 receptors in their brain. Therefore they cannot experience pleasure to the same extent as people without this gene and seek out addictive behaviors as compensation.
A1 Allele: Those carrying the A1 allele tend to have insufficient D2 receptor development. The A1 allele associated with reward-deficiency syndrome and is present in approximately 25% of the general population. Blum’s research has been able to pinpoint this specific allele being linked to addictions such as alcoholism among first-degree relatives and families. When this specific allele gets passed on, the kids who inherit it are naturally more susceptible to developing addictions.
P300 waves: This is electrical activity in the brain that is common among alcoholics. The P300 waves have been measured among sons to alcoholic fathers, and even from a young age, there is a significant increase in this “positive 300-millisecond” wave. This specific brain wave is also associated with some cases of RDS.
Smoking: Among smokers, approximately 48% carry the A1 allele. Those who carried the A1 allele tend to smoke from an earlier age and have a more difficult time when they try to quit smoking. In people who had been able to successfully quit smoking or had never smoked at all, the prevalence of the A1 allele was significantly less.
Studies have determined that over 50% of those who are pathological gamblers carry the A1 allele. Those with more severe cases of gambling were more likely to carry the A1 allele. Furthermore, in a sample of men who had comorbid drug and gambling problems, the A1 allele was found among 76% – very significant.
In the human genome, chromosome #11 is responsible for containing the gene that codes the D2 dopamine receptor; this is one of 6 total receptors.
In cases of reward deficiency syndrome, many neurotransmitter receptors have been investigated. Although there is generally a complex interplay between receptors that contribute to this condition, the most influential type is the dopamine receptor. Specifically the D2 dopamine receptor count tends to be reduced among those with RDS. This receptor is responsible for regulating attentional processes, motor control, motivation, and other important executive functions. Deficiencies in the D2 dopamine receptor can contribute to a variety of different disorders depending on the individual. Mathematically speaking, based on a predictive model called the “Bayes Theorem” – people carrying the A1 allele for the D2 receptor has approximately a 74% chance of developing a disorder as a result of reward deficiency syndrome. The specific disorder that a person develops will depend on other genetics and environmental influences.
It is believed that the D4 receptor may also have an influence in cases of RDS. Those who carry a certain variation of this gene are more likely to be thrill seekers and/or seek out reward. This receptor is believed to contribute to RDS significantly less compared to variants of the D2 receptor.
There is a major underlying genetic component to reward-deficiency syndrome. Kenneth Blum has determined that it can be passed on throughout generations and tends to run in families. For example, his research has shown that alcoholism can run in families as a result of those carrying a certain allele. Researchers believe that an inherent chemical imbalance or abnormal D2 activity influences how people react to certain events and situations. Among those with the A1D2 gene, it is believed that people experience alterations with the signaling processes in the reward center of the brain. This leads to feelings of anxiety, anger, and craving for a certain substance to help alleviate negative emotions. The addictive behavior such as using drugs, gambling, or alcohol makes the individual feel more “normal.”
How many less D2 receptors do those with the A1 allele have? Approximately 30%-40% less than a person without it. It is hypothesized that the A1 allele is capable of reducing the expression of the D2 gene compared to individuals carrying the A2 allele. It is also possible that sites for the D2 receptors become altered among those with the A1 allele.
Essentially the reduced numbers of D2 receptors among those with the A1 allele results in reduced dopamine activity in reward centers. Those carrying the A1 allele may not feel pleasure from certain stimuli that brings others pleasure. It is also suggested that those with the A1 allele may have a tougher time coping with stress because their dopamine levels are significantly lower than average; dopamine tends to reduce stress.
Pleasure deprivation within the reward centers of the brain
Those afflicted with RDS are believed to experience a significant degree of pleasure depravation within the reward center of the brain. The severity of the condition is subject to variation based on the individual; other traits can play a role. Early research believed that reward-seeking behavior was an animal’s “learned” response to pleasurable stimuli.
Based on addiction research, dependency of various drugs such as alcohol, opiates, and stimulants all seem to have a similar biological basis in the brain. Addictions and reward-deficiency behaviors seem to stem from within the limbic system, specifically in two regions. These regions are known as the “nucleus accumbens” and the “globus pallidus” – and express reward among those with various addictions.
When D2 receptor activity is inadequate, activity levels of neurons within the nucleus accumbens and hippocampus becomes reduced. The individual feels unpleasant emotions and/or cravings for substances that will release dopamine, thereby providing temporary relief from these emotions.
Neurons responsible for releasing serotonin in the hypothalamus become excited and release enkephalin (an opioid peptide). This inhibits activity of neurons that release GABA (an inhibitory neurotransmitter) and dopaminergic neurons release dopamine which leads to a “cascade effect.”
Despite the fact that specific drugs have different effects on these reward regions, the final outcome is the same: doapmine gets released in the nucleus accumbens and hippocampus. Dopamine is considered the primary neurotransmitter associated with rewards in these particular regions. Serotonin in the hypothalamus, opioid peptides in the nucleus accumbens, and GABA in the ventral tegmental area can also have a lesser influence.
It is also believed that norepinephrine in the hippocampus can influence reward in an alternative pathway. Among individuals with normative functioning in the reward center, these neurotransmitters work collectively to either excite or inhibit excitement which helps create feelings of well-being and pleasure from life. Those with disrupted functioning of these neurotransmitters are thought to experience negative emotions and seek out substances that allow them to feel “reward.
Reward Deficiency Syndrome: Symptoms
Those with reward-deficiency syndrome tend to experience a variety of symptoms. These symptoms cannot necessarily be used to “diagnose” the condition because there is no specific diagnostic criteria. However, those who are aware of the condition may realize that they may be dealing with a case of reward-deficiency.
People with RDS may develop addictions as a way to feel engaged with life. Using drugs or gambling may make someone with this condition feel some degree of pleasure and/or thrill. This allows them to feel more “normal” and experience the same level of reward that others get from more mundane activities. Therefore certain addictions such as using drugs or gambling may become the focal point of the individual’s life.
Most people get excited while anticipating an event such as the first day on a new job, first day at school, going on a vacation, or a wedding. For most people, the excitement leading up to these events is significant. Those with reward-deficiency may not feel any excitement leading up to these major events. Essentially the excitement that normal people experience is heavily muted for those with RDS.
Due to the significantly reduced number of D2 receptors, many individuals don’t get a thrill from any activity. Certain events such as going on a big date, taking a vacation, or getting a good grade on a test may not make a person with RDS feel good. Some individuals with this condition may experience very little pleasure from “rewarding” activities, while others may experience none at all.
People with RDS don’t just have a few less D2 receptors, they tend to be severely deficient compared to a normal individual. It is estimated that they have 40% fewer D2 receptors in specific areas of the brain such as the nucleus accumbens. This leads people to be less excited about pursuing goals and staying motivated. The functioning of their brain’s reward system is essentially nonexistant.
People with RDS tend to lack arousal and excitement during activities that would be considered thrilling to a normal individual. Reduced levels of arousal are associated with less production of dopamine as well, which may also contribute to the RDS. Activities that result in high levels of stimulation such as using drugs may increase the person’s arousal and make them feel better.
Based on Blum’s research, people with RDS tend to seek out the biggest thrills possible, given their circumstances. They do this because it allows them to feel pleasure and raises the amount of dopamine in their brain.
Self-Medicating with Reward-Deficiency Syndrome
Individuals with reward-deficiency syndrome often self-medicate with illicit drugs. This allows them to experience adequate levels of “pleasure” that they aren’t able to feel from other activities. It allows these individuals to function well and takes away their agitation, low mood, and anxiety.
Note: Someone with RDS may have other addictions than simply what is listed above. Additionally a person with this condition may develop multiple addictions such as gambling and smoking.
Genetic Addiction Risk Score
The Genetic Addiction Risk Score (GARS™) is the innovation of Geneus Health co-founder Dr. Kenneth Blum. The science is derived from the early groundbreaking findings of Dr. Kenneth Blum and Dr. Ernest P. Noble (former director of the National Institute on Alcohol Abuse and Alcoholism). The research was published in JAMA (1990), discussing the first association of the dopamine D2 receptor gene and severe alcoholism. This was the first ever confirmed gene in the field of Psychiatric Genetics. The importance of this discovery paved the way for subsequent gene variations involved in what has been defined as the Brain Reward Cascade (BRC) [see figure 1].
It is the interaction of many chemical messengers (neurotransmitters) in the BRC, that enables the release of the molecule dopamine at just the right amount to the reward site of the brain called the nucleus accumbens. While there are many interacting systems involved in this process, the following neurotransmitter pathways are required in this complicated process:
The final interaction of these systems provide the net release of dopamine that then stimulates 9 receptors (the D1 and D2 most prominent) to induce a feeling of well-being and even heightened pleasure states. Humans are therefore wired to achieve this feeling in spite of daily stress and trauma. In simpler terms, if the exact amount of dopamine is compromised or potentially reduced, then the individual cannot deal with typical every day events, and finds unnatural ways to obtain a “dopamine fix” leading to all types of additive behaviors. These addictive behaviors include:
All of these substance and non-substance behaviors have at one thing in common…they cause dopamine to be released at the reward site of the brain. So in essence by seeking out anything that will fix the low dopamine function, the individual finds resolve by self-medicating to overcome what has been termed “hypodominergia” (low levels of dopamine). While initially this seems beneficial over time, both substance and even non-substance addictive behaviors attack the reward centers of the brain locking people into unwanted dependence.
GARS™ helps identify the various genes tied to the normal release of dopamine via the BRC and pinpoints any variation of these required reward genes. GARS™ is based on the primary genes identified in the BRC and subsequent variations (alleles) or polymorphisms (a single nucleotide switch -SNPS) [see Figure 2].
The collective research by numerous global scientists, Geneus Health scientists, and the Colorado Institute of Behavioral Genetics, have clearly identified ten reward genes across the BRC and eleven SNPS that predicted clinical severity outcomes (drug and alcohol severity as measured by Addiction Severity Index: ASI).
Each risk variation utilized in GARS™ has been the subject of thousands of published articles. Following a four year observation evaluating GARS™ and its predictive abilities in a multi-centered study, it was found that individuals carrying any combination of seven alleles or more predicts clinical alcohol severity, while four alleles or more predicts clinical drug severity.
Through the understanding of “reward deficiency” and associated compromised genes as identified by GARS™, we can accurately pinpoint brain dopamine function.
Simple Testing Process
GARS™ is performed from a simple cheek swab. All reporting is provided through secure and confidential handling.
It is recommended to get the GARS™ test to be guided to the appropriate restoreGen™ formulation.
restoreGen™ Helps Control Substance and Non-Substance Cravings Now
restoreGen™ is a patented neuro-nutrient formulation unlike any other product in the recovery market. It works as a pro-dopamine regulator that decreases substance and non-substance behaviors and cravings*.
An unprecedented 37 published clinical studies have validated this neuro-nutrient technology for re-balancing brain chemistry and optimizing dopamine sensitivity and function to help with:
Reducing addictive cravings
Optimizing brain health
Enhancing energy levels
Improving overall well-being
The patented neuro-nutrient restoreGen™ has been genetically formulated to provide maximum results based on GARS™ results. The different formulations were scientifically developed based on the genetic risk variants a person might carry.
Even a moderate amount of drinking can screw up your brain
Drinking even moderate amounts of alcohol is linked to changes in brain structure and an increased risk of worsening brain function, scientists said on Tuesday.
In a 30-year study that looked at the brains of 550 middle-aged heavy drinkers, moderate drinkers and teetotallers, the researchers found people drank more alcohol had a greater risk of hippocampal atrophy – a form of brain damage that affects memory and spatial navigation.
People who drank more than 30 units a week on average had the highest risk, but even those who drank moderately – between 14 and 21 units a week – were far more likely than abstainers to have hippocampal atrophy, the scientists said.
“And we found no support for a protective effect of light consumption on brain structure,” they added.
The research team – from the University of Oxford and University College London – said their results supported a recent lowering of drinking limit guidelines in Britain but posed questions about limits recommended in the United States.
How To Use SAM-e (S-Adenosylmethionine) For Alcohol Recovery
If you have high whole blood histamine levels SAM-E is a co-factor for the enzyme HMNT which breaks down histamine in the brain. High brain levels of histamine lowers dopamine, serotonin and norepinephrine. This is what is could very well be causing you to be addicted to drugs, alcohol, nicotine, sugar, etc. By increasing the enzyme that breaks down the histamine you’ll start losing the cravings of your addictions.
SAM-e is produced in the liver from an amino acid called methionine, which is found naturally foods like beef, eggs, and cheese. SAM-e is a cofactor for a cellular process called methylation. To make a long story short, methylation occurs throughout the body and is absolutely critical for the maintenance of health on a cellular level.
SAM-e is a precursor for glutathione, which is a very powerful antioxidant produced in the liver. Increasing glutathione levels can help to restore liver function during alcohol recovery.
Even more importantly, adequate levels of SAM-e are required for the last steps in the production of three important neurotransmitters:
- Serotonin – Associated with feelings of confidence and relaxation
- Dopamine – Associated with reward, motivation, and learning
- Norepinephrine – Associated with arousal and memory (aka adrenaline)
Most drinkers subjectively understand the importance of these neurotransmitters. You feel giddy, blissful, or invincible while alcohol causes its (temporary) cascade of artificial neurotransmitter boosts.
What heavy drinkers fail to realize is that chronic alcohol consumption actually depletes the natural production of these neurotransmitters over time.
Research on SAM-e
Research supports the use of SAM-e for many symptoms involved in protracted alcohol withdrawal:
- SAM-e significantly reduces symptoms of depression, with scientists calling for further investigation. (source)
- Clinical trials have shown that SAM-e is as effective as prescription antidepressants, with fewer side effects. This makes SAM-e a good option if alcohol withdrawal is causing depression. (source)
- In addition to its antidepressant effects, SAM-e is very safe at recommended dosages because it is an essential amino acid. (source)
- In treating alcoholic liver injury, SAM-e can attenuate the pain and effects caused by alcohol and other hepatotoxins. (source)
- SAM-e offers promise for treating alcoholic liver disease because it is a precursor for glutathione, an antioxidant produced in the liver. (source)
Because SAM-e may help to alleviate depression and restore liver health, further research on SAM-e for alcohol recovery should be conducted.
If you have recently quit drinking alcohol, 800-1600 mg per day of a high-quality SAM-e supplement may help to alleviate the depression and sluggish liver that often accompany protracted alcohol withdrawal.
However, because I am cautious with supplements I have not taken before, I would personally start with 200 mg. Many people have begun to feel noticeably better after using this smaller dosage of SAM-e.
I would therefore start with SAM-e 200mg Tablets.
If you respond well to 200mg (or if you felt nothing), I would increase the dosage until I reached the optimal level. You can increase up to 400 mg 3 times a day.
SAM-e has a short half-life, meaning that its effects are noticeable within minutes and last for only a few hours after each dose.
Too much SAM-e prior to bedtime can cause insomnia because it generally increases energy levels, due to its restoration of the body’s supply of norepinephrine (an energy-promoting neurotransmitter).
** DO NOT TAKE SAM-E IF YOU ARE ALREADY TAKING AN ANTI-DEPRESSANT!**