Giving up drugs - it's easy!

[scott nathaniel]

Funken! You're freakin me friggin' out: 5 consecutive posts without a response. I defended you in private, strictly on principal, and here you are gabbing like a lunatic. Please, Funken, cogency, please!

http://www.youtube.com/watch?v=YPIsTKpAoE4

Thanks! I needed that! So, we're cool?

[Forge.]

phew... 4am in England, I think he's finally gone to bed.

[artpunk]

...no, they act on different receptors to the best of my knowledge.

I've quoted some research in this thread and the other one.

"But how is marijuana addictive? What’s the link to heroin?

What most people don’t know is that there is quite a bit of interaction between the cannabinoid receptor system (especially CB1 receptors) and the opioid receptor system in the brain. In fact, research has shown that without the activation of the µ opioid receptor, THC is no longer rewarding.

If the fact that marijuana activates the same receptor system as opiates (like heroin, morphine, oxycontin, etc.) ....

etc etc etc...
Funken, funken, funken.... WTF?
I was addressing this statement here.

They all act on the same brain receptors and reward pathways in fact.

Yes, they do influence the reward pathways, but (now please, pay attention to this simple thing I am saying here) they act on different receptors. Not only that but they also affect the reward pathways in different complex ways - I know it is being pedantic, but surely there is nothing wrong with clarifying so-called 'facts'. You can refer to other documents, 'research' and what have you stating 'same receptors' all you like, but it will not change simple established knowledge of neurophysiology, neurotransmitters and the physiology of cell membranes, transport mechanisms, receptors, agonists and antagonists. I just don't like 'fuzzy' science.
I stand by my other statements regarding addictions as well. These issues are often far too complex to solve every individuals addiction problems through answers provided in any one book or approach...


ALCOHOL

Alcohol affects the brain’s neurons in several ways. It alters their membranes as well as their ion channels, enzymes, and receptors. Alcohol also binds directly to the receptors for acetylcholine, serotonin, GABA, and the NMDA receptors for glutamate.

OPIATES

The reason that opiates such as heroin and morphine affect us so powerfully is that these exogenous substances bind to the same receptors as our endogenous opioids. There are three kinds of receptors widely distributed throughout the brain: mu, delta, and kappa receptors.

These receptors, through second messengers, influence the likelihood that ion channels will open, which in certain cases reduces the excitability of neurons. This reduced excitability is the likely source of the euphoric effect of opiates and appears to be mediated by the mu and delta receptors.

This euphoric effect also appears to involve another mechanism in which the GABA-inhibitory interneurons of the ventral tegmental area come into play. By attaching to their mu receptors, exogenous opioids reduce the amount of GABA released. Normally, GABA reduces the amount of dopamine released in the nucleus accumbens. By inhibiting this inhibitor, the opiates ultimately increase the amount of dopamine produced and the amount of pleasure felt.

COCAINE

Cocaine acts by blocking the re-uptake of certain neurotransmitters such as dopamine, norepinephrine, and serotonin. By binding to the transporters that normally remove the excess of these neurotransmitters from the synaptic gap, cocaine prevents them from being reabsorbed by the neurons that released them and thus increases their concentration in the synapses. As a result, the natural effect of dopamine on the post-synaptic neurons is amplified. The group of neurons thus modified produces much more dependency (from dopamine), feelings of confidence (from serotonin), and energy (from norepinephrine) typically experienced by people who take cocaine.

NICOTINE

Nicotine imitates the action of a natural neurotransmitter called acetylcholine and binds to a particular type of acetylcholine receptor, known as the nicotinic receptor.

Whether it is acetylcholine or nicotine that binds to this receptor, it responds in the same way: it changes its conformation, which causes its associated ion channel to open for a few milliseconds. This channel then allows sodium ions to enter the neuron, depolarizing the membrane and exciting the cell. Then the channel closes again, and the nicotinic receptor becomes temporarily unresponsive to any neurotransmitters. It is this state of desensitization that is artificially prolonged by continual exposure to nicotine.

Tobacco dependency, which then develops very quickly, arises because nicotinic receptors are present on the neurons of the ventral tegmental area which project their terminations into the nucleus accumbens. In smokers, repeated nicotine stimulation thus increases the amount of dopamine released in the nucleus accumbens. Between cigarettes, however, chronic smokers maintain a high enough concentration of nicotine to deactivate the receptors and slow down their recovery. This is why smokers develop a tolerance to nicotine and experience reduced pleasure from it.


CANNABIS

The sensations of slight euphoria, relaxation, and amplified auditory and visual perceptions produced by marijuana are due almost entirely to its effect on the cannabinoid receptors in the brain. These receptors are present almost everywhere in the brain, and an endogenous molecule that binds to them naturally has been identified: anandamide. We are thus dealing with the same kind of mechanism as in the case of opiates that bind directly to the receptors for endorphins, the body’s natural morphines.

Anandamide is involved in regulating mood, memory, appetite, pain, cognition, and emotions. When cannabis is introduced into the body, its active ingredient, Delta-9-tetrahydrocannabinol (THC), can therefore interfere with all of these functions.

THC begins this process by binding to the CB1 receptors for anandamide. These receptors then modify the activity of several intracellular enzymes, including cAMP, whose activity they reduce. Less cAMP means less protein kinase A. The reduced activity of this enzyme affects the potassium and calcium channels so as to reduce the amount of neurotransmitters released. The general excitability of the brain’s neural networks is thus reduced as well.

However, in the reward circuit, just as in the case of other drugs, more dopamine is released. As with opiates, this paradoxical increase is explained by the fact that the dopaminergic neurons in this circuit do not have CB1 receptors, but are normally inhibited by GABAergic neurons that do have them. The cannabis removes this inhibition by the GABA neurons and hence activates the dopamine neurons.

[Forge.]

GO TO BED!

[artpunk]

You really should try and at least get a few winks!

About the 'research' yeah, well, I will admit I didn't even read it, or it source, or in what journal or papers it was published, but if it doesn't actually negate my points about what affects what specific receptor(s), then it probably isn't relevant...
Regarding what the/any research shows, I'm happy to examine scientifically rigourous data, at least until a different data set is presented by different researchers... Over the years especially in medical science, I've seen a great deal of supposedly scientifically 'proven' data that later on turned out to be 'not so' accurate... enough to maintain a healthy cynicism, no matter what papers/journals they are published in!

Now... Get some sleep!

[Machinesworking]

I CAN"T SLEEP!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!

Insomnia is the absolute worst part of the first month of sobriety, it gets better after a couple weeks for most people.

Since you've spent this thread essentially spamming your favorite addiction therapy author I have one for you.
http://www.amazon.com/Seven-Weeks-Sobri ... 0449002594

Mostly because it deals with the chemical imbalance people often suffer when quitting drinking.
IE the inability to sleep, irritability etc. I don't subscribe to her method whole heartedly, I simply watched what I ate, and ate some vitamins.

She did a pretty intensive study of the body types and chemical dependance variations that happen depending on type. All northern europeans for instance should definitely consider taking into account a regiment of omega 3 fatty acids etc. Especially if signs of depression occur after quitting.

[Forge.]

Vitamin B12 is a big one for alcohol... sometimes doctors actually give injections of it when people quit heavy drinking

[Machinesworking]

If I remember right all the B's are a big part of it....

[artpunk]

If I remember right all the B's are a big part of it....

...and Diazepam (Valium) when symptoms of Delerium Tremens kick in...
We have 'alcohol withdrawal charts' in E.D. so we can assess our patients using a reasonably objective tool with clear guidlines for treatment depending on the score they get on the chart...

[cmcpress]

stop smoking! go on! stop!

I was waiting for someone to do that.

he's poised willing to cure Funken from his heterosexuality.

[Machinesworking]

Funny, even though I'd been arguing on here, which was probably another reason I was wide awake, I never missed alcohol all evening. Never really thought about it.

The insomnia doesn't come from desire for booze or anything, it comes from the simple fact that booze is a downer, and over the years you train your body to think it needs be slightly toasted to sleep. So when you quit your sleep patterns get all out of whack.

It's not just booze though, I get this every time I'm off of work for a while because my work is physically exhausting and I like to play guitar and with the computer etc. which isn't physically active enough.


http://www.youtube.com/watch?v=Tusig-UmukU

[cmcpress]

hmm, no offence to Allan but he wouldn't be my first choice I don't think. Funny bloke though.

massive cock though.

[artpunk]

If I remember right all the B's are a big part of it....

...and Diazepam (Valium) when symptoms of Delerium Tremens kick in...
We have 'alcohol withdrawal charts' in E.D. so we can assess our patients using a reasonably objective tool with clear guidlines for treatment depending on the score they get on the chart...

Did you read the bit in the op about the supposed dangers of stopping alcohol suddenly? Maybe you can comment on that?

Yes, I already did, on page 7 of this thread... But it probably wasn't very obvious as I simply posted some links...

note - it is said that stopping alcohol suddenly can be dangerous to a small percentage of alcoholics. I will try to find out more.

http://en.wikipedia.org/wiki/Delirium_tremens

http://www.ncbi.nlm.nih.gov/pubmedhealth/PMH0001771/

[d.reamonn]

"I read the book in two days, and had my last drink about two months ago. Since then, I have had no desire whatsoever to have a drink; which is pretty astounding as I used to love it!"

[Forge.]

I had a lie down later and crashed out for 3 hours anyway, woke up dreaming about Black Sabbath.
.

one sure fire way to inspire yourself to get off the booze is to watch Ozzie in action

got a great quote from a doco of him the other day: "yeah 1 + 1 = 2 but what the fuck does 1 mean?"

small bit of trivia... his son Louie included my first release on his DJ mix compilation