Does anyone know the scientific explanation of someone being HIGHLY resistant to all kinds of addiction?

I understand the concept of addiction coming from high levels of dopamine, but I really  can't even begin to think about what would cause someone to be almost completely resistant to addiction. I am not a science aficionado  (or any core academic subject for that matter) so if anyone has any knowledge or maybe theories about this I really would like to hear it. Google searches didn't pull up shit.

 

I'm just speculating, but I would say it has to do with your post synaptic receptors not being downregulated, so you wouldn't need more and more dopamine each time you shot up or smoked or w.e.  If you didn't lose receptors you wouldn't require the drug to get to your initial state of happiness, in other words wouldn't be dependent on it.  
Meditation.
Chemical & physical dependency is simply unavoidable with certain drugs like opiates, amphetamines or benzos. Once you take the drug X number of days in a row, your brain slowly starts to rewire and downregulate those receptors. Which is what causes tolerance and chemical dependency. Psychological addiction can be more tricky and is really the only varying factor at play. A person can be chemical dependent to a substance they take daily but not psychologically addicted. Someone can be hopelessly addicted in both forms as well of course. I've personally experienced both sides and id say the trickiest substance to gauge in this regard would be Cannabis. 
That's interesting. I have done my fair share of things which are considered to be extremely addictive (sometimes on a semi regular basis for weeks/months) and for some reason addiction just never happened. I mean I enjoyed it and felt good obviously but when I ran out withdrawal symptoms was something that just never happened. 
For some people that particular X number of days that a substance needs to be taken to cause withdrawal will vary a bit. The dosage being taken also will matter a lot. Example being someone taking 0.25mg of xanax everyday for 2 weeks wouldn't feel much, if any withdrawal symptoms at all upon stopping. Change that dose to 2-3mg everyday instead and it can make a huge difference. 

From a clinical psych. blog

 

RE: Internet addiction


Ask a 20 year crack addict when was the last time they used powder cocaine.  Do they miss it?  Are they in withdrawal?  "But crack is cocaine."  No, it isn't, or else they would be using both, wouldn't they?  "But crack is more potent and addictive."  Then why don't cocaine adicts move over to crack? 

Do you know how many Xanax addicts I've had throw back at me a prescription for Klonopin? It wasn't availability, I was giving it to them, they had it in their hands, and they refused it.  In theory it should have been "good enough."  It wasn't. 

By age 25, every guy has been with a girl that-- sorry, let me start over--

By age 25, every guy that has been with a girl has been with a girl that they couldn't get enough of, couldn't live without, called all the time, left school work undone, called into work sick, code-named "Freebird" in a journal entry,  etc, etc-- but the relationship sucked, this girl was so evil that all his friends wanted to hit him with a sack of doorknobs.  Was he addicted to her?  Technically, yes-- but really, no.  More to the point: she wasn't actually evil, and he wasn't addicted to her, at all.  (I mean, now that you're 40, you see that, right?)

"Yes, but there's a common addiction pathway..."  Oh, I don't know.  If this was true, chemical addicts would have generally substitutable addictions, and they don't.  Experiments with mice strongly support the idea of substitution  (e.g. cocaine addicted mice will thirstily self-administer amphetamine)  but humans don't really do this.  (1)  And chemical addicts should also have very high rates of other (non-chemical) addictions as well, and they don't. (2)

These non-chemical, behavioral addictions are more properly labeled obsessions but-- and this is the point-- an obsession is not a disorder.  Obsessions can cause harm, we can try to help people with them, but they are not themselves the problem, they are symptoms of something else.

That something else may not be a disorder, either: fragile self; guilt or shame; low or high self esteem; flawed but automatic assumptions, whatever-- but trying to "treat" internet addiction without addressing the underlying problem is like treating cancer with Tylenol.  Not only does it not help, it actually makes the situation worse.

Dr. Block's intention was to describe a series of behaviors, not to create a new disease.  He's already established believer in the positive power of the net, online games, etc.  Unfortunately, psychiatrists will only see this editorial, and come to the wrong conclusions.

In the article he cites research from South Korea, where the average kid (supposedly) uses the internet 23 hours a week, and thus is at risk for addiction.  Compare that to the U.S. 20 years ago, where the concern was 20+ hours of TV a week.  I do not recall discussion about kids becoming addicted to TV; we worried they were becoming stupid.  What's changed isn't the medium or the amount of time on it, or the harm to the intellect or society; what's changed is the social movement to pathologize, rather than condemn, behaviors.

I'm not saying let's go back to condemnation, but to put "Internet Addiction" into the DSM legitimizes the symptom-is-disease approach that has caused such great difficulty for patients, and nearly irreparable harm to humanity.

(1) Please do not say the words "dopamine" and "nucleus accumbens" anywhere near me, I still have my old sack of doorknobs.  These explanations could not be more general and useless.  Using those two in support of a common addiction pathway is like involving "gasoline" and "spoons" in the diathesis for serial rapes.  Even though these are involved in various "addictions"-- cocaine, alcohol, internet, sex-- these "addictions" and their associated behaviors are so disparate that the pathway serves no useful clinical target.  Haldol blocks dopamine in the nucleus accumbens, but you can't cure alcoholism with it, can you? 

I'm not denying that such a pathway exists, I'm doubting the utility of this information, even if true.  Call me when science catches up to your lies.

(2) Here's an example: why do so "sex addicts" or gamblers have such high rates of drug abuse, but the converse is not true?

http://www.chron.com/news/health/article/Houston-scientists-see-hope-in-...

The needle may be one of addiction's enduring symbols, but two Houston researchers hope injections of modified cocaine actually provide the first-ever medication for people hooked on the destructive drug.

1996: cocaine vaccine was developed by ImmuLogic (defunct), announced in Nature.
1999: sold to Cantab Pharmaceuticals
2001: Cantab merges into Xenova
2005: Xenova bought by Celtic Pharma (really a private equity firm, that also holds the nicotine vaccine.)

In an attempt to see if there is an interaction between cocaine and Provigil, 20mg or 40mg IV cocaine was given pre and post Provigil (400mg or 800mg) for 7 days. There was an interaction, but it turned out to be positive: Provigil reduced systemic cocaine exposure.

 

A safety study investigated (in 7 people) the interaction between cocaine (30mg IV) and Provigil (modafinil) 200mg or 400mg, or placebo, and found no synergistic effect on vital signs (T, BP, HR) or EKG.  Not only did it not augment cocaine euphoria, it blunted it in one person. 

 

In another study, 62 (mostly black) males addicted to cocaine were randomized to placebo, CBT, or Provigil 400mg.  Abstinence, the primary outcome, was measured by benzoylecgonine in the urine.  Patients on Provigil were abstinent longer, and produced fewer positive urines (i.e. fewer relapses.)  Importantly, no one got addicted to Provigil.


Unlike cocaine and Ritalin (methylphenidate) Provigil did not produce "cocaine like discriminitive stimulus" (i.e. didn't feel like cocaine; Ritalin and cocaine do feel like cocaine.)

 

That's all we know about Provigil vs. cocaine so far, which is pitiful but not inconsequential.  Given Provigil's near absence of terrible side effects, I say it's worth a try.

 

In the interest of completeness (and correctness) I have to correct the major paper, above (the 62  people with the urine tests) .  The authors of that paper propose the following potential mechanism:

 Its glutamate-enhancing action (Ferraro et al, 1998; 1999) might be clinically advantageous in cocaine dependence because the repeated administration of cocaine depletes extracellular glutamate levels

Except that the Ferraro paper doesn't actually say that. What it says is that it inhibits striatal and globus pallidus GABA, but doesn't directly affect glutamate.   In order for it to have any effect on  striatal glutamate, you needed 300mg/kg (i.e. 21,000mg.  See you on the other side.)  Given that GABA and glutamate are opposites (i.e. glutamate goes up because GABA goes down), it's probably a small point, but not an insignificant one: if it directly increases glutamate, it could antagonize Lamictal or even potentially cause seizures (and it does neither.)

The second  Ferraro reference finds essentially the same thing: inhibition of medial preoptic area and posterior hypothalamus GABA, and consequently glutamate increases.  And again, all of this occurs at preposterously high doses (100-300mg/kg.)

In interesting side finding of Ferraro's study is that the medial preoptic area and posterior hypothalamus are primarily controlled by tonic GABA inhibition; consequently modafinil's (or any drug's) effect of increasing glutamate in these areas can be blocked by giving a GABA-A antagonist.

So Provigil operates by  (probably) by antagonizing GABA, not specifically by enhancing glutamate (neither synthesis of or transport of). 

To further complicate this picture, it may be that the effects on GABA and glutamate are both indirect, and really the result of serotonin agonism. In an earlier study by the same guy, the decreases in GABA were partially prevented by a 5HT3 blocker (think Zofran, Remeron).  Does Provigil work through serotonin?  In a later study, the same guy finds that at 100mg/kg, Provigil does, after all,  increase serotonin in the medial preoptic area and posterior hypothalamus.   (At lower doses, 10-100mg/kg, it increases serotonin in the cortex, dorsal raphe and the amygdala.)  (And in another study, (yes, by that same guy again,) 3mg/kg Provigil, which in itself has no effect on serotonin, synergistically augmented serotonin increase to fluoxetine and imipramine.)

We already know that Provigil can reduce the sedation that comes from varying drugs, like SSRIs, general anesthesia,  haloperidol, and chlorpromazine. It would be interesting to see if Provigil was unable to improve sedation on Remeron, supporting the 5HT3 hypothesis.

 

Good luck out there. 

Provigil is an interesting drug. I've researched it a bit for treating adhd vs amphetamine treatments. It's still a relatively new treatment for it but what you can read up about it seems promising. I could still get a sample packet of it if I want to. 

"Do you know how many Xanax addicts I've had throw back at me a prescription for Klonopin? It wasn't availability, I was giving it to them, they had it in their hands, and they refused it.  In theory it should have been "good enough."  It wasn't."  

I find that hard to believe lol, no benzo addict I know would do that. Only odd thing from that blog. 

 

Well, that was written 8 years ago.
That could explain the weird deja vu feeling I got from reading it lol. Probably read it a long time ago.   
A square....
Killed it.