Im not going to post to anyone in particular because they think Im here to endlessly argue. I will address the neuroscience part of it. The blockade of opioid receptors is the basis behind Naltrexone's action in the management of opioid dependence—it reversibly blocks or attenuates the effects of opioids, meaning the neurotransmitter stays in the synapse longer, instead of being 'reuptaken'. There are three classes of opioid neurotransimtters as well.

The way Naltrexone works in addiction medicine is not fully understood, but as an opioid-receptor antagonist it's likely to be due to the modulation of the dopaminergic mesolimbic pathway which ethanol is believed to activate(from wiki, which actually gives a good summary of it)

Also from wiki, which I explained before concerning the safety of the medication .....

"""Safety
In alcohol dependence, naltrexone is considered a safe medication. Control of liver values prior to initiation of treatment is recommended. There has been some controversy regarding the use of opioid-receptor antagonists, such as naltrexone, in the long-term management of opioid dependence due to the effect of these agents in sensitising the opioid receptors. That is, after therapy, the opioid receptors continue to have increased sensitivity for a period during which the patient is at increased risk of opioid overdose. This effect reinforces the necessity of monitoring of therapy and provision of patient support measures by medical practitioners"""

So I dont need a lecture or a crayon drawing from anybody, thanks.

My feeling is that people are looking at alcoholism(a form of addiction) from the standpoint that the basis(cause) is behavioral. It is not the cause or the basis of the disease. If it were, anyone who has ever experimented with drugs/aocohol/gambling/etc would have learned the disease and become addicts, which is not the case. The basis(cause) is genetic. The learned behavior happens only with people who have the genetic basis for the disease. It explains why the vast majority of the population who casually gamble, drink, etc do not turn into addicts.

I appreciate everyone's help here, and I let the sarcastic stuff roll off. Doesnt bother me.

My motivations are primarily to show the genetic basis of addiction, not any one way to go about addressing it, although as I have said, TSM is a step in the right direction, although a bit off the path. Its a pharmacological approach to a genetic disease. Its appealing to addicts, except for the opioid sensitivity part, which increases the chance for overdose(not from endorphins, which are the response from a drug, but from the drug itself)

Im not sure what you mean my pre-synaptic. Re-uptake means it allows whatever drug to stay in the synapse longer, thereby increasing its effects. Pre or post synaptic are just terms describing the duration, not the mechanism. It certainly would not increase the re-uptake. The whole point of reuptake is to let the NT float around in the synapse. Im fairly certain most here do not have a background in neuroscience. I do, and would gladly explain the function and mechanisms.

"Exogenous opiates"? Is alcohol not exogenous to the brain or did I miss that class where the brain produces alcohol? People overdose on alcohol, as well as heroine all the time. They are both exogenous. Endogenous opiates you can't OD on, you are correct. You equate alcohol incorrectly.

The manner you are describing have to do with duration, not mechanism. The drug Naltrexone blocks this reabsorbtion, allowing the opioid neurotransmitters to float in the synapse longer. You are respectfully confusing duration of NT transmission with mechanism.

Alcohol is ethanol technically. Opioids are the neurotransmitters that are released with alcohol comsumption. Alcohol, Heroin, Morphine, etc act upon the opioid neurotransmitters. Neither Heroine nor alcohol nor any other drug are opioids. Some are opiates, which act on human opioid neurotransimtters. Look up the definition of opiates and opioids and then get back about neuroscience, which I will say again, few here seem to have a background on. Very respectfully.


I should have been more careful with the terms opiates and opioids in my previous post

Alcohol works the same pathways as opiates. The main NT is Dopamine that is involved in opiate addiction.

You are correct. Heroin is an opiate. Alcohol is not. They both work on the same limbic pathways.

Actually heroin is an opioid, as are all other synthetic and semi-synthetic narcotic analgesics. Opiates are naturally occurring substances which have similar effects (a background in linguistics helps sort this one out).

The difference between the direct effect of an exogenous opioid (such as heroin) and the indirect action of alcohol through endorphin release is an important distinction. You can OD on alcohol, and you can probably OD on jellybeans, but you can't OD on the sweet endorphins they both release.

But more importantly, what is it exactly you're trying to prove here? We all know that we can't drink without taking nal - it's written on the blackboard right under the teacher's name

Why don't you do this: read the book. If, after that you would still rather debate TSM than try it, we'll still be here.

Heroin is a opiate. Heroin is not naturally occuring in the brain. An opioid is a neurotransmitter in brains, which is triggered by opiates. There is no such thing as an exogenous opioid. An opioid is a class of NT that are produced by the brain. Ive stated what Im trying to prove here a few posts ago. which is addiction is fundamentally genetic. And that is where the focus should be. Not behavioral. Behavioral is just the sub-component of the underlying disease.

http://en.wikipedia.org/wiki/Heroin
http://www.druglibrary.org/Schaffer/heroin/opifaq.htm
http://www.ceida.net.au/depressants/heroin.asp

- just to clarify the minor point.

But despite your explanation, the major question remains: why would you spend countless hours trying to convince people who's lives have been positively transformed by TSM that somehow it doesn't work? Do you think we're just making it all up? I'm just really, honestly curious.

G'night all

OK I lied, I'm not going to bed yet. I just wanted to relate something: I have bad vision. Really bad vision, as in feel my way through the house without the coke bottle bottoms bad vision. It's genetic. That has been well established. My dad's the same way, and so is my mom (that explains "love at first sight"). I've done pretty well with glasses, and even better with contacts, even though they don't address the underlying problem. They are kind of like the AA or Rational Recovery of eye treatment. Just something to get you through, but without them you're pretty much screwed.

I'm thinking I might go get lasic surgery (I can spell, it's just that one key doesn't work on my computer). That surgery would be awesome. It's very safe (like TSM), it's proven (ditto), It's a real fix (again), and it's cutting edge (haha) technology. Nothing to be afraid of.

Does it address the genetic component to my eye problem? Absolutely not! Do I give a s h i t? Not even one! I just want my damn eyes fixed, to go along with my newly fixed brain!

OK this time for real, G'Night all

great analogy by Firebird regarding the eye-surgery

However, regarding the nature vs nurture argument, we have two extremes on the spectrum

a) It is 100% genetic
b) It is 100% acquired

If it is (a) then everyone who has the genetic disposition would be a raging alcoholic, there'd be no point in AA or any other form of therapy, and all pre-disposed people in 'non-drinking' societies such as in the Muslim world, would have broken out and gone on life-long benders.
If it is (b) then anyone who ever put a drink to their lips would never have stopped, while the horrified onlookers of all genetic backgrounds would have vowed to stay away from such a dangerous substance

I assume we can all acknowledge we're not at either end of this spectrum, which forces us to accept that we're somewhere in between - i.e. there are both components to the disease. This explains why not everyone who drinks becomes an alkie and why not everyone with the disposition continues to problem drink.

Regarding two points that dreadnought makes

1) My understanding of the problems with Naltrexone and (exogenous) opiates is that an opium addict will not be getting the 'hit' due to the action of the Naltrexone and may therefore take ever increasing doses to the level of being life-threatening
2) My understanding of the effect of Naltrexone on the sensitivity is that it is a short-term phenomonen, so that someone taking Naltrexone who stops is not going to suddenly face (any more than normal) mortal danger from alcohol.

Finally, those wondering about the motives of dreadnought ought to maybe ponder on his choice of username

Dreadnought, you misapprehend the discussion of alcoholism as learned behavior. You seem not to understand that term as we use it here. No one here would ever say alcoholism is behavioral; you must have missed the rants about Rational Recovery on this board. By learned behavior we mean learning in the classical-conditioning sense. We mean repeated behavior that strengthens neural pathways in our brain each time we repeat the behavior. Sinclair's work has demonstrated that those with a genetic predisposition to alcoholism are especially efficient at building neural pathways into "superhighways", although, given enough time and effort, those without the gene can strengthen the same neural pathways. When this learning has progressed to the point where can stop drinking, if at all, only with herculean effort, we are addicted to alcohol.

Your mantra is, "It's genetic." So what? What then? Apparently your choice is to wring your hands because you have the gene, and pound beer daily in the double digits. You repeatedly duck the question, put to you by Firebird and others, of why we should stop doing what we are doing, because it obviously is working.

I'm going to reprint part of my earlier post.

No one denies there is a genetic component to addiction. No one can credibly deny alcoholism is learned behavior. Anyone who drinks hard enough for long enough can certainly become addicted to alcohol over time. I am an example of that. If I have the gene, it is so far back in my family no one knows of it. To me, it doesn't matter. The words "addicted" and "cured" mean very little to me.

Here's what does mean a great deal to me: I was drinking very unhealthy amounts, and found I couldn't stop drinking on my own, so I started doing TSM. After twentysomething weeks, I am drinking less all all the time, without effort, and AF days are coming more easily. I'm nearly drinking at safe limits as defined by the W.H.O. I was forced by illness to stop naltrexone for a while, and was not able during that time to abstain from alcohol. Nothing terrible happened to me, and I resumed my progress once I was able to resume TSM. Based on what I've learned, the experience of others here, and my own progress, I can expect that I will be at safe limits shortly and that my interest in alcohol will continue to decrease.

I have not read one single word on this thread that would convince any sane and sensible person that TSM is a bad idea, or that I should stop doing it.

Dreadnought: Please comment.

You have an axis II personality disorder called narcissism. Look it up, you`ll probably like the traits that describe you. No hard feelings, its common and usually comorbid with substance abuse. The only person you are fooling here is yourself.