There is no evidence that cocaethylene per se has activity that is different from cocaine itself or alcohol itself, other than the potential for prolongation of the usually short half-life of cocaine.  However, in conversations with thousands of people who used cocaine and alcohol together, patients have told me they felt the cocaine more intensely but not for a more prolonged period of time. However, there is clinical evidence that the cardiac toxicity of cocaine may be prolonged in drinkers, perhaps because of the chronicity of cocaethylene duration.  Interesting question whether cocaethylene may have prolonged psychoactive effects, but am aware of no evidence on that.

You are right there is a dearth of research and data on the subject.  It is not a legal treatment for cocaine use disorder (CUD) in the US, nor in my opinion, should it be. As Dr. Wartenberg said - it is pharmacologically (and experientially) virtually identical to the simultaneous use of alcohol and cocaine.  I have heard (anecdotally) that ED presentations are on the rise (somewhat dramatically - is cocaethylene easy to synthesize?) and therefore we should expect to see them in SAMHSA/DAWN data soon.  However, if there's really no material difference between cocaethylene and polysubstance use (cocaine+alcohol) then I don't see, from a clinical or policy perspective, why treatment protocols should be any different than for the "sub-disorders" (CUD and AUD) that are presented by cocaethylene misuse.  

One treatment to consider would be disulfiram.  Disfulfram (antabuse) will make pt sick when she uses cocaethylene, but I'm not sure if it's approved for cocaethylene OR, more importantly, if if disulfiram might interact in a negative way with the cocaine side of the compound.  You also might look into naltrexone (or extended release Vivitrol), which is pretty effective in neutralizing the (euphoric) effects of alcohol by blocking a set of receptors.  The problem with both disulfiram and naltrexone is pt compliance - they both have negative effects; nausea in the case of disulfiram and blocked euphoria in the case of naltrexone, so it is VERY HARD to get patients to take these meds long-term, as far as I know.  

You might also look into substitution therapy being developed for cocaine and other stimulants in other countries - it is presently illegal in the US, and I'm not personally optimistic that it will work, but who knows.  I have seen some interesting papers on stimulant substitution therapy (SST) but I don't have the cites handy - you can find them on medline.  [My concern with SST is that, unlike OST, you are trying to upregulate domaine and other neurotransmitters INDIRECTLY, by downregulating their reputake inhibitors -- whereas with OST you're administering medications (methadone/buprenorphine) that hit receptors directly after they are metabolized and pass the blood-brain barrier.  I'm just guessing that SST is going to be tougher than OST to get efficacy (even OST is arguably not the optimal standard of care) because of that key difference in neurophysiology.  

Given the lack of evidence-based Tx protocols for cocaethlyne, I would merge those available for cocaine and alcohol.  Probably, you're looking at an abstinence-based approach, at least in the US.  Treat comorbid psych conditions, encourage 12-step attendance, etc, etc.  There's no magic bullet for cocaine, or alcohol, much less the combination in one substance.  

Thank you for tending to my question. I suppose we could look at Cocaethylene as equal to the simultaneous use of cocaine and alcohol, except for the fact that it is produced and has its own unique chemical entity. That makes the need for further research necessary. My experience talking and a few qualitative questions I have kept by me over the years suggests ethylbenzoylecgonine (Cocaethylene) has an entirely separate set of presentations than other polysubstance abuse markers. Many addicts combine Xanax with cocaine when they run out of the cocaine or to "come down".  100 interviews with Cocaethylene addicts revealed that the addicted individuals simply cannot just use on or the other. Patient John Doe "I have to drink when I smoke dope, I could never take a hit unless I had a drink, and the second I have a drink, I have to run for the coke." These types of responses suggest, to me, an addiction to the actual "drug" Cocaethylene. I have heard many personal accounts of how the drug addiction was noticed and reinforced the binging behavior. I have heard an astonishing amount of clients explain that they started out as heavy drinkers and discovered they can drink much more and function sometimes, feeling as if they are stronger for long periods of time, even days and then when one or the other drug runs out the person crumbles into crying hysterically and deep depression. 

Please forgive the typos in my previous response. Something went wrong with my spell check. 

Hi Devin,

You wrote; >

ED presentations may be increasing simply because more practitioners are aware of this issue and because toxicology labs are actually looking for this metabolite?

I am not aware of any cases of synthetic coca-ethylene being produced and marketed as a drug of abuse. As far as I am aware, the only clinically significant cases of coca-ethylene synthesis take place in the livers of people who consume alcohol and cocaine concurrently.

http://www.ncbi.nlm.nih.gov/pubmed/7616402

A similar process produces the active metabolite ethylphenidate in people who drink alcohol whilst affected by Ritalin (methylphenidate). This substance has been synthesized industrially and over the last couple of years ethylphenidate has been marketed as a research chemical and as an ingredient in some "legal high" products.

https://www.caymanchem.com/app/template/Product.vm/catalog/13896

.

https://www.erowid.org/chemicals/ethylphenidate/ethylphenidate.shtml

.

But in the case of coca-ethylene, what we are talking about is poly-drug use.

Hi Marilyn,

There are synergistic effects involved in most poly-drug use- (if you watch people trying to give up smoking tobacco you'll see they often struggle with not having a cigarette with their coffee- this is not just psychological- they are habituated to the combined effects of nicotine and caffeine).

Most stimulant users are "poly-drug users", and the majority do use depressant drugs to regulate their level of arousal or to mediate the symptoms of "coming down" or of withdrawal from dependent use of their stimulant drug of choice. Alcohol and/or cannabis are the substances most commonly used in conjunction with cocaine or methamphetamine, although use of benzodiazepines and/or opioids is also not uncommon.

When people use alcohol in combination with either cocaine or methamphetamine, they quickly discover they can consume much larger quantities of alcohol and remain relatively functional. The subjective reward of the ethanol is increased while the negative symptoms are obscured by the stimulant. In someways this is similar to the way people use Red Bull or other caffeine/energy drinks in combination with alcohol.

http://onlinelibrary.wiley.com/doi/10.1111/j.1530-0277.2006.00070.x/abstract;jsessionid=94293C10A21686617D74BDF56482412E.f03t01?deniedAccessCustomisedMessage=&userIsAuthenticated=false

.

http://onlinelibrary.wiley.com/doi/10.1111/j.1553-2712.2008.00085.x/full

Typically people report that the rewarding effects of methamphetamine or cocaine can be prolonged by co-administration of alcohol. There are a bunch of increased health risks involved, especially increased risk of cardiac problems.

http://www.ncbi.nlm.nih.gov/pubmed/21463066

.

http://www.ncbi.nlm.nih.gov/pubmed/7768079

However there are behavioral or social risks as well-  people affected by stimulants AND alcohol may be more likely to argue with significant others, may be more likely to become involved in incidents of aggression or violence, and people affected by stimulants and alcohol may misjudge their ability to drive or perform other functions, underestimating how intoxicated they are.

There has been some attention paid to the issue of cocaine + alcohol, , see, for example;

http://ranzetta.typepad.com/files/cocaethylene_academy-briefing-paper-april-2010-8.pdf

I would support Devin's suggestion;

>

Regards,

Paul.

Paul:

I understand your scholarly explanation of this being a case of poly-substance use; however, the production of cocaethylene by the liver, to me, is astonishing. But, more importantly, my dissertation was Substance Abuse in the Workplace. This combination has the potential to reach the workplace. I am not suggesting a different treatment protocol (other than an added educational component), I am suggesting further research, including qualitative prior to quantitative. There is too much of a black hole in the literature regarding the subject matter. Thank you for your response.

Best Regards,

Marilyn

Esteemed Collegues"

The difference between poly-substance abuse is that Cocaethylene (etylobenzoiloekgonina) is not a street drug nor can be somehow introduced into one's bloodstream. I find that incredibly worth the scientific study of such a chemical/drug manufactured in the human body which is then sought after..

Marilyn