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Ketamine Therapy Can Be effective for Alcoholism
Ketamine has efficacy in the treatment of drug and alcohol disorders. More studies need to evaluate the benefits and negative aspects of Ketamine treatment. In this post, I am reviewing some information of ketamine use for Alcohol Use Disorder (AUD).
Our brain is designed to respond to rewards. The original reward pathway is effectively for food, and dopamine is the core molecule for this pathway. Anything that acts as a reward, such as food, sex, a glass of wine, a win at the casino, causes the release of Dopamine. In fact, it is the unexpected rewards that cause the larger release of dopamine as our brain is assessing errors in reward prediction as part of its learning about the environment. When we get a larger than expected reward, our brain emits larger amounts of dopamine. A part of our brain, called the amygdala-striatum neural complex, motivates us to achieve rewards. The VTA (Ventral Tegmental Area) is, in part, involved with error-reward prediction. If we get more or less than expected, we will release more or less dopamine and each is a learning event. These errors in prediction of rewards offer an opportunity of the brain to learn more about the environment and create new neural pathways and behaviors to drive continued acquisition of those rewards. Those rewards can be good or bad, such as excess alcohol or cocaine, each of which increase dopamine A link forms between automatic, repetitive behaviors, such as pouring a drink, and increased dopamine and as we repeat this behavior, it becomes solidified and habitual.
Increasing dopamine activity also accelerates the change between the first steps of choosing to have a drink and later craving a drink. New pathways in the brain form with repetitive behavior. Cues and memories in the environment to drink are noticed more quickly, like hearing glasses clink, or walking in the front door after work. At the time of the unexpected reward or experience, our brain tries to learn everything about the environment that got it the reward, such as the music playing, the smells, the people you are with, and even the location. These cues drive the compulsion to drink.
The Prefrontal cortex is the CEO of the brain that is involved with executive functioning and decision making so as the appropriately control impulses and act appropriately. This means we can trade short term rewards, like a drink, for possibly greater long-term goals, such as avoiding a DUI charge. One explanation is that there is a balance between a “cool” and “hot” system that works out how we respond to triggers or cravings. The “cool” refers to basic working memory and inhibition of impulses. The “hot” involves numerous emotional responses that are possible. The hot system is the lizard brain that exists in all of us. It is the reward-driven side of us that only wants to reward itself with food, sex, shelter, fighting, and anything else pleasurable. The lizard brain is suppressed by our prefrontal cortex so that we act appropriately and socially to achieve rewards. Damage to either of these systems may impair the ability to say “no” to situations, or drugs like alcohol, that can harm us. Either the impulse side or the emotional side wins when we lose a health balance. The Lizard brain works off the impulsive, emotional components.
When we drink or use drugs, we effectively cause damage or a ‘concussion’ to our executive functioning center, the prefrontal cortex. This, over time, erodes the ability of an individual to act appropriately in social settings, such that they may begin to act poorly, such as becoming aggressive or undressing in public as simple examples.
Poor decision making in alcoholics may also be explained by yet another system called the insular cortex. It responds to imbalance in our bodies from things like sleep deprivation, anxiety and stress. These stressors may hijack our impulse/habit system and increase cravings while promoting decisions to seek out alcohol. Repeated cycles of increased cravings can also essentially rewire brain circuits, reinforcing continued destructive behavior.
Addiction can be viewed as a disease of choice. People don’t think of choice or poor choosing as being a disease, but when an individual cannot understand the salience of a reward or have introspection of their behaviors due to damage form substance abuse, their choices can be viewed a s a disease process. There are studies that support that “faulty brain connections” related to decision-making which can lead to addictive behaviors and relapse.
Genetics can also play a role in alcoholism and substance abuse. Family history of alcoholism is a risk factor for developing alcohol addiction. A study by Petrakis et al showed one answer may lie in the NMDA (N-Methyl-D-Aspartate) receptor, which is vital to the glutamate system in the brain. Alcohol alters this receptor’s function, but if the receptor is not normal, that person may be more susceptible to alcohol abuse.
It is possible a rewarding memory of taking a drink, for example, can be triggered repeatedly by seeing a glass of beer, going to a restaurant, or maybe returning home from work and having the habit to pop the top of a beer can. These triggers lead to the urge to drink as they have become habitual and the compulsion is the routine and the provided cues, such as cigarettes, location, and smells that are associated with the reward (alcohol). It is much like the old song you hear on the radio station that takes you back to the day when….something awesome was happening and makes you recall a wonderful date or event.
Why can’t an alcoholic just stop drinking? Ravi Das from University College London explains why people often quit but return to drinking. “The main problem is the really high relapse rate after treatment,” said Das. “People can successfully quit using over the short term while they’re being monitored in the hospital … but when they return home, they’re exposed to those environmental triggers again.” The good news is that each time the brain accesses that rewarding memory, the neural connections that code the memory are destabilized. It is at this moment that ketamine, which blocks the brain receptor required for the formation of memories (NDMA), can help weaken or even erase the memory. In other words, ketamine will help break the power of that trigger.
How can Ketamine help this process? The benefits from the psychedelic experience while receiving a ketamine treatment may be due to the neuroplastisticity and new synapsis that form with Ketamine use. This offers an opportunity for learning, I.e. learning new and safer habits.. Dr. Tobias Stevens, in his presentation on ketamine as a treatment for alcohol use disorder, postulates the hallucinations and altered mental state from ketamine may help change lifestyle choices. He suggests the experience may alter perceptions and break routine behaviors. Therefore, a combination of psychotherapy with ketamine, (ketamine psychotherapy or KPT) may prove helpful for some folks. KPT allows the psychedelic effects from ketamine to enhance a psychotherapy session and is shown to be effective helping those with addiction, including heroin and alcohol by Dr. Evgeny Krupitsky.
Part of the reason that relapse rates are so high in alcoholism is that the alcoholic brain can’t learn new skills due to fewer synapse formation. There is a proven decrease in neural growth factors in the brain, BDNF, with alcohol addiction. With fewer connections between nerves, and less ability to make new connections, the brain cannot learn new skills. With ketamine and synaptogenesis, which happens to peak 24 hours after a treatment, well timed psychotherapy can have a greater impact. Clearly Ketamine used in combination with therapy can provide a new direction in alcohol treatment.
Ketamine therapy can be combined with Naltrexone and other therapies to potentially decrease cravings. Naltrexone is supposed to reduce the reward pathways of drinking but it does not result in abstinence. This medication does decrease overall drinking amounts. Baclofen, gabapentin, and topirimate are other examples of medications that can assist in decreasing cravings in alcoholism.
One significant problem after a person becomes sober is the post-acute withdrawal syndrome. The depression that results can inspire relapse due to altered brain function. This is where the use of Ketamine can be of value as it can help decrease the degree of depression, increase synaptogenesis, and enable new and more functional pathways of sobriety. This therapy needs to be incorporated into psychotherapy, CBT, eating well, exercise, and other modalities to maximize recovery in the setting of a comprehensive program.
[i] Noël X,Brevers D, et al. A neurocognitive approach to understanding the neurobiology of addiction Curr Opin Neurobiol . 2013 August ; 23(4): 632–638. doi:10.1016/j.conb.2013.01.018. link
[ii] Bergland C, The Neuroscience of Making a Decision: Various brain regions work together during the decision-making process. Psychology Today online, 05/06/2015. link
[iii] Petrakis I, Limoncelli D, et al Altered NMDA glutamate receptor antagonist response in individuals with a family vulnerability to alcoholism. The American Journal of Psychiatry Oct-2004 161 1776–1782 0002-953X link
[iv] Devlin H, Radical ketamine therapy could treat alcohol addiction. Theguardian.com, 01/24/2017. link
[v] Stevens T. Ketamine as a Treatment For Alcohol Use Disorder. Breaking Convention 2017, YouTube 09/13/2017. link
[vi] Krupitsky E, Ketamine psychotherapy for heroin addiction: immediate effects and two-year follow-up. Journal of S/ubstance Abuse Treatment 23 (2002) 273–283.link
[vii] McAndrew A, Lawn W, et al. A proof-of-concept investigation into ketamine as a pharmacological treatment for alcohol dependence: study protocol for a randomised controlled trial. Trials (2017) 18:159 DOI 10.1186/s13063-017-1895-6. link
[viii] KARE: Ketamine for reduction of Alcoholic Relapse. University of Exeter, England. link
[ix] Krystal J, Madonick S, et al. Potentiation of Low Dose Ketamine Effects by Naltrexone: Potential Implications for the Pharmacotherapy of Alcoholism. Neuropsychopharmacology (2006) 31, 1793–1800 link
[x] Krupitsky E, Burokov A, et al. Attenuation of Ketamine Effects by Nimodipine Pretreatment in Recovering Ethanol Dependent Men: Psychopharmacologic Implications of the Interaction of NMDA and L-Type Calcium Channel Antagonists. [Neuropsychopharmacology 25:936-947, 2001 link
[xi] Krystal J, Petrakis I et al. Dose Related Ethanol-like Effects of the NMDA Antagonist, Ketamine, in Recently Detoxified Alcoholics. Arch Gen Psychiatry Vol 55, April 1998, 354-360 link