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Traumatic Brain Injury: Definition, Classification, and Management

We hear a lot about traumatic brain injury (TBI) nowadays: among NFL players (as in the movie ‘Concussion’), and as a signature diagnosis among recent combat veterans. What doesn’t get as much press coverage is the impact of TBI on those suffering from addiction. Having an alcohol or other substance use disorder greatly increases the risk of TBI. But what is TBI? How do I diagnose it? How does it manifest? How do I manage it?

Defining TBI
Although there is no universally accepted definition for TBI, recently updated guidelines from the Department of Veterans Affairs (VA/DoD Clinical Practice Guideline for the Management of Concussion-mild Traumatic Brain Injury, 2016; https://tinyurl.com/y8e6owdx) state that a TBI is an injury to the brain caused by an external force accompanied by one of several clinical signs following the event). These signs can be an intracranial lesion, loss of consciousness, amnesia, confusion, slowed thinking, muscle weakness, sensory loss, or another neurological deficit. The severity of a TBI (mild, moderate, or severe) is determined by the symptoms immediately following the injury (see the VA TBI severity table below). If the patient meets different ratings for the different criteria, go with the more severe rating. The lay term “concussion” equates to a mild TBI. In addition to the neurological symptoms, patients may experience cognitive problems affecting their attention, memory, processing speed, and executive function. Mental health effects include irritability, impulsivity, depression, and anxiety. However, these symptoms can be an effect of the TBI or part of a comorbid, major depressive disorder, posttraumatic stress disorder (PTSD), or substance use disorder.

Table: Classification of TBI Severity

Table: Classification of TBI Severity

(Click to view full-size PDF.)

Assessment and treatment
But what symptoms should I really be concerned about? For any TBI that is associated with progressively declining neurological function or worsening headache, pupil asymmetry, seizures, intractable vomiting, ongoing disorientation or neurological deficit, slurred speech, or new bizarre behavior, you should immediately refer for emergency evaluation.

The good news is that the vast majority of mild TBI cases resolve without any intervention. It’s important for the physician to provide education and reassurance to the patient and family. Any interventions should be tailored to the specific symptoms while reinforcing good sleep hygiene, relaxation techniques, and limiting use of caffeine, tobacco, and alcohol. Return to normal functioning at work or school should be encouraged in a gradual, monitored fashion. Patients with a TBI who report ongoing symptoms need appropriate referral and a comprehensive treatment plan (Silver JM et al, Textbook of Traumatic Brain Injury, American Psychiatric Publishing, Inc; 2nd ed;2011).

Cognitive rehabilitation therapy (CRT) 
You may have heard of cognitive rehabilitation therapy (CRT) as a treatment for TBI. But what exactly does it involve? And does it work? After a TBI there may be functional deficits that are both physical and mental in nature. CRT is a therapeutic process structured to improve the patient’s functioning in their daily lives. Patients are first guided through recognizing their strengths, weaknesses, and what deficits they want to improve. Then techniques are relearned when possible (solve the problem), or compensatory strategies are identified (work around the problem). The last step is to incorporate these relearned or new skills into daily life. This process can be applied to both physical and cognitive deficits that arise from a TBI.

CRT sessions should be tailored to the individual but most incorporate memory compensation techniques. Such techniques include having the patient write down at each session what was important to them, then reviewing their notes and memory of what was said during the next session. This method not only increases their participation in the therapy sessions but teaches them how to use the memory compensation techniques in their daily lives.

The evidence for CRT after stroke and moderate to severe TBI has long been established, showing improvement in the domains of memory, attention, and communication (Cicerone KD et al, Arch Phys Med Rehabil 2005;86(8):1681-1692). However, for mild TBI, CRT remains more controversial as there isn’t strong evidence for improved functional outcomes. The 2016 VA clinical guidelines recommend short-term CRT for moderate to severe TBI and discourages prolonged treatment courses without measurable improvements.

Sometimes the most concerning symptoms the patient will come to us for are the cognitive deficits and they may press for neuropsychological (NP) testing early. However, NP testing should not be done in the first 30 days. Most cognitive deficits of mild TBI will improve within this time period. And if the problems last longer than 30 days, NP testing may be helpful. Whenever referring for NP testing, be specific in why you are making the request. A targeted referral allows the NP examiner to choose the right tests to provide the most useful information.

Pharmacologic treatment 
When considering medication treatment for symptoms following a TBI, there are several general guidelines to follow (Silver JM et al, Neurology 2006;67(5):748-755.2011). Again, most symptoms of a mild TBI will abate within a month, so watchful waiting and reassurance are important. Symptom improvement may continue throughout the first year as the brain continues to heal, so be sure to reassess the need for the medication intervention. Many times, the neuropsychiatric symptoms after a TBI can be complicated by concurrent major depressive disorder, PTSD, or a substance use disorder. Untreated depression can be the root cause of cognitive problems, irritability, sleep disturbance, fatigue, and headache. Be sure to perform a thorough psychiatric assessment so that you can tailor the treatment plan accordingly. Target specific symptoms or concurrent conditions with your medication choices. After a TBI the brain can be more susceptible to side effects of medications, underscoring the importance of “starting low, and going slow.”

Here are a few specific medication recommendations to target neuropsychiatric symptoms (Silver JM et al, 2011). For improving processing speed, methylphenidate has the most evidence. Donepezil and rivastigmine also may have some utility for treating memory impairment. When targeting depression and anxiety, SSRIs are first-line and choose a specific SSRI based on side effect profile and limiting medication interactions (sertraline, citalopram, and escitalopram are favorable choices) (Salter DL et al, J Head Trauma Rehabil 2016;31(4):E21-32). Be cautious with bupropion due to increased seizure risk. Caution is also advised with typical antipsychotics as they may inhibit neuronal recovery, and also benzodiazepines due to the memory impairment effects. For controlling mania or irritability, valproate is preferred due to its anti-seizure effect as well as having less cognitive side effects in long term treatment than other mood stabilizers (carbamazepine or lithium). Atypical antipsychotics may also be helpful in controlling irritability especially when combined with psychosis, and are preferred over typical antipsychotics. More recent research shows beneficial effects of amantadine in treating aggression from TBI even 6 months post-injury and more studies are evaluating its use in the acute phase after a severe TBI (Hammond FM et al, J Head Trauma Rehabil. 2017;32(5):308-318).

CATR Verdict: When treating patients with TBI, always remember that the brain has a great capacity for plasticity and recovery. Encourage patients to see their treatment as a process and journey. Take care to evaluate for comorbid mental health disorders, and handle accordingly. Those with substance use disorders, whether existing pre-TBI or newly occurring, should be encouraged to enter into treatment promptly. With the right combination of cognitive rehabilitation, pharmacotherapy, and a good therapeutic alliance, your patients can make great strides in recovery after a TBI.

Ohio State TBI

Alcohol use and TBI are closely related. Up to two-thirds of people with TBI have a history of alcohol abuse or risky drinking. Between 30-50% of people with TBI were injured while they were drunk and about one-third were under the influence of other drugs. Around half of those who have a TBI cut down on their drinking or stop altogether after injury, but some people with TBI continue to drink heavily, which increases their risk of having negative outcomes.

After TBI, many people notice their brains are more sensitive to alcohol. Drinking increases your chances of getting injured again, makes cognitive (thinking) problems worse, and increases your chances of having emotional problems such as depression. In addition, drinking can reduce brain injury recovery. For these reasons, staying away from alcohol is strongly recommended to avoid further injury to the brain and to promote as much healing as possible.

Facts about TBI and alcohol

Alcohol and brain injury recovery

  • Recovery from brain injury continues for much longer than we used to think possible. Many people notice improvements for many years after injury.
  • Alcohol slows down or stops brain injury recovery.
  • Not drinking is one way to give the brain the best chance to heal.
  • People’s lives often continue to improve many years after brain injury. Not drinking will increase the chance of improvement.

Alcohol, brain injury and seizures

  • Traumatic brain injury puts survivors at risk for developing seizures (epilepsy).
  • Alcohol lowers the seizure threshold and may trigger seizures.
  • Not drinking can reduce the risk of developing seizures.

Alcohol and the risk of having another brain injury

  • After a brain injury, survivors are at higher risk (3 to 8 times higher) of having another brain injury.
  • Drinking alcohol puts survivors at an even higher risk of having a second brain injury. This may be because both brain injury and alcohol can affect coordination and balance.
  • Not drinking can reduce the risk of having another brain injury.

Alcohol and mental functioning

  • Alcohol and brain injury have similar negative effects on mental abilities like memory and thinking flexibility.
  • Alcohol magnifies some of the cognitive problems caused by brain injury.
  • Alcohol may affect brain injury survivors more than it did before their injury.
  • The negative mental effects of alcohol can last from days to weeks after drinking stops.
  • Not drinking is one way to keep your mental abilities at their best and stay sharp and focused.

Alcohol and mood

  • Depression is about 8 times more common in the first year after TBI than in the general population.
  • Alcohol is a “depressant” drug, and using alcohol can cause or worsen depression.
  • Alcohol can reduce the effectiveness of anti-depressant medications. People who are taking antidepressants should not drink alcohol.
  • One way to improve problems with sadness or depression after TBI is to stop or cut down on the use of alcohol.

Alcohol and sexuality

  • Lowered desire is the most common effect of TBI on sexuality.
  • Alcohol reduces testosterone production in males.
  • Alcohol reduces sexual performance (erection and ejaculation) in men.
  • Alcohol reduces sexual satisfaction in men and women.
  • Avoiding alcohol improves sexual ability and activity in men and women.

How much alcohol is “safe” after TBI?

After TBI the brain is more sensitive to alcohol. This means that even one or two drinks may not be safe, especially when you need to do things that require balance, coordination and quick reactions, such as walking on uneven surfaces, riding a bicycle or driving a car. The fact is, there is no safe level of alcohol use after TBI.

Alcohol and medications

Alcohol is especially dangerous after TBI if you are taking certain prescription medications. Alcohol can make some medicines less effective and can greatly increase the effects of others, potentially leading to overdose and death. Using alcohol along with anti-anxiety medications or pain medications can be highly dangerous because of the possible multiplying effect.

What about using other drugs?

Alcohol is a drug. Almost everything mentioned above about alcohol applies equally to other drugs. If your drug of choice is something other than alcohol-such as marijuana, cocaine, methamphetamine or prescription drugs, anti-anxiety medications (benzodiazepines such as Ativan, Valium, or Xanax), or pain medication (opioids like Percocet, Oxycodone or Oxycontin)-many of the same principles apply. In addition, use of illegal drugs or misuse of prescription drugs can lead to legal problems.

If you use multiple drugs like alcohol and marijuana, or alcohol and pain pills, there is a higher risk of addiction and overdose. Using alcohol and pain medications together, or alcohol and anti-anxiety medications, has killed many people. Contact your doctor if you are drinking and using prescription drugs.

What should you do?

The stakes are higher when people choose to use alcohol after having a TBI. Some people continue drinking after a TBI and don’t have any desire to change that behavior. Others know they probably should stop or reduce alcohol use, but don’t know how or have tried in the past and not been successful.

There are many ways to stop using alcohol or other drugs and many ways to reduce the potential for harm. The great majority of people who have stopped having alcohol problems did it on their own. They got no professional help or counseling and did not use Alcoholics Anonymous (AA). Don’t underestimate your ability to change if you want to.

There are many ways to change, cut down or stop drinking

The key ingredients to changing your drinking are: (1) find people who will support your efforts to change your drinking; (2) set a specific goal; (3) make clear how you will meet your goal; (4) identify situations or emotions that can trigger drinking, and figure out ways to cope with those triggers ahead of time; and (5) find ways to reward yourself for sticking to your plan and meeting your goals.

If you have questions or concerns about your drinking, there are many ways to get information or help:

  • Take a confidential on-line drinking assessment: http://www.alcoholscreening.org/.
  • Talk to your physician about your concerns, and ask about medications that can help you resist relapse or reduce cravings for alcohol, such as naltrexone (Revia).
  • Psychologists or other counselors in your brain injury rehabilitation program can help you get started on a treatment program that is right for you.
  • Alcoholics Anonymous (AA) has helped millions of people. There are meetings in most towns and cities (http://www.aa.org/).
  • Moderation Management (http://www.moderation.org/) and Smart Recovery (http://www.smartrecovery.org/) are alternatives to AA that do not use the 12-step model.
  • Substance Abuse and Mental Health Services Administration (SAMHSA) is a federal program that can help you find a treatment facility wherever you live (http://findtreatment.samhsa.gov/; 800-662-4357).
  • Private treatment: look in the Yellow Pages under substance abuse, chemical dependency counselor, or addiction treatment.

Reduce the harm from drinking

For those who don’t want to stop drinking, it is still possible to reduce some harm from drinking:

  • Eat food and drink water before you drink alcohol. This will help reduce the sharp spike in blood alcohol level that can cause nausea, vomiting, falls, blackouts and alcohol poisoning.
  • Plan your transportation so you don’t drink and drive: have a non-drinking designated driver; plan to spend the night where you are doing your drinking; or drink only at home.
  • To avoid dangerous peaks in blood alcohol concentrations, drink beer rather than hard liquor, or mix hard liquor with water instead of with sweet, carbonated beverages.
  • Sip your drinks slowly (no more than one per hour). Drinking too fast can make the pleasant feelings of alcohol go away.
  • Drinking in bars slows some people down because of the expense. However, be sure you do not drive after drinking.
  • Take vitamins B1 (thiamine), B12 and folate to reduce the chances of alcohol-related brain damage.
  • Keep your drinking to no more than two drinks per day. Or cut back on certain days of the week, such as weeknights.
  • Take a drinking “holiday” (days or weeks when you decide not to drink at all). This can remind you of some of the benefits of being sober.

How family members can help

No one can force another person to stop using alcohol or drugs, but you can have an influence. Attending Al Anon meetings can be a good source of support for a friend or family member of someone who abuses alcohol or drugs, and it can help promote change. Planning an “intervention” where family and friends confront the person may help.

A program called Community Reinforcement and Family Training (CRAFT) has been found to work best. CRAFT takes a more positive, motivational approach that helps loved ones make not drinking more rewarding for the person with the alcohol problem. Research has shown that alcoholics are more likely to go into treatment if their loved ones follow the CRAFT method. To learn about CRAFT, see the book Get Your Loved One Sober in the Resources section below, or find a counselor familiar with this approach.


Bombardier, C.H. & Turner, A. (2009). Alcohol and traumatic disability. In R. Frank & T. Elliott (Eds.), The Handbook of Rehabilitation Psychology, Second Edition (pp. 241-258). Washington, DC: American Psychological Association Press.


  • Brown, J., Corrigan, J., & Hammer, P. (2010). “Substance Abuse and TBI.” Brainline Webcast #4, Defense and Veterans Brain Injury Center. (http://www.brainline.org/webcasts/4-TBI_and_Substance_Abuse/index.html)
  • Corrigan, J., & Lamb-Hart, G. (2004). Alcohol, Other Drugs, and Brain Injury. Columbus, Ohio: Ohio Valley Center for Brain Injury Prevention and Rehabilitation, Ohio State University Dept. of Physical Medicine and Rehabilitation. (Available from the Brain Injury Association, http://www.biausa.org/LiteratureRetrieve.aspx?ID=43235. )
  • Meyers, R.J., & Wolfe, B.L. (2004). Get Your Loved One Sober: Alternatives to Nagging, Pleading, and Threatening. Center City, MN: Hazelden Publications.
  • Substance Abuse Resources and Disability Issues (SARDI); http://www.med.wright.edu/citar/sardi/index. html.


This information is not meant to replace the advice from a medical professional. You should consult your health care provider regarding specific medical concerns or treatment.


Our health information content is based on research evidence whenever available and represents the consensus of expert opinion of the TBI Model System directors.


Alcohol Use After Traumatic Brain Injury was developed by Charles Bombardier, PhD, in collaboration with the University of Washington Model Systems Knowledge Translation Center.



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New Drug Combo Shows Promise for Treatment of Depression and Addiction

Drug Combo Shows Promise for Depression and Addiction
Ketamine Treatment for alcoholism | Call 703-844-0184 | Alexandria, Va 22306 | NOVA Health Recovery

The combination of naltrexone and ketamine can help treat both symptoms of addiction and depression, a preliminary study by Yale University researchers suggests.

Substance abuse and depression are common in many patients, and efforts to treat both conditions simultaneously have had limited success. One recent study suggested that the antidepressant effects of ketamine might blunted by administration of naltrexone, used to limit cravings of those addicted to opioid drugs and alcohol.

A preliminary study of five patients suffering from both depression and substance abuse disorders suggest that isn’t the case. The study was published Jan. 9 in the journal JAMA Psychiatry.

The results “raise the possibility that for people who have depression complicated by substance abuse disorders, the combination of ketamine and naltrexone may be a strategy to explore in the effort to optimally treat both conditions,” said senior author John Krystal, Yale’s Robert L. McNeil Jr. Professor of Translational Research; professor of psychiatry, neuroscience, and psychology; and chair of the Department of Psychiatry.

Krystal and lead author Gihyun Yoon, assistant professor of psychiatry, treated the five patients suffering from depression and alcohol use disorder with a long-lasting form of naltrexone and then administered ketamine. Four of the five responded to the first ketamine dose and all five found relief from depression after multiple doses.

The study also challenges the idea that ketamine might produce antidepressant effects by stimulating opiate receptors.

Krystal cautioned that larger studies are needed to confirm beneficial effects of the combination treatment.

Krystal and Yoon have provisional patents on the use of ketamine and naltrexone to treat comorbid depression and substance abuse.

The study was primarily funded by the U.S. Department of Veterans Affairs.

Publication: Gihyun Yoon, et al., “Association of Combined Naltrexone and Ketamine With Depressive Symptoms in a Case series of Patients With Depression and Alcohol Use Disorder,” JAMA Psychiatry, 2019; doi:10.1001/jamapsychiatry.2018.3990

At NOVA Health Recovery, we do use Ketamine and other combinations to treat Alcoholism and Opioid and Pain pill addiction using Ketamine Treatment. Dr. Sendi is Board Certified in Addiction Medicine. Call 703-844-0184 Today. Fairfax, Va 22304.

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Prazosin for Harm Reduction in Alcohol Use Disorder?



Double-Blind Randomized Clinical Trial of Prazosin for Alcohol Use Disorder


Increasing doses of prazosin reduced heavy drinking, but adverse effects were common.

In some patients with post-traumatic stress disorder (PTSD), the alpha-1 noradrenergic blocker prazosin has been helpful for nightmares and, in open-label studies, has decreased stress reactivity, alcohol craving, and alcohol use. The alpha-1 noradrenergic blocker doxazosin has also been found to be useful for alcohol and other substance use disorders. These investigators conducted a randomized, placebo-controlled, double-blind, 12-week study of prazosin for alcohol use disorder in 92 outpatients without PTSD (mean age, 48; 79% men).

Participants averaged >67% heavy drinking days and 12 drinks per drinking day in the prior 90 days. After two 1-mg bedtime test doses, prazosin and placebo were up-titrated, depending on adverse effects, over 2 weeks; prazosin targets were 4 mg in the morning, 4 mg in the afternoon, and 8 mg at bedtime. Twelve patients dropped out during titration; of the 80 completers, 70 reached the target dose. The prazosin group took ≥1 dose on a mean of 65% of days and all 3 doses on 55% of days.

Prazosin was associated with self-reported fewer heavy drinking days and fewer drinks per week (–8 vs. –1.5 with placebo); differences in drinks per week accelerated after 8 weeks. Drinking days per week and craving showed no group differences. Mean systolic blood pressure decreased by 3.5 mm Hg with prazosin. Frequent adverse effects with prazosin were drowsiness (64% vs. 31% with placebo) and edema (20% vs. 4%). Symptomatic (1 patient in each group) and asymptomatic orthostatic hypotension did not differ between groups.



Evidence suggests that elevated brain noradrenergic activity
appears to be involved in the initiation and maintenance of
alcohol use disorder (1, 2). A clinically feasible approach to
reducing brain noradrenergic activity is to reduce activation
by norepinephrine at the postsynaptic a-1 adrenoceptor.
Prazosin is a clinically available lipid-soluble a-1 adrenoceptor
antagonist that reduces brain a-1 adrenoceptor–
mediated signaling when administered peripherally (3). In
rodents, prazosin has been shown to decrease withdrawalinduced
alcohol intake (4), alcohol drinking by alcoholpreferring
(P) rats (2), and stress-induced alcohol seeking
(5), and it has been shown to block yohimbine-induced reinstatement
of alcohol seeking (6). In human alcohol use disorder
studies, prazosin has been shown to reduce reactivity
to stress and to result in reduced craving (7), reduced drinks
per week (8, 9), and reduced drinking days per week (8). In
persons with DSM-IV alcohol dependence and comorbid
posttraumatic stress disorder (PTSD), one study found that
prazosin reduced drinking but not PTSD outcomes (10), and
another study found no prazosin effect on either outcome (11).
Doxazosin, another a-1 adrenoceptor antagonist, did
not outperform placebo on drinking outcomes in a study of alcohol treatment seekers, but among those with a high family
history density of alcohol problems, the active medication
was associated with improved drinking outcomes (12). Across
the entire sample, alcohol treatment seekers with higher
standing diastolic blood pressure receiving active medication
had better outcomes than those receiving placebo (13).
After obtaining positive results in a pilot study (8), we
conducted a 12-week randomized controlled trial comparing
prazosin and matched placebo in 92 participants who met
diagnostic criteria for alcohol use disorder but not PTSD.
Individuals with PTSD were excluded because there is evidence
that prazosin reduces symptoms of PTSD (14), and we
were interested in isolating the effects of prazosin on drinking
alone in light of evidence linking excessive drinking to
stress and the adrenergic system. Both treatment arms included
medical management (15), and daily symptoms were
monitored via a telephone-based interactive voice response
system to obtain close to real-time data regarding alcohol
consumption. Our primary hypotheses were that prazosin
would lead to a decreased likelihood over time of any drinking
and of heavy drinking (i.e., $4 drinks for women, $5 drinks
for men) as well as a decrease in number of drinks consumed.



These results indicate that prazosin has the potential to
reduce the likelihood of heavy drinking and number of
drinks per week over time but not the number of drinking
days per week. They suggest that prazosin may be most
useful in reducing heavy drinking associated with negative
consequences (29), which is consistent with a harm reduction
approach characterized by safer consumption rather
than full abstinence.

 In addition to reducing rodent self-administration of
alcohol (33), prazosin compared with vehicle has also been
shown to reduce self-administration of cocaine (34), heroin
(35), and nicotine (36). In humans, the previous positive pilot
studies of prazosin for alcohol use disorder (8, 10) and the
present study provide preliminary support for an effect of
prazosin on heavy drinking and number of drinks per week.
Another a-1 antagonist, doxazosin, has shown a signal for
reducing drinking in alcohol-dependent individuals who
have a positive family history of alcohol problems (12).
Doxazosin has also been found to reduce cocaine use in
cocaine-dependent individuals compared with placebo (37)





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Health relevance of the modification of low grade inflammation in ageing (inflammageing) and the role of nutrition.

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Stopping Alcohol Abuse with Ketamine

ReachMD Ketmaine on Roundtable talk

ketamine-to-treat-alcoholism transcript

Stopping Alcohol Abuse with Ketamine   << Article Link

A currently ongoing study based at University College London (UCL) involves giving a dose of ketamine to alcohol abusers. Yes, you read that correctly. Ketamine is a legal tranquilizer, used mainly on small animals by veterinarians. However, ‘Special K’ doubles as a recreational drug, found most often at dance parties and nightclubs. So how the heck does ketamine stop alcohol abuse? The answer is by manipulating alcohol-associated memories.

Let’s start over.


Certain things make drinkers want to drink. Ask anyone who consumes alcohol often, and they’ll tell you it’s true. Maybe the smell of alcohol triggers the desire to drink. Maybe it’s a certain place, or some classic rock song. When this happens, the drinker’s memories of alcohol giving pleasure are recalled, and his or her brain wants that alcohol-induced pleasure again. This is the precursor to alcoholism, wherein the brain can’t function without alcohol.

Cravings are essentially fond memories. You are recalling the pleasure of something and desiring it again. During this memory recall, “…the neural connections that encode [the memory] are temporarily destabilized, meaning that our recollection can be slightly altered before it goes back into storage,” as written in The Guardian, linked above.

Ketamine causes memory loss and/or disruption, by blocking a receptor in the brain called NMDA. This particular receptor is partly responsible for our ability to form memories. The UCL research team believes they can use this effect of ketamine to ‘erase’ the memories associated with craving alcohol. “There is evidence that it could be useful as a treatment for alcoholism,” said lead researcher Ravi Das.

The Library Book Metaphor

Every time you access a memory, you are basically removing it from your mental library. In a real library, a book can be removed and read, like a memory can, but it also becomes vulnerable. The book borrower could rip a page out, cross out some text, or even damage the book. The same thing goes for memories. This is why we give slightly different accounts of our past each time we do so.

Because ketamine disrupts the memory-formation process, the idea of the UCL study is to trigger alcohol cravings in participants, and then give them ketamine. The hope is to weaken the alcohol-related memories, ultimately to the point of non-existence.

A dose of ketamine administered at the time of alcohol-related memory recall, the researchers hope, will make it so you lose the book of alcohol-craving from your mental library. The ‘temporary destabilization’ of our memories, when recalled, acts as the window of opportunity for ketamine to work. The ultimate goal is to eliminate the triggers for craving a drink.

The UCL Study

The research team consists of psychologists from University of Exeter, Imperial College London, and UCL. Participants must consume at least forty drinks per week, drinking four or more days per week. This qualifies them as heavy drinkers. However, participants cannot be clinical alcoholics. Anyone with diagnosable alcohol dependence would be excluded. They are aiming for 90 people to participate, and at the time of a July 2016 publication, over 50 people were already in.

Apparently no further details have been published yet about whether or not the quota has been met. Some details on what the study involves have been published, and as of the time of this writing, a flyer advertising the study is still online. So far, here’s what we know the study entails:

The psychologists intentionally trigger the craving for alcohol in the participants. A glass of beer is placed directly in front of each person. This is a surefire trigger – no scientific explanation needed. The details of what happens next are being withheld by the team. However, according the Guardian, “They will then disrupt the memory, by surprising the participant (the team is not disclosing the exact details as this could bias the results).”

The ketamine comes next. After the memory is triggered and disrupted, each participant is either given “a ketamine infusion, with a concentration equivalent to a high recreational dose, or a placebo.” The team then stays in touch with all 90 people for one full year after the ketamine dose, to see how their drinking habits have changed.

Short-term Results are Promising

One participant, who already received the ketamine dose, claims that it worked. According to the Guardian article, 31-year-old Nikki, a consultant in London, took part in the study when she realized she was drinking heavily. She was even drinking more than she wanted to. “It’s just in the culture. That’s what all my friends are like… everyone drinks to excess,” she said before the study.

After her alcohol craving was triggered and her memory was manipulated, Nikki was given her ketamine dose. She described the experience as overwhelming and intense, but not unpleasant. “It was quite psychedelic. I felt untethered from my body,” she said.

One week later, Nikki reported an “incredible positive mood,” and said she was much more aware of her decisions regarding drinking. She didn’t say she gave up alcohol completely. However, she did praise the study. “In the past, there were occasions where I would be drinking and I’d be on autopilot: ‘Let’s get another drink’,” said Nikki.

Although one week is only 1/52nd of a year, Nikki’s story proves as a promising example of how a ketamine dose could prevent heavy drinking.

Similar Approaches to Different Problems

Using one drug to fight the abuse of another drug is not unheard of. Actually, two years ago, Merel Kindt and Marieke Soeter of University of Amsterdam performed a study that used a beta-blocker to get rid of arachnophobia. Beta-blockers are used primarily for cardiac care. The particular one used in the study, propranolol, treats high blood pressure, and is also used to reduce performance anxiety.

Fifteen participants with diagnosed arachnophobia, a fear of spiders, were shown a giant tarantula, and told they had to touch it. Then they were each given a dose of propranolol. The arachnophobia was gone for good.

According to the article linked above, “They erased their spider fear memories and then rewrote them with one of triumph — touching the tarantula a week after their treatment. When they returned to her lab three months and a year later, the effects stuck.”

Michael Saladin is attempting to end tobacco addiction with a similar approach. He is a professor at the Medical University of South Carolina, and he believes smoking addictions can be ended by getting rid of the cues (triggers) that make addicts smoke.

“There is a vast animal research literature that suggests memories can be manipulated following reactivation,” Saladin said. “I am convinced that there is sufficient evidence to believe that memory reconsolidation can be harnessed for clinical purposes.”

Memory Reconsolidation

The process being utilized in the UCL study, as well as in both studies mentioned above, is known as memory reconsolidation. The entire concept is relatively new. Essentially, the idea is to replace the bad memories associated with certain things with good memories, feelings of accomplishment and healthy pride. In the case of resisting alcohol, the already-consolidated memories of drinking will be replaced with new memories of feeling proud of not drinking. The ketamine allows this process to occur.

This may seem futuristic to you, and frankly it is. Scientists discover new information every day, and in the age of the microchip, our limits are becoming harder to see. New methods for how we do just about everything are being found. Yet when the use of illegal drugs, (ketamine is illegal to possess and is not a prescribed drug), becomes one of the methods that scientists discover, there tends to be a lot of pushback.

The scientists wish people would stop resisting.

Just because something is illegal and/or looked down on by society doesn’t mean that something isn’t effective in another way. We are seeing this nationwide with marijuana.

The Pushback

Lead researcher Das spoke to this resistance the public has for illegal/illicit drugs being used as medicines: “There’s just the general social attitude that everything that’s illegal is terrible. There will obviously be that kind of narrow-sighted pushback, but if it’s safe and effective enough it should be recommended.”

Das isn’t implying that ketamine is safe to use for anyone who wants to fix a bad memory. What he’s implying is that in a controlled, medical environment, a one-time dose of ketamine could help heavy drinkers relax on the booze.

Quoted in the Guardian article, Andrew Misell is a spokesman for Alcohol Concern, a non-profit charity working to reduce alcohol harm in the UK. Speaking about the UCL study in particular, he said, “The researchers have quite rightly highlighted what a lot of people in recovery from alcohol problems know from experience, namely that cues or triggers like the smell of beer can cause a relapse even after long periods of abstinence. Any work looking at how people can overcome these pitfalls is going to be useful.”

Misell added that he knows ketamine-based therapy has risks. What Misell didn’t add is that alcohol abuse has much more inherent risk than drug-based therapy. Not to mention, ketamine itself is significantly safer, and much less abused, than xanax, the number one drug used in all of psychotherapy.

Why the Pushback?

Medicine is medicine. Unless you the reader are a scientist or a doctor, you and I have no influence on what becomes medicine. If a one-time dose of ketamine can prevent alcoholism, why would anyone resist? Xanax is the most prescribed drug in all of psychotherapy, yet people abuse it WAY more often than ketamine. The NY Post published an article just last year explaining this, going so far as to say that xanax is ruining lives.

OxyContin, a drug used rather commonly for chronic pain, legal with a prescription, ends the lives of 100,000 people every single year. So why the pushback for ketamine?

In Conclusion

Drug/alcohol abuse is a horrible thing. People are dying in mass numbers from drug/alcohol abuse, and not just in America. This author does not condone the abuse of alcohol, nor does this author condone the use of illicit drugs. However, as this author wrote prior, what becomes a medicine is not a decision for anyone but scientists and doctors. If yours truly was a heavy drinker, and a doctor told me that habit could be stripped away with a one-time dose of ketamine, believe that no more questions would be asked.

One can only wait for the final results from the UCL study to see how many more participants turn out like Nikki. If and when the study proves effective for more and more people, we may begin to see a radical change in the way we fight addiction. It may seem like fighting fire with fire, but sometimes it works. Brushfires that spread rapidly are sometimes stopped by deliberately burning a section of earth where the fire is headed. Maybe ketamine is that deliberate burn in the realm of alcohol addiction

Tip sheets:

Prof Evgeny Krupitsky – Ketamine Psychotherapy For Heroin Addiction: Immediate Effects and Two-Year Follow- up

 1997 Apr-Jun;29(2):165-83.

Ketamine psychedelic therapy (KPT): a review of the results of ten years of research.


Ketamine is a prescription drug used for general anesthesia. In subanesthetic doses, it induces profound psychedelic experiences and hallucinations. The subanesthetic effect of ketamine was the hypothesized therapeutic mechanism in the authors’ use of ketamine-assisted psychotherapy for alcoholism. The results of a controlled clinical trial demonstrated a considerable increase in efficacy of the authors’ standard alcoholism treatment when supplemented by ketamine psychedelic therapy (KPT). Total abstinence for more than one year was observed in 73 out of 111 (65.8%) alcoholic patients in the KPT group, compared to 24% (24 out of 100 patients) of the conventional treatment control group (p < 0.01). The authors’ studies of the underlying psychological mechanisms of KPT have indicated that ketamine-assisted psychedelic therapy of alcoholic patients induces a harmonization of the Minnesota Multiphasic Personality Inventory (MMPI) personality profile, positive transformation of nonverbalized (mostly unconscious) self-concept and emotional attitudes to various aspects of self and other people, positive changes in life values and purposes, important insights into the meaning of life and an increase in the level of spiritual development. Most importantly, these psychological changes were shown to favor a sober lifestyle. The data from biochemical investigations showed that pharmacological action of KPT affects both monoaminergic and opioidergic neurotransmitter metabolism, i.e., those neurochemical systems which are involved in the pathogenesis of alcohol dependence. The data from EEG computer-assisted analysis demonstrated that ketamine increases theta activity in cerebrocortical regions of alcoholic patients. This is evidence of the reinforcement of limbic cortex interaction during KPT session.

Ketamine is gaining widespread acceptance as a fast and effective treatment for depression. It is so successful that ketamine has been called “the most important discovery in depression research in half a century” says Ronald Duman MD, Professor of Psychiatry at the Yale University School of Medicine. “A single dose of ketamine alleviates depressive symptoms within hours in patients who have failed to respond to two or more conventional antidepressants” he states in a scientific article published in the respected journal Science.

Researchers now believe it can treat more than depression and anxiety. Ketamine has recently generated a lot of interest among psychiatrists and addiction medicine physicians as a potential new and rapidly effective approach to treating struggling with other difficult-to-treat conditions such as substance abuse disorders and alcohol dependence.

“Current treatments benefits for alcoholism are at best modest, about three quarters of people return to drinking after 6 months, so there is a great need for new and more effective therapies” said Dr. Grass, Director of the Ketamine Institute in Pensacola Fl. “Many patients who come to us for ketamine therapy with conditions such as depression, anxiety or PTSD have self-medicated with alcohol or opioids to find relief. Initially, they find that alcohol seems to help their symptoms until it doesn’t anymore and it then become another serious medical issue in their lives” says Dr. Grass.

Can Ketamine Cure Alcoholism or Drug Addiction?

Research studies are currently underway at Yale and Columbia University in the United States and the University of Exeter in the United Kingdom to explore the beneficial effects of ketamine infusions on substance abuse disorders. Ketamine has already been shown to be an effective for depression, something that many people with substance abuse issues encounter as they try to become sober. As an antidepressant, it’s unique in that it acts very quickly, with patients often reporting an improvement in their mood over just one or two days. That could make it ideal for treating active, as well as, recovering alcoholics, who often suffer from depression immediately after quitting.

“This form of therapy is not new, says Dr. Grass. We have known for almost 30 years that ketamine may be effective in dealing with substance abuse issues.” In the 1990’s, Dr. Evgeny Krupitsky published research documenting over 10 years of observations utilizing ketamine for substance abuse disorders. His results suggest that ketamine can be remarkably more effective that current treatment options. Few people with substance abuse disorders can maintain abstinence following therapy with traditional approaches. However, Krupitsky found that as many as 66% remained alcohol free after one years as compared to only 24% with traditional treatment.

In addition, Krupitsky also found that the beneficial effects were dose dependent and that those people who received higher dosages of ketamine did better than those who received lower amounts. Following the study, psychological testing revealed that ketamine treated patients showed improvement on tests such as the Minnesota Multiphasic Personality Inventory (MMPI) personality profile. Changes seen included a positive transformation of self-concept and emotional attitudes, positive changes in life values and purposes. Patients also experienced important insights into the meaning of life and an increase in the level of spiritual development. Most importantly, these psychological changes tend to favor a sober lifestyle.

“We see many patients with depression, anxiety or PTSD who have at one point or another turned to alcohol or other substances to find relief only to become dependent upon these drugs”, says Dr. Grass. “A ketamine infusion, given at the right dose, can be a remarkably effective therapy in reversing these symptoms and alleviating their dependence upon alcohol or opioids. Often after just several ketamine treatments they can stop drinking and have no interest in alcohol or drugs after that.”

Ketamine – It’s Just the Beginning

Although more research is needed to determine exactly why there’s such a strong correlation between ketamine therapy and decreased use of alcohol and opioids, this observation does appear to validate the experiences of many people who have found substances like ketamine be life-changing tools that have helped them lead happier, more fulfilling lives. For many, this therapy has helped them cut back or quit their use of alcohol, opioids or other substances with which they have had a problematic relationship. One day, doctors may use ketamine routinely not only to help severely depressed people, but many who suffer from related conditions such as alcohol and substance abuse issues. “While the science is very promising, ketamine is not to be considered lightly and must be carefully monitored when used. But with the excitement generated by early results, we will have more information soon,” Grass says.


Duman RS, Aghajanian GK, (2012) Synaptic Dysfunction in Depression: Potential Therapeutic Targets. Science. 338(6103):68-72.

Synaptic Dysfunction in Depression Potential Therapeutic Targets

Krupitsky EM, Grinenko AY, (1997) Ketamine Psychedelic Therapy (KPT): A Review of the Results of Ten Years of Research. Journal of Psychoactive Drugs. 29(2):165-83

Ketamine therapy in Virginia | Ketamine for depression \ 703-844-0184 | Dr. Sendi | Ketamine for alcohol and drug abuse | Ketmaine psychotherappy

ketamine-and-rehab-therapy – Thailand

Ketamine Therapy

One of the most controversial issues surrounding ketamine is that it has been found to be an effective tool in therapy for addiction and depression. Researchers studied the effects of the drug on individuals who suffered severe depression and found that it was effective in relieving both symptoms and increased the effectiveness of psychotherapy. The drug has had interesting and astonishing results when used on patients who suffer from difficult depressive conditions, including bipolar disorder. The fast-acting nature of the drug proved to be the most interesting anti-depressant effect. Typically, anti-depressant medications can take days or weeks to start working which can prove ineffective if someone is suffering from a depression crisis. Administration of ketamine has provided immediate and short-acting results against depression, though it has been found ineffective in the long term.

Ketamine has been used as an alternative drug and alcohol therapy for nearly 30 years. The drug is administered under clinical conditions to individuals who are suffering the effects of chronic addiction and depression and the results have proved to be effective for some people. The drug has been found to only provide positive outcomes after detoxification from other drugs has occurred, and it is combined with effective professional psychotherapy. One study showed that there was a significant increase in the level of anhedonia, depression and anxiety that recovering heroin addicts experienced when they had been through ketamine psychedelic therapy. This is a significant result and such information may increase the use of ketamine as a therapeutic tool.



Clinical Trial:


Detailed Description:

Major depression and alcohol dependence are both within the ten disorders for highest worldwide disease burden as identified by the World Health Organization (WHO), and these disorders frequently co-occur, especially in high-service utilizing patients with severe and persistent mental illness. Currently available treatments are inadequate for both chronic conditions alone, and the inadequacy is even clearer in people meeting criteria for both disorders. Ketamine was first reported as a rapidly-acting antidepressant in 2000 via research occurring at Yale, and, since that time, in several small randomized controlled trials, a single subanesthetic dose of intravenous ketamine has demonstrated efficacy in improving mood in unipolar and bipolar depression within only hours after administration. These effects can last at least a week. Interestingly, ketamine has been demonstrated to produce a more robust effect in treatment-refractory unipolar depressed subjects with a family history of alcoholism relative to similarly difficult-to-treat subjects without a family history of alcohol problems. In addition, recently-detoxified alcoholics have been safely administered subanesthetic doses of ketamine, and, during these infusions, alcoholics (and even those with only a family history of alcoholism) displayed a differential response to ketamine, e.g. blunted psychotic-like and cognitive effects, relative to healthy controls. Therefore, ketamine may reduce depressive symptoms and alcohol consumption compared to placebo in patients with comorbid major depression and current alcohol dependence. Positive results will mark a major advance in the clinical care of those being treated for both conditions and will open the door for further scientific investigations into the clinical neuroscience of these highly comorbid and prevalent conditions.

This is a two phase, double-blind, randomized, placebo-controlled, cross-over, proof-of-concept study designed to determine the effects of a single dose of ketamine, administered IV, on mood and alcohol consumption, in psychotropic medication-free patients meeting DSM-IV-TR criteria for a major depressive episode (MDE) and current alcohol dependence. Participants will be assigned randomly to receive either intravenous ketamine (0.5mg/kg) or saline solution 2 weeks apart in a cross over design. The ketamine dose was based on previous studies in patients with depression and bipolar disorder. A team member experienced with ketamine infusions will administer the study medication over a 40-minute infusion in a blinded fashion at the Biological Studies Unit at the WHVA.

20 depressed alcohol dependent subjects between the ages of 21-65 will be recruited for this study through advertising and the West Haven VA clinics. Subjects will complete an informed consent process and will be thoroughly screened for inclusion and exclusion criteria as described below. Individuals will be given a post consent test to evaluate their understanding of the procedure. For subjects who provide incorrect answers to any of the test items, the research staff will review the correct answers with the subject and show the subject where the correct answers are found in the consent form. Those who get more than 60% of the questions wrong and are still unable to understand the procedure after reviewing it with the research staff will be excluded from the study. They will be referred to appropriate resources for outpatient treatment of their depression and alcoholism. Before start of the study all patients will be free of any psychotropic medications.

Ketamine for cocaine treatment

On the motivational properties of reward cues Individual differences

Subanesthetic ketamine decreases the incentive-motivational value of reward-related cues.

The effects of subanesthetic ketamine infusions on motivation to quit and cue-induced craving in cocaine-dependent research volunteers.

Ketamine emerging as top treatment for cocaine dependence



– The prospect on the horizon of two new effective therapies for chronic cocaine dependence – sustained-release dextroamphetamine and subanesthetic ketamine infusions – was among the top developments of the year in addiction medicine, Wim van den Brink, MD, PhD, said at the annual congress of the European College of Neuropsychopharmacology.Other highlights on his list included:• Studies establishing that comorbid attention-deficit/hyperactivity disorder (ADHD) and substance use disorder now can be treated effectively with either extended-release mixed amphetamine salts or high-dose methylphenidate.

Dr. Wim van den Brink

Dr. Wim van den Brink

• Evidence that the alpha-1 blocker doxazosin is an effective treatment for alcoholism in a specific well-defined subset of patients, opening the door to a personalized medicine approach to this disease.• Release of a puzzling array of conflicting studies on the use of high-dose baclofen for treatment of alcohol dependence. It’s tough to reconcile this mishmash of polar opposite results. And that dictates it’s time to declare a moratorium on the use of this therapy in clinical practice, which in many places is now widespread, said Dr. van den Brink, professor of psychiatry and addiction at the University of Amsterdam and director of the Amsterdam Institute for Addiction Research.

“It’s too strange that we have such conflicting evidence out there. Too many people are prescribing crazy-high doses of baclofen with no strong supporting evidence,” Dr. van den Brink said.

Cocaine dependence

Dr. van den Brink was a coinvestigator in a Dutch multicenter randomized, double-blind, placebo-controlled trial of multitreatment-refractory comorbid cocaine dependence in 73 heroin-dependent patients in heroin-assisted treatment. Patients assigned to 60 mg/day of sustained-release dextroamphetamine, in addition to the background methadone and diacetylmorphine all participants were on for their heroin dependence, had significantly fewer days of cocaine use in the 12-week study: a mean of 44.9 days, compared with 60.6 days in placebo-treated controls. Adverse events were transient and well tolerated (Lancet. 2016 May 28;387[10034]:2226-34).

“A lot of medications have been tried for treatment of cocaine dependence, but actually none of them has been shown to be effective with the exception of substitution treatment with stimulants. Ours is one of the most successful trials. These patients were using cocaine an average of 24 days per month along with a lot of other drugs, despite being in heroin treatment for 4 years,” Dr. van den Brink said. “Patients were very willing to take the sustained-release dextroamphetamine. In the last 4 weeks, 84% of them used at least 80% of their medication. And they were blinded to what they were using.

“We saw good effect sizes: 0.6-0.7 for self-report measures and 0.31 for negative urine samples. So this is a very promising approach. But it also means that, like with tobacco dependence or alcohol dependence, we have to start thinking about substitution therapy in stimulant-dependent patients,” he said.

Dr. van den Brink said subanesthetic ketamine as a novel treatment for cocaine dependence is not yet ready for prime time use in clinical practice, because it’s just not practical to bring patients in for a roughly hour-long intravenous infusion on a daily basis, as was done in a highly impressive proof-of-concept study. But new formulations of ketamine are under development that should better lend themselves to use in clinical practice.

In the proof-of-concept study, investigators at the New York State Psychiatric Institute brought into the laboratory cocaine-dependent volunteers not seeking treatment or abstinence and administered 52-minute infusions of ketamine at 0.41 or 71 mg/kg or lorazepam at 2 mg (Biol Psychiatry. 2014 Jul 1;76[1]:40-6). Lorazepam had absolutely no effect on motivation to change, but ketamine was a different story.

“As soon as you give a low dose of ketamine, you see a wonderful effect on motivation to change and on craving ratings in assessments at 24 hours post infusion. This looks like another promising way of treating cocaine dependence,” he said.

Doxazosin for alcoholism

Investigators at the National Institute on Alcohol Abuse and Alcoholism and several U.S. universities hypothesized that the norepinephrine system could be an important treatment target in alcohol dependence. They conducted a double-blind, placebo-controlled randomized trial in which alcohol-dependent patients seeking outpatient treatment were assigned to the alpha1-adrenergic blocker doxazosin (Cardura) titrated to a maximum of 16 mg/day or placebo. They found doxazosin significantly reduced drinks per week and the number of heavy drinking days per week, but only in the subgroup of patients with a strong family history of alcoholism. In patients without such a family history, doxazosin paradoxically increased drinking (Addict Biol. 2016 Jul;21[4]:904-14).

One of the reasons adult ADHD is greatly underrecognized is that it tends to occur in combination with flashier substance use disorders. “Addiction is very comorbid with all kinds of disorders, but especially with externalizing childhood disorders like conduct disorder and ADHD,” Dr. van den Brink said.

It was shown half-a-decade ago that normal doses of methylphenidate have no effect on ADHD symptoms or substance use in comorbid adults. Then Swedish investigators reported that treating criminal offenders with high-dose methylphenidate – roughly three times greater than standard dosing – was effective in reducing both ADHD symptoms and comorbid substance use in criminal offenders. Those findings prompted investigators at the New York State Psychiatric Institute and the University of Minnesota to examine whether prescribing extended-release mixed amphetamine salts in adults with comorbid cocaine use disorder and ADHD would achieve improvement in both conditions. Indeed, it did, Dr. van den Brink said.

One hundred twenty-six affected patients were randomized to 60 or 80 mg/day of extended-release mixed amphetamine salts or placebo for 13 weeks coupled with weekly individual cognitive-behavioral therapy for all in this double-blind, three-arm clinical trial.

“They showed a number-needed-to-treat of about 2.5 in order to achieve a significant reduction in cocaine use and a very nice reduction in ADHD symptoms with a number-needed-to-treat of 3,” Dr. van den Brink said.

The rate of continuous cocaine abstinence in the last 3 weeks of the trial was 30% in the 80-mg group and 17.5% with 60 mg of extended-release mixed amphetamine salts, compared with just 7% with placebo (JAMA Psychiatry. 2015 Jun;72[6]:593-602).

Interpreting baclofen studies

The first high-quality multicenter, randomized, placebo-controlled, double-blind clinical trial, conducted in Germany, showed baclofen (Lioresal) at a mean dose of 180 mg/day was effective in maintaining alcohol abstinence (Eur Neuropsychopharmacol. 2015 Aug;25[8]:1167-77).

“They got wonderful results, with a number-needed-to-treat of 2.3. That is something we’re not used to seeing in the treatment of alcoholism. But there was no dose-response effect, which is a little unusual,” the psychiatrist observed.

Then a multicenter group of Dutch investigators, including Dr. van den Brink, carried out what they believed would be a confirmatory randomized, double-blind, placebo-controlled trial. However, it showed no difference between high- or low-dose baclofen and placebo in time to relapse (Eur Neuropsychopharmacol. 2016 Dec;26[12]:1950-9).

Little further light was shed by the two large French randomized, placebo-controlled clinical trials presented at the 2016 World Congress for Alcohol and Alcoholism in Berlin. One, the BACLOVILLE trial, included 320 patients treated in 60 family practice clinics; it showed strongly positive results for high-dose baclofen. In contrast, the 316-patient ALPADIR study proved negative. These conflicting results were particularly disappointing because France has been at the forefront of using high-dose baclofen to treat alcoholism, Dr. van den Brink said.

“Maybe some 100,000 people have been treated with high-dose baclofen for alcoholism in France,” he said. “What is the conclusion from all these baclofen studies? You can interpret them in many ways. Maybe there are two positive trials and two negative trials, or maybe there are two positive trials and two failed trials. The debate is not closed, even after four randomized trials.”


Ketamine trials –

Researchers in the UK and US are running studies to see if ketamine could help prevent alcoholics from relapsing.

Ketmaine 703-844-0184 infusions| Fairfax, Va | 22308 |Woodbridge Ketamine | Ketamine for depression

People looking to quit problematic drinking in the UK could one day have access to a new, quick-acting treatment to help them cope with the difficult first few weeks of sobriety: ketamine.

In a new trial taking place at the University of Exeter and University College Hospital in London, researchers are using small shots of the tranquilizer—perhaps best known in the country as a popular party drug that can ruin the bladder lining of heavy users—alongside standard psychotherapy treatments to see if it can help treat alcoholism.


“Current effects of treatments for alcoholism are at best modest, about three quarters of people return to drinking after 6 months, so there is a dire need for new treatments,” said Celia Morgan, a professor of psychopharmacology at the University of Exeter, and one of the lead researchers on the study.

“It could help people who are stuck in a rut with alcoholism. It may prime your brain to take on new experiences from the world.”

Ketamine has already been shown to be an effective treatment for depression, something that’s done a lot to rehabilitate its reputation. As an antidepressant it’s unique in that it acts very quickly, with patients often reporting an improvement in their mood over just one or two days.

That could make it ideal for treating recovering alcoholics, who often suffer from depression immediately after quitting.

“We know that in alcohol dependence, depression is a predictor of relapse in the first couple of weeks. So we’re able to give people the ketamine package in the time at which they might be particularly susceptible to relapse,” said Morgan.

The trial, which is funded by the UK government’s medical research charity, will have participants take part in seven therapy sessions, three with shots of ketamine. Control groups will receive no drug and no therapy conditions. Ideally, the ketamine will act as a sort of stabiliser for depression, and possibly increase the power of the therapy.

Morgan said experiments with animals show that ketamine may help form neuronal connections in the brain, and that could mean that in humans the therapy will be more effective or more likely to “stick.”

“There’s new scientific evidence in animal models suggesting that their brains might be primed to learn more [after taking ketamine,]” she said. “So it could help people who are stuck in a rut with alcoholism. It may prime your brain to take on new experiences from the world.”

“We’re not going for the full-blown mystical experience”

Morgan is not the only one pursuing this theory. Elias Dakwar, a Professor of Clinical Psychiatry at Columbia University in New York, is currently recruiting patients for a similar trial that will use ketamine treatment alongside motivational therapy for alcoholism. He says that the way people’s brains adapt to addiction is similar to that of depression.

“People sort of forswear their own agency and self-efficacy, and there’s a sense of resignation,” he said. “The thinking on ketamine’s effect on depression is that it reverses depression-related adaptation through neuroplasticity.”

In other words, it could make the brain more ready to create new connections and move away from old patterns of behaviour, making it an ideal companion for therapy that’s meant to help people re-evaluate and change their lives.

The ketamine doses Morgan plans to use are higher than those used in standard depression treatment, but they’re not quite enough to cause the sort of total dissociation that has led some scientists to class ketamine as a psychedelic drug, and far less than the maximum safe dose as an anaesthetic.

“We’re not going for the full-blown mystical experience,” Morgan said. “We’re looking at treatment we can do within the National Health Service as well; this is something that is funded by the government, so we are looking at things that are acceptable in that context.”

Both trials are still in the early stages: Morgan’s started in June and is set to run until 2017, and Dakwar’s should wrap up next year. But if the results are positive, ketamine’s use could expand quickly. Alcoholism, like most addictions, is notoriously difficult to treat, with few effective drugs available. And according to the NHS, nine percent of men and four percent of women in the UK show signs of alcohol dependence.

“It’s one of those really intractable disorders that people have been trying to find a drug therapy for some time,” said Dr Dakwar.