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Finally have some time to really dive into this.

Is anyone out there aware of any published responses to this AA Cochrane review yet, from Div 50 or others? How are folks in your systems using these findings?

One thing I am particularly concerned about is mid-levels justifying AA over everything else based on this report. Interesting findings but it seems there are more than some methodological concerns. Also, one of the major points is that the findings are for "clinically delivered" and "manualized" programs. What community meetings are run this way? I know of none.

Some interesting articles being written in the media about the report:
 
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1)It's a sneaky trick. AA treats "Alcoholism", NOT the DSM5 or ICD10 alcohol disorders. AA defines alcoholism as a spiritual disease, mixed in with some physical cravings, and some mental stuff.
2) They don't define success like you'd think. Hint: it's not sobriety.
3) AA's early publications claimed success for 50-75%. But no data.
4)In the early 2000s, AA made some national news because someone obtained their data. Long story short, AA excluded the fact that the majority of people drop out after one meeting, and even more drop out within a few meetings. Throw those people in, and their combined success rate was like 5-10%. Not that great. And their version of "success" is not necessarily life time sobriety.
5) There was some conflict stuff with the legality of the courts mandating religious treatment.
6) And the self medication hypothesis isn't supported.
7) But all of this is a cheap way for society to deal with a problem, kinda.
 
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Source? To my knowledge results are mixed (PTSD examples: 1, 2), but curious what led you to make such a strong statement.

(1) Error - Cookies Turned Off
(2) Ecological momentary assessment of PTSD symptoms and alcohol use in combat veterans - PubMed
A. Strap yourself in, it's a crazy ride. Gonna give you some names, but this is more of a rant than an academic treatise. Feel free to look up the names.


1) To start, my source for refutation is ANY ELEMENTARY SCHOOL SCIENCE BOOK THAT COVERS THE SCIENTIFIC METHOD.

a. Most academic is predicated upon the assumption that the people involved use the commonly accepted professional terms and methods of that field. For example, there is a defined meaning to the term "hypothesis", and the term "theory" and "scientific method".

b. Most academia would immediately refute works that do not use the accepted methods, terms, and literature, without explanations for deviations from professional standards. Most normal people also seem to demand such things, which is why we find humor in claims from QAnon, sovereign citizens, and that random guy in the bar who claims to have genitals the size of an elephant.

c. Confronted with a hypothesis that isn't a hypothesis, a lack of empirical supported, and a creator doesn't follow the scientific method, etc...... it is wise to accept the null hypothesis.


2) Formalized circa 1985, with some lead up articles starting in 1974, the self medication hypothesis (i.e., SMH) is presented as a VERY VERY SPECIFIC HYPOTHESIS that has 2-3 components.

a. There is a CAUSAL relationship between affective/mental disorders and substance abuse.
b. The characteristics of the affective/mental disorder PREDICTS which substance will be used.
c. The individual's functioning would IMPROVE through the use of the substance.

It is important to note that this hypothesis is essentially an A/B design, with the added components of specificity of substance, and improved functioning. It is X disorder, caused abuse of Y substance which did not exist before, and not cause abuse of Z substance. Causation requires that Y use was not present before X disorder, just like in infectious disease stuff. And before you start talking about trait whatever blah blah blah, the SMH says that ADHD causes cocaine use, so ...NO.

This theory is NOT "My abuse of Y substance went into overdrive when I got X diagnosis.", nor is it "I got X symptoms and went on a polysubstance bender.".

History: So the SMH gets published in 85. People like Deykin and/or Dackis tested it, and showed that the onset of the affective/mental diagnosis had no relationship with the onset of substance use. Showed that the characteristics of the mental disorder did not predict which substance was used. Then people like Weiss and/or Morrisey showed that people will say they abuse substances because they are depressed, but that their self report is completely contradicted by years of medical records that show the SUD predated any mood complaints by years. (This is one of the starting points in the literature showing self report is HIGHLY unreliable. ) Then the epidemiology literature showed that polysubstance abuse is MUCH more common than abuse of one substance, which would contradict the specificity requirement of the SMH. And some experimental studies from authors like Castenda, Greene, Mueser, Schink, or Swenden who showed that there was no relationship between the type of mental/affective disorder and which substances used, that onset of substance use typically predated the onset of the affective/mental disorder, and that patients reported that the substance use actually made their symptoms worse. Not good enough for you? THE ARCHITECT OF THE DSM-IV INDICATED THAT THE SMH IS MISGUIDED!!!!! Try coming back from that one!

Now most elementary school kids would accept the null hypothesis, or get more data, or give a completely different hypothesis for testing.

3) INSTEAD THE AUTHOR LITERALLY ADMITTED HE WAS WRONG IN 1997, "Diagnostic studies provide evidence that variously supports and fails to support a self-medication hypothesis of addictive disorders." AND HE THEN HE CHANGED THE SELF MEDICATION HYPOTHESIS!!!!!!!!! No, he didn't give a new hypothesis. He just changed the old one. Anyone else remember that part of elementary school science? Or that part of stats where Type I and II errors can be avoided by changing the hypothesis? No? Because that is NOT how hypotheses work.

So now the 2nd version of the SMH basically says the substance of choice is caused by the individual's current mood, and NOT the affective/mental disorder. Which essentially means the "self medication" is really just about mood state.

Some people decided to study the new SMH. Studies from people like Aharanovich, or Hodgins showed that state emotions had no relationship to which substance was used, and that affective state did not happen BEFORE onset of substance abuse. This even went on at the National Comorbidty Study. Ten YEARS of follow up showed that there was no relationship between the specific mental disorder and the specific substance of abuse; and that the onset of substance use had little relationship to the onset of mental disorder (e.g., breslau; Kessler, etc).

Must be the end of the story, right?

4) Not even joking, HE CHANGED THE SELF MEDICATION HYPOTHESIS A 3RD TIME!!!!!!! In 2003, the SMH essentially became "you know, there's this entire dual diagnosis thing. Since addictive disorders are caused by people trying to self medicate an underlying disorder, the substance use will disappear once you treat it." Now Mueser had already disproved that idea, and Brown disproved this idea like 15+ years before, but why stop now? People like Hall, or Nunes, showed that treating the the supposed underlying mental disorder does nothing to change substance abuse. Even on meta-analysis.

5) To be fair, there is another self medication theory based upon operant conditioning, published by Duncan around 1974. Interesting idea. However, he seemed to experience some difficulty in studying this idea AFTER HE WENT TO PRISON FOR KIDDIE PORN IN 1989.

6) In comparison, other theories have stronger evidence. Heritability of SUD is around 30-60% on monozygotic twin studies (e.g. ,Goldman, 2006ish). There seems to be some genetic vulnerability, and trait vulnerability, which interacts with the environment (e.g., Belcher, 2015ish; Read, 2014 ish; etc).




B. Now let's go to your citations:


1) In order to accept the works as supporting evidence, we would need them to:

a. study the subject of relevance,
b. use a methodology relevant to the subject of relevance.

2) They don't use any definitions consistent with the SMH, which means they're not studying the SMH.

a. The authors from your citations ignored the 1985 definition, and the 1997 definition, and then defined the SMH as, " ...the self-medication hypothesis, a causal model that postulates that individuals with PTSD are more prone to developing problematic drinking behaviors due to a tendency to drink to cope with negative internal experiences (Khantzian, 1997)". The VERY SAME 1997 paper defines the SMH as, " First and foremost, drugs of abuse relieve psychological suffering. Second, a person's preference for a particular drug involves some degree of psychopharmacological specificity. ". Kinda weird that the authors didn't reference the definition on the first page. Even weirder is that their definition ignores the specificity part of the SMH. Still weirder is that they reduced the SMH to problematic drinking in PTSD, when the 1997 article actually says alcohol and drugs. And even weirder that instead of using the SMH, they use Duncan's theory, which differs from the SMH, and fell into disfavor after Duncan went to prison for kiddie porn. Don’t they know what the SMH is?

b. The authors' method is essentially asking people if they drink to cope with PTSD, when the literature, over the last 30+ years, has shown this is an unreliable method.

c. There are no efforts to determine if the substance abuse or PTSD came first. As required by the SMH, and recommended by Allen Frances. And, you know... like the DSM requires....
 
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AbnormalPsych

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I've written some about this (SMH and others), back in my academic days.

I'll just say, yep. Aside from #5. No idea about any of that. Duncan or the kiddos.

99% of midlevels and a good amount of PhD/PsyDs will only answer SMH when you ask them to tell you what they know about theory and treatment of SUD. It's a blindspot in our training for sure, given the prevalence of substance related d/o.
 
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1)It's a sneaky trick. AA treats "Alcoholism", NOT the DSM5 or ICD10 alcohol disorders. AA defines alcoholism as a spiritual disease, mixed in with some physical cravings, and some mental stuff.
2) They don't define success like you'd think. Hint: it's not sobriety.
These 2 are of big concern, because lay people are not picking up on this.

7) But all of this is a cheap way for society to deal with a problem, kinda.
Fair and good for those who need it.

But, this (money, politics) is why I think this report is getting more publicity that it should be in medical circles, at least in my neck of the woods. People are also looking for something or somewhere to send difficult patients and this report is their golden ticket to justify that.
 

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A. Strap yourself in, it's a crazy ride. Gonna give you some names, but this is more of a rant than an academic treatise. Feel free to look up the names.


1) To start, my source for refutation is ANY ELEMENTARY SCHOOL SCIENCE BOOK THAT COVERS THE SCIENTIFIC METHOD.

a. Most academic is predicated upon the assumption that the people involved use the commonly accepted professional terms and methods of that field. For example, there is a defined meaning to the term "hypothesis", and the term "theory" and "scientific method".

b. Most academia would immediately refute works that do not use the accepted methods, terms, and literature, without explanations for deviations from professional standards. Most normal people also seem to demand such things, which is why we find humor in claims from QAnon, sovereign citizens, and that random guy in the bar who claims to have genitals the size of an elephant.

c. Confronted with a hypothesis that isn't a hypothesis, a lack of empirical supported, and a creator doesn't follow the scientific method, etc...... it is wise to accept the null hypothesis.


2) Formalized circa 1985, with some lead up articles starting in 1974, the self medication hypothesis (i.e., SMH) is presented as a VERY VERY SPECIFIC HYPOTHESIS that has 2-3 components.

a. There is a CAUSAL relationship between affective/mental disorders and substance abuse.
b. The characteristics of the affective/mental disorder PREDICTS which substance will be used.
c. The individual's functioning would IMPROVE through the use of the substance.

It is important to note that this hypothesis is essentially an A/B design, with the added components of specificity of substance, and improved functioning. It is X disorder, caused abuse of Y substance which did not exist before, and not cause abuse of Z substance. Causation requires that Y use was not present before X disorder, just like in infectious disease stuff. And before you start talking about trait whatever blah blah blah, the SMH says that ADHD causes cocaine use, so ...NO.

This theory is NOT "My abuse of Y substance went into overdrive when I got X diagnosis.", nor is it "I got X symptoms and went on a polysubstance bender.".

History: So the SMH gets published in 85. People like Deykin and/or Dackis tested it, and showed that the onset of the affective/mental diagnosis had no relationship with the onset of substance use. Showed that the characteristics of the mental disorder did not predict which substance was used. Then people like Weiss and/or Morrisey showed that people will say they abuse substances because they are depressed, but that their self report is completely contradicted by years of medical records that show the SUD predated any mood complaints by years. (This is one of the starting points in the literature showing self report is HIGHLY unreliable. ) Then the epidemiology literature showed that polysubstance abuse is MUCH more common than abuse of one substance, which would contradict the specificity requirement of the SMH. And some experimental studies from authors like Castenda, Greene, Mueser, Schink, or Swenden who showed that there was no relationship between the type of mental/affective disorder and which substances used, that onset of substance use typically predated the onset of the affective/mental disorder, and that patients reported that the substance use actually made their symptoms worse. Not good enough for you? THE ARCHITECT OF THE DSM-IV INDICATED THAT THE SMH IS MISGUIDED!!!!! Try coming back from that one!

Now most elementary school kids would accept the null hypothesis, or get more data, or give a completely different hypothesis for testing.

3) INSTEAD THE AUTHOR LITERALLY ADMITTED HE WAS WRONG IN 1997, "Diagnostic studies provide evidence that variously supports and fails to support a self-medication hypothesis of addictive disorders." AND HE THEN HE CHANGED THE SELF MEDICATION HYPOTHESIS!!!!!!!!! No, he didn't give a new hypothesis. He just changed the old one. Anyone else remember that part of elementary school science? Or that part of stats where Type I and II errors can be avoided by changing the hypothesis? No? Because that is NOT how hypotheses work.

So now the 2nd version of the SMH basically says the substance of choice is caused by the individual's current mood, and NOT the affective/mental disorder. Which essentially means the "self medication" is really just about mood state.

Some people decided to study the new SMH. Studies from people like Aharanovich, or Hodgins showed that state emotions had no relationship to which substance was used, and that affective state did not happen BEFORE onset of substance abuse. This even went on at the National Comorbidty Study. Ten YEARS of follow up showed that there was no relationship between the specific mental disorder and the specific substance of abuse; and that the onset of substance use had little relationship to the onset of mental disorder (e.g., breslau; Kessler, etc).


Must be the end of the story, right?

4) Not even joking, HE CHANGED THE SELF MEDICATION HYPOTHESIS A 3RD TIME!!!!!!! In 2003, the SMH essentially became "you know, there's this entire dual diagnosis thing. Since addictive disorders are caused by people trying to self medicate an underlying disorder, the substance use will disappear once you treat it." Now Mueser had already disproved that idea, and Brown disproved this idea like 15+ years before, but why stop now? People like Hall, or Nunes, showed that treating the the supposed underlying mental disorder does nothing to change substance abuse. Even on meta-analysis.

5) To be fair, there is another self medication theory based upon operant conditioning, published by Duncan around 1974. Interesting idea. However, he seemed to experience some difficulty in studying this idea AFTER HE WENT TO PRISON FOR KIDDIE PORN IN 1989.

6) In comparison, other theories have stronger evidence. Heritability of SUD is around 30-60% on monozygotic twin studies (e.g. ,Goldman, 2006ish). There seems to be some genetic vulnerability, and trait vulnerability, which interacts with the environment (e.g., Belcher, 2015ish; Read, 2014 ish; etc).




B. Now let's go to your citations:


1) In order to accept the works as supporting evidence, we would need them to:

a. study the subject of relevance,
b. use a methodology relevant to the subject of relevance.

2) They don't use any definitions consistent with the SMH, which means they're not studying the SMH.

a. The authors from your citations ignored the 1985 definition, and the 1997 definition, and then defined the SMH as, " ...the self-medication hypothesis, a causal model that postulates that individuals with PTSD are more prone to developing problematic drinking behaviors due to a tendency to drink to cope with negative internal experiences (Khantzian, 1997)". The VERY SAME 1997 paper defines the SMH as, " First and foremost, drugs of abuse relieve psychological suffering. Second, a person's preference for a particular drug involves some degree of psychopharmacological specificity. ". Kinda weird that the authors didn't reference the definition on the first page. Even weirder is that their definition ignores the specificity part of the SMH. Still weirder is that they reduced the SMH to problematic drinking in PTSD, when the 1997 article actually says alcohol and drugs. And even weirder that instead of using the SMH, they use Duncan's theory, which differs from the SMH, and fell into disfavor after Duncan went to prison for kiddie porn. Don’t they know what the SMH is?

b. The authors' method is essentially asking people if they drink to cope with PTSD, when the literature, over the last 30+ years, has shown this is an unreliable method.

c. There are no efforts to determine if the substance abuse or PTSD came first. As required by the SMH, and recommended by Allen Frances. And, you know... like the DSM requires....
Really appreciate the background and history. I see what you're saying regarding the label "self-medication hypothesis" -- it clearly ought to be "self-medication model" or "theory". I haven't been able to gain access to the actual 1997 Khantzian article, but the abstract makes the claim: "clinical observations and empirical studies that focus on painful affects and subjective states of distress more consistently suggest that such states of suffering are important psychological determinants in using, becoming dependent upon, and relapsing to addictive substances." To me, this implies a much more flexible model or theory than what you're attributing.

Regarding the accuracy of the theory/model, it sounds like you're disputing the claim that negative affective/mood states are related to subsequent substance use behaviors. It looks like you've pointed to a lot of cross-lagged panel data or epidemiological research to support your disputation. Am I understanding you correctly?

If so, I'd point out that those methods (cross-lagged panel or epidemiological surveys) are not sensitive to momentary fluctuations in affect/mood or subsequent substance use behaviors. Meanwhile, research that uses more sensitive assessment methods (e.g., intensive longitudinal, ecological momentary assessment), and thus has greater temporal resolution, does indicate that this "using to cope" or "self-medication theory/model" seems to be supported by findings.

(1) https://www.tandfonline.com/doi/full/10.1080/00952990.2019.1635606
(2) Ecological momentary assessment of acute alcohol use disorder symptoms: associations with mood, motives, and use on planned drinking days - PubMed

Yes, there is a sordid history for the so-called "self-medication hypothesis", but when appropriate assessment methods are used there does appear to be empirical support for the related model/theory.
 
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WisNeuro

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"a. There is a CAUSAL relationship between affective/mental disorders and substance abuse.
b. The characteristics of the affective/mental disorder PREDICTS which substance will be used.
c. The individual's functioning would IMPROVE through the use of the substance."

Those articles don't seem to cover points B and C at all, and they only look at correlations, so don't really get at A either.
 

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"a. There is a CAUSAL relationship between affective/mental disorders and substance abuse.
b. The characteristics of the affective/mental disorder PREDICTS which substance will be used.
c. The individual's functioning would IMPROVE through the use of the substance."

Those articles don't seem to cover points B and C at all, and they only look at correlations, so don't really get at A either.
Again, I'm talking about the 1997 article, you're referring to the 1985 article. My understanding is that the 1997 article proposes a much more flexible theory/model, but I haven't actually been able to gain access to it. Either way, I do think that point a is retained in the 1997 proposal, albeit without the disorder/abuse threshold. More of a "negative affect/mood states increase probability of subsequent use".

How would you recommend a study test for causality in a more rigorous way than the cited studies? My first thought is randomization, but it's obviously impossible to randomly assign someone to have a mood/affect. Experimentally controlling mood/affect also seems extremely challenging and would have extremely limited external validity. I suppose there could be laboratory studies that could cue certain mood/affective states, but the ecological validity of a study like that would be vastly inferior to the cited studies.
 
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WisNeuro

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Again, I'm talking about the 1997 article, you're referring to the 1985 article. My understanding is that the 1997 article proposes a much more flexible theory/model, but I haven't actually been able to gain access to it. Either way, I do think that point a is retained in the 1997 proposal, albeit without the disorder/abuse threshold. More of a "negative affect/mood states increase probability of subsequent use".

How would you recommend a study test for causality in a more rigorous way than the cited studies? My first thought is randomization, but it's obviously impossible to randomly assign someone to have an emotion. Experimentally controlling emotions also seems extremely challenging and would have extremely limited external validity. I suppose there could be laboratory studies that could cue certain emotions, but the ecological validity of a study like that would be vastly inferior to the cited studies.
Well, first things first, they'd actually need to use the disorders themselves to study this, rather than emotional states, as most studies do. Second, you'd have to do more case control studies rather than traditional experimental studies. As one of the major critiques is that problematic substance use usually predates the onset of diagnosable syndrome, you'd have to look at case controlled individuals over time to see if the substance use patterns differed in some meaningful way. Otherwise, you just fall victim to the fallibility of self-report in these individuals. For example, we have numerous studies that show people with the fake "postconcussive syndrome" will time lock everything to their concussion, when in fact on in-depth record review, almost all of their symptoms were frequently cited in their medical charts well before any head injuries.
 

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Well, first things first, they'd actually need to use the disorders themselves to study this, rather than emotional states, as most studies do. Second, you'd have to do more case control studies rather than traditional experimental studies. As one of the major critiques is that problematic substance use usually predates the onset of diagnosable syndrome, you'd have to look at case controlled individuals over time to see if the substance use patterns differed in some meaningful way. Otherwise, you just fall victim to the fallibility of self-report in these individuals. For example, we have numerous studies that show people with the fake "postconcussive syndrome" will time lock everything to their concussion, when in fact on in-depth record review, almost all of their symptoms were frequently cited in their medical charts well before any head injuries.
Again, my understanding is that the 1997 article proposes a hypothesis that is not restricted to disorder. I think we would need to get the actual full-text of the 1997 article to discuss this further.

As to the "fallibility of self-report", are you suggesting that people fail to accurately report their mood/affective state at a given moment in time when they complete a self-report survey? Or are you just suggesting that people who report "using to cope" are not able to accurately report on the causal relationship between mood/affect and subsequent behavior? If it's the former then I think we'd have to throw out a huge amount of psychological science, no? If it's the latter, that's still a high bar, but it's at least an empirical question (which we could use the former to at least test).

Your example of post-concussive syndrome is not relevant to discussions of ecological momentary assessment methods. EMA is not retrospective in the way that you're describing -- people are reporting their affect/mood and then on a later survey during the same day they're reporting use behaviors.
 

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Again, my understanding is that the 1997 article proposes a hypothesis that is not restricted to disorder. I think we would need to get the actual full-text of the 1997 article to discuss this further.

As to the "fallibility of self-report", are you suggesting that people fail to accurately report their mood/affective state at a given moment in time when they complete a self-report survey? Or are you just suggesting that people who report "using to cope" are not able to accurately report on the causal relationship between mood/affect and subsequent behavior? If it's the former then I think we'd have to throw out a huge amount of psychological science, no? If it's the latter, that's still a high bar, but it's at least an empirical question (which we could use the former to at least test).

Your example of post-concussive syndrome is not relevant to discussions of ecological momentary assessment methods. EMA is not retrospective in the way that you're describing -- people are reporting their affect/mood and then on a later survey during the same day they're reporting use behaviors.
It is absolutely relevant to the discussion. The self-medication hypothesis, in whatever form that it has existed posits that the negative state causes the substance use in some way. One of the criticisms is that a person can have problematic drinking behaviors prior to significantly altered affective states. So, in effect, they are not necessarily "using to cope" as opposed to just engaging in a pre-existing behavior pattern. As to the tangentially related issue of not trusting self-report, it is absolutely a problem in psychological science. It's a good starting point, but in many cases, unreliable when we look at more objective information.
 
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beginner2011

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It is absolutely relevant to the discussion. The self-medication hypothesis, in whatever form that it has existed posits that the negative state causes the substance use in some way. One of the criticisms is that a person can have problematic drinking behaviors prior to significantly altered affective states. So, in effect, they are not necessarily "using to cope" as opposed to just engaging in a pre-existing behavior pattern. As to the tangentially related issue of not trusting self-report, it is absolutely a problem in psychological science. It's a good starting point, but in many cases, unreliable when we look at more objective information.
Are you arguing that the self-medication hypothesis is flawed because people can use substances in a problematic way before they have "altered affective states"? What do you mean by "altered affective states"? Are "altered affective states" mood/anxiety disorders? If so, again, I'll point out that it seems the 1997 proposal does not require disorder diagnosis. If "altered affective states" is just deviation from an individual's mean, or the population mean...then the EMA studies I mentioned are addressing precisely that question and have reported that momentary "altered affective states" are associated with subsequent use behavior.

As to the underlined/italicized statement, it seems like you're suggesting that you can't establish causality without temporal precedence -- but that's exactly what these EMA studies have done. They have extremely precisely and in the context of peoples' daily lives demonstrated that there is temporal precedence to this association. Specifically, these EMA studies are demonstrating that momentary deviations from average mood/affective states ("altered affective states"?) are significantly associated with temporally subsequent probability of use behavior. In other words, the presence of a "pre-existing behavior pattern" is not sufficient to explain use patterns because results show that in-the-moment reports of mood/affect predict subsequent reports of use. To me, this is all very different than the post-concussive example.
 
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"a. There is a CAUSAL relationship between affective/mental disorders and substance abuse.
b. The characteristics of the affective/mental disorder PREDICTS which substance will be used.
c. The individual's functioning would IMPROVE through the use of the substance."

Those articles don't seem to cover points B and C at all, and they only look at correlations, so don't really get at A either.
I generally agree with this criticism, but regarding point c, I think the goal of the substance use in many of these cases would be to relieve distress, not necessarily to improve functioning.
 

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Are you arguing that the self-medication hypothesis is flawed because people can use substances in a problematic way before they have "altered affective states"? What do you mean by "altered affective states"? Are "altered affective states" mood/anxiety disorders? If so, again, I'll point out that it seems the 1997 proposal does not require disorder diagnosis. If "altered affective states" is just deviation from an individual's mean, or the population mean...then the EMA studies I mentioned are addressing precisely that question and have reported that momentary "altered affective states" are associated with subsequent use behavior.

As to the underlined/italicized statement, it seems like you're suggesting that you can't establish causality without temporal precedence -- but that's exactly what these EMA studies have done. They have extremely precisely and in the context of peoples' daily lives demonstrated that there is temporal precedence to this association. Specifically, these EMA studies are demonstrating that momentary deviations from average mood/affective states ("altered affective states"?) are significantly associated with temporally subsequent probability of use behavior. In other words, the presence of a "pre-existing behavior pattern" is not sufficient to explain use patterns because results show that in-the-moment reports of mood/affect and subsequent reports of use. To me, this is all very different than the post-concussive example.
You're missing the point here, in that the self-medication hypothesis would need to show a change in use dependent on these states in some meaningful way, most likely increase of use, either in frequency or amount. I guess you could over-generalize this to include any affective mental state, regardless of diagnosis, but then how do we use this in SUD tx? And, how is it tied to disordered use and such? We seem to be getting very far from the original model in many ways. Furthermore it gets at another issue brought up in that people still explain things in the SMH model that was posited as ABC in the above example.

So, to get us back on the same page, what is the SMH as you are defining it, and what research backs up that definition? Because, there doesn't seem to be much backing up the definitions of the models that have been explicitly spelled out.

I generally agree with this criticism, but regarding point c, I think the goal of the substance use in many of these cases would be to relieve distress, not necessarily to improve functioning.
I'd tend to agree, from what I gather, this was an early operational definition. Although, we'd also have to see that it actually relieves distress in some meaningful way.
 

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A tangent but related aspect to theory and assessment that grinds my gears is midlevels I see are using the specifiers early remission and sustained remission solely based upon sober time (e.g., 90 days, 365 days). Without any regard for the actual 11 DSM-5 criteria, functional impairment, clincal distress, etc. It's driving me insane.
 
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You're missing the point here, in that the self-medication hypothesis would need to show a change in use dependent on these states in some meaningful way, most likely increase of use, either in frequency or amount. I guess you could over-generalize this to include any affective mental state, regardless of diagnosis, but then how do we use this in SUD tx? And, how is it tied to disordered use and such? We seem to be getting very far from the original model in many ways. Furthermore it gets at another issue brought up in that people still explain things in the SMH model that was posited as ABC in the above example.

So, to get us back on the same page, what is the SMH as you are defining it, and what research backs up that definition? Because, there doesn't seem to be much backing up the definitions of the models that have been explicitly spelled out.



I'd tend to agree, from what I gather, this was an early operational definition. Although, we'd also have to see that it actually relieves distress in some meaningful way.
Personally, I find Marlatt's dynamic model of addictive behaviors/relapse the most useful. My read of it is that the self-medication hypothesis is a component of the model, but does not encompass the entirety.

1600280290940.png


You can see "Affective State" linked to "Substance Use Behavior (quantity or frequency)", which is how I would interpret the more constrained conclusions that can be drawn from results of tests of the "self-medication hypothesis". This model does a good job of acknowledging the many other factors at play. The EMA studies seem to support this conclusion with greater consistency than the cross-lagged panel or epidemiological studies were able to, probably mostly due to the research design being more appropriate to the research question.
 

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Ok, what are the key tenets of the SMH that you are advocating for?
The formulation implied by the systematic review I linked seems reasonable (1) and well-supported. Again, I don't have access to the 1997 Khantzian article, so I'm not sure about the details. Would love to see it if someone is able to share.

(1) Error - Cookies Turned Off

From the article:

the self‐medication hypothesis, a causal model that postulates that individuals with PTSD are more prone to developing problematic drinking behaviors due to a tendency to drink to cope with negative internal experiences (Khantzian, 1997).
Edit: I gained access to the original 1997 article that "reconsiders" the 1985 hypothesis. (https://www.researchgate.net/public...ations/link/553e934f0cf210c0bdaaa91f/download)

My read of it is that there are two claims (again, this should probably be considered the "self-medication theory"):

(1) drugs of abuse relieve psychological suffering
(2) a person's preference for a particular drug involves some degree of psychopharmacological specificity

I think there's a ton of evidence for #1. I'm not very familiar with the evidence for #2.
 
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Ok, so what evidence do we have that the problematic drinking behavior is directly related to the PTSD or immediate negative affect state? and what evidence do we have that it alleviates the "negative internal experience?"

Also, from that systematic review

"Despite its popularity, a systematic review of the literature revealed a lack of rigorous empirical evidence in support of the self‐medication model, which is likely due to several important methodological considerations. Such considerations, deduced from this systematic review, include the lack of specific operationalization of trauma‐specific drinking‐to‐cope, lack of longitudinal study designs and mediational analyses to account for the temporal and causal assumptions underlying the self‐medication model, heterogeneity in alcohol assessment, and failure to account for potential confounding variables, such as sample selection (e.g., sex, race/ethnicity), trauma type and timing, and other commonly comorbid internalizing disorders, such as depression and anxiety."
 

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Ok, so what evidence do we have that the problematic drinking behavior is directly related to the PTSD or immediate negative affect state? and what evidence do we have that it alleviates the "negative internal experience?"

Also, from that systematic review

"Despite its popularity, a systematic review of the literature revealed a lack of rigorous empirical evidence in support of the self‐medication model, which is likely due to several important methodological considerations. Such considerations, deduced from this systematic review, include the lack of specific operationalization of trauma‐specific drinking‐to‐cope, lack of longitudinal study designs and mediational analyses to account for the temporal and causal assumptions underlying the self‐medication model, heterogeneity in alcohol assessment, and failure to account for potential confounding variables, such as sample selection (e.g., sex, race/ethnicity), trauma type and timing, and other commonly comorbid internalizing disorders, such as depression and anxiety."
The EMA studies suggest this. I cited a few above.

The bolded section from the systematic review basically says exactly what I've been saying. Lack of evidence to date "is like to due to several important methodological considerations..." Again, results from EMA studies substantiate this.
 
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The EMA studies suggest this. I cited a few above.

The bolded section from the systematic review basically says exactly what I've been saying. Lack of evidence to date "is like to due to several important methodological considerations..." Again, results from EMA studies substantiate this.
But it doesn't really.

Let's take your edits from above

(1) drugs of abuse relieve psychological suffering
(2) a person's preference for a particular drug involves some degree of psychopharmacological specificity

As for #1, the EMA study actually suggests that the substance use increases negative affect. As for #2, I have never seen evidence to this effect.

If anything, the evidence is weak at best. The systematic review actually says that they are worried about a file drawer effect, these are not that hard to run. If anything, it would negate the weak findings if one were actually done, most likely. Are there other EMA studies, or more recent work that supports this?
 

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Can I ask, as clinicians how do we integrate this into our practice? I have patients with PTSD who tell me that their drinking is secondary. I assume that I'm not supposed to say "uhhh well actually research suggests otherwise," lol. Is it more for case conceptualization?
 
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beginner2011

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But it doesn't really.

Let's take your edits from above

(1) drugs of abuse relieve psychological suffering
(2) a person's preference for a particular drug involves some degree of psychopharmacological specificity

As for #1, the EMA study actually suggests that the substance use increases negative affect. As for #2, I have never seen evidence to this effect.

If anything, the evidence is weak at best. The systematic review actually says that they are worried about a file drawer effect, these are not that hard to run. If anything, it would negate the weak findings if one were actually done, most likely. Are there other EMA studies, or more recent work that supports this?
Here's a statement from one study (Duif, 2019): https://www.tandfonline.com/doi/pdf/10.1080/00952990.2019.1635606?needAccess=true

Within-person daily NA preceding the first drinking event was associated with increased likelihood of same-day alcohol consumption.
Here's a statement from another study (Dvorak, 2014): Ecological Momentary Assessment of Acute Alcohol Use Disorder Symptoms: Associations With Mood, Motives, and Use on Planned Drinking Days

Additionally, an affect regulation model of drinking to cope with negative mood was observed. Specifically, on planned drinking days, the temporal association between daytime negative mood and the experience of acute AUD symptoms was mediated via coping motives and alcohol use.
It's still a bit mixed, with one study (Possemato, 2015): Ecological momentary assessment of PTSD symptoms and alcohol use in combat veterans - PubMed

Our results support the finding that increases in PTSD are associated with more drinking within the same 3-hr time block, but not more drinking within the following time block.
This could be explained by a lack of temporal resolution. That is, more frequent assessment might reveal that the increases in PTSD symptoms occurred prior to use (as was seen in Duif2019, and suggested by Dvorak2014), or vice-versa.

Of course, this is not a comprehensive review, and I'm sure there is more data on this question.
 

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In the Duif study, drinking does not decrease NA, if anything it's a slight increase, but commensurate with non-drinking days. It does seem to lower PA, though. How exactly does this support that substance use relieves psychological suffering?

I can't access the PTSD study at the moment, for some reason, just the abstract, so I can't comment on that one. But, after nearly a decade of working and doing research in the VA, I take anything coming out of there with a HUGE grain of salt unless the data has been scrubbed of at least obvious malingerers.
 

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@beginner2011

My read of it is that there are two claims (again, this should probably be considered the "self-medication theory"):

(1) drugs of abuse relieve psychological suffering
(2) a person's preference for a particular drug involves some degree of psychopharmacological specificity

I think there's a ton of evidence for #1. I'm not very familiar with the evidence for #2.
NONE OF WHAT YOU ARE CALLING THE SMH IS THE SMH!!!!

1) In regards to #1, you'd be wrong.

a. There evidence for #1 is based upon self report, but NOT objective evidence. There is a significant degree of evidence that shows that people will attribute their substance abuse to negative mood states, despite objective data that shows onset of substance abuse far before their mood problems (e.g., de Graaf, 2004; Falk; 2008; Goodwin, 2004; Kushner, 1990; Morrissey, 1978; Weiss, 1992; etc, etc etc.). Likewise, there is significant evidence that people will retroactively claim their substance use helped their mood symptoms, despite evidence showing that it made them worse (e.g., Weis, 2004; Wilkinson, 2015 for PTSD; all of the anabolic steroid literature literature for men right now which is essentially a repeat of the...., the HRT replacement literature for menopausal women in the early 2000s, the opiioid induced hyperalgesia literature, the opioid hypogonadism stuff, generally just all of the opioid literature, etc). Despite this clear methodological problem, a bunch of modern researchers still just rely upon self report without any reference to the central problems of their method.

b. Then there is the DSM5 problem, which requires the psychologist to rule out other causes of the symptoms, including ruling out substance abuse.

c. And then there is the entire literature based that shows substance use independently causes mood problems, sleep problems, cognitive stuff, etc.

d. Then there is the incredible problem of REVERSIBILITY. If the people are trying to relieve suffering of A kind, using a substances B that have properties opposite A, then we should see a reversal. Then we would expect, if A mood state causes the use of B substance, then the absence of A mood should stop use of B substance. This does not happen on review, meta-analysis, or double blind (Nunes, 1991; Nunes, 2004; Cornelius, 2001; Conrnelius, 1997; Pennitti, 2004; McHugh, 2015; etc. Likewise, pharmacoloigcal treatments only for mood do not show efficacy in treating SUDs, aside from quetiapine.

e. Then you'd the problem of SPECIFICITY, which has significant evidence against it (e.g., Ahranovich, 2001). In short, If the people are using substances to relieve suffering of A kind, using B substances that have properties opposite A, then there should be very specific correlations. Like CRAZY HIGH correlations. But the National Comorbidity Study, its replication, the Detroit Survey, and international replications failed to not show any type of specificity (e.g.,Kessler, et al., 2004; Breslaud, 1998; Breslau, et al., 2004 ; Merikangas, 1998).A simple pubmed search of PTSD and SMH has cocaine use disorder on the first page. You'd have to explain why an anxious person is choosing a highly stimulating substance, when the SMH says the choice will be a sedating substance. Which is why the National Comorbidity Study, and its repetition are bad for the SMH. They definitely show comorbidity, but NOT SPECIFICITY OR CAUSATION. Do you use meth because you have PTSD, or did you get PTSD from living around methheads?

2. Going back to your EMA study: the SMH's revision literally states that PTSD would cause alcohol abuse for states of rage, anxiety, and panic. Let's see how that works. First, did the authors address onset of PTSD and onset of alcohol use? No? Well how the hell are we gonna determine causation? Ask anyone who has gotten an STD from their partner. Who had it first is a pretty big component of determining causation. Second, notice how the authors lump all the negative moods together? This is basically ignoring the specificity component of the SMH. Why wouldn't they want to show that alcohol use went up on anxious days, and no effect on depressive days? This should be the end of this article. Third, they included individuals with AUD, which is an incredible covariable. No kidding drinkers are gonna drink. And look! The AUD subjects say they drink because of negative mood and positive mood! Sounds a lot like inaccurate self report. Fourth, the inclusion of Positive Mood/Enhancement is just crazy. The SMH is about treating negative mood states, not keeping the good times rolling. Fifth, their findings disprove the SMH when you remove the AUD subjects. Do X mood states predict Y substance use? Nope! Even when coping factors are accounted for? Nope!
 

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We have had this discussion here before. It is usually worth reminding everyone that "failure to support the original self medication hypothesis as laid out by X in Y article" is a VERY different thing from "we now and forever categorically reject the notion that substances could sometimes be used with the intention of alleviating symptom X."

The latter falls under the broader umbrella of self medication research, but is a drastic departure from the original article. It could apply whether or not the drugs are effective. If the drugs are effective, it could be due to expectancies that have minimal relationship to the actual pharmacological effects of the drugs. It could apply to symptoms that are not formal DSM criteria (e.g. effects of nicotine on sensory gating deficits). It could be true only for a small subset of individuals with a particular genotype. It could be that healthy populations sometimes use substances to alleviate sub-threshold symptoms.

Psydr is 100% correct that the former is not supported....at all. At the same time, I don't know any serious scientist who categorically rejects the latter as a possibility. It is very much an active research area with millions and millions of dollars being pumped into it at the highest levels. I am not sure any reasonable person could try to argue there is not additional work to be done in the area or that there remains some possibility that people sometimes use drugs to improve certain symptoms.
 

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It could apply whether or not the drugs are effective. If the drugs are effective, it could be due to expectancies that have minimal relationship to the actual pharmacological effects of the drugs. It could apply to symptoms that are not formal DSM criteria (e.g. effects of nicotine on sensory gating deficits). It could be true only for a small subset of individuals with a particular genotype. It could be that healthy populations sometimes use substances to alleviate sub-threshold symptoms.
THIS. I think this is a critical point. If people think that are self-medicating, that can still reinforce the substance use/abuse behavior.
 
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@Ollie123 I see things differently. The SMH is a myth that is not supported. Since that time, people have been scrambling to try to find something, anything, about this idea that can be supported. It is rare that this type of frantic behavior pans out in favor of science. It sure as hell didn't work out for Reik. As for the the amount of money invested... See: well... the presidential campaign...all of 2020... certain politicians....climate change deniers...

My read on the situation:

1) Substances are pleasurable. Anyone that fails to acknowledge that fact is paternalistic at best, and an aggressively idiotic person otherwise. People use substances because they feel good. The simplicity of that explanation can be very uncomfortable for some people due to a myriad of social, moral, ethical, financial, legal, and relational implications. However, it is pure collusion to ignore the hedonistic explanation. One calls to mind the southpark episode featuring tiger wood's infidelity. If the pleasure is NOT a factor, then show me anyone who has binge ate cabbage, or self medicated using the things we know work against mental disorders.

2) There are clearly genetics at play. It is intellectually dishonest to ignore this fact. Anyone who remember the Minnesota Twin study knows that substance abuse is highly heritbale. Further twin studies show about 30-60% heritability of substance abuse (depending on substance and population...looking at you, the Irish), which demonstrates the entire penetrance vs expressivity vs pleiotrophy stuff (Goldman, 2006; Ducci,& Goldman, 2012; etc). Those numbers will look familiar to anyone who has looked that the literature about the heritability of FSIQ stuff where heritablilty is like 75% (mediated by environment), the heritbality of achievement stuff which pegs heritability at around 60% (obkay, 2016), heritbaility of 5 factor models, or whatever Cloninger is up to nowadays. Kinda weird those numbers are circling each other.

If we can address differential responses to substances in some ethnic groups (e.g., flush reactions in alcohol secondary to AD1HB-2 polymorphisms in some asian ethnic groups such as the Han, and in some european group like the Askanzai jews), then we have already accepted that there is some genetic basis. If 30-75% of SUD susceptibility is due to genetics, it is just plain MEAN to try to get people to give another explanation. However, if individuals want to ignore the genetic basis of response, then they need to also ignore other genetically based responses.


3) Some people have some susceptibility to specific substances that appears to be mediated via genetics and environment. It is likely that some individuals are susceptible to the effects of a specific class of substances. It is also likely that there is a range of problematic behaviors that vary from physiological dependence to engaging in completely socially unacceptable behaviors while under the influence. We are AWFUL at describing these variations.

This susceptibility likely has little to do with any other mental disorders, aside from common sense implications (e.g., maybe it is not a great idea to drink a ton of 4Loko with a someone with bipolar disorder). .

Exceptions are obvious, like how smoking cigarettes in over medicated schizophrenics reduces oversedation of FGAs through CYP induction via cigarettes.

4) People who abuse substances are obviously going to reach out to use substances when there are good times, bad times, and boring times. This isn’t self medicating anything. Treating some mood stuff isn't going to do a damn thing for these people. Giving people false promises, and letting them feel as if it is their fault that said promises don't work.... that is awful. No better than telling them that their SUD is hurting baby jesus, or whatever.

5) People can have 2+ problems. Professionals should be able to deal with this. The reductionist idea of that every problem can be explained by something is just dumb.

6) If the literature shows that treating an underlying mood disorder has little effect on substance use.... this entire theory is wrong. If the literature predominantly shows that the only pharmacological treatments that work are naltrexone and such ... it's not a self medication anything. It's a SUD.

7) There are many many many social, financial, legal, religious, moral, relational, etc implications for SUDs. The SMH offers people a socially accepted excuse from this stuff. There is no science to this idea. It takes real character to not collude with people.

8) People are not accurate in what they say, across the board. It is unclear as to whether this is straight up lying, or some human tendency. It doesn't matter. The literature shows that substance abuse typically comes BEFORE mood problems. We know that treating mood problems does not stop substance abuse. Therefore, we should treat the substance abuse, and ignore any patient attributions. Anyone who has treated a delusional person knows how this works.

9) Which is preferable:

a. Telling a patient that he/she has a substance use problem, and that their mood problems will get better when that is under control. When asked, telling that patient, "We don't know why some people use drugs. It looks like there's some genetics, some environment, and some personal choice. What matters is that we treat that, and get you better."

b. Telling a patient that his/her substance abuse is caused by some underlying thing that may or may not be present. Getting them to believe that their SUD is caused by this mood thing. Getting them to believe that if this mood thing is treated, that they will get sober. Treating the mood thing, and then having them believe that any resulting SUD is a matter of personal choice?
 
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@Ollie123 I see things differently. The SMH is a myth that is not supported. Since that time, people have been scrambling to try to find something, anything, about this idea that can be supported. It is rare that this type of frantic behavior pans out in favor of science. As for the the amount of money invested... See: well... the presidential campaign...all of 2020... certain politicians....climate change deniers...


My read on the situation:

1) Substances are pleasurable. Anyone that fails to acknowledge that fact is paternalistic at best, and an aggressively idiotic person otherwise. People use substances because they feel good. The simplicity of that explanation can be very uncomfortable for some people due to a myriad of social, moral, ethical, financial, legal, and relational implications. However, it is pure collusion to ignore the hedonistic explanation. One calls to mind the southpark episode featuring tiger wood's infidelity. If the pleasure is NOT a factor, then show me anyone who has binge ate cabbage, or self medicated using the things we know work against mental disorders.

2) There are clearly genetics at play. It is intellectually dishonest to ignore this fact. Anyone who remember the Minnesota Twin study knows that substance abuse is highly heritbale. Further twin studies show about 30-60% heritability of substance abuse (depending on substance and population...looking at you, the Irish), which demonstrates the entire penetrance vs expressivity vs pleiotrophy stuff (Goldman, 2006; Ducci,& Goldman, 2012; etc). Those numbers will look familiar to anyone who has looked that the literature about the heritability of FSIQ stuff where heritablilty is like 75% (mediated by environment), the heritbality of achievement stuff which pegs heritability at around 60% (obkay, 2016), heritbaility of 5 factor models, or whatever Cloninger is up to nowadays. Kinda weird those numbers are circling each other.

If we can address differential responses to substances in some ethnic groups (e.g., flush reactions in alcohol secondary to AD1HB-2 polymorphisms in some asian ethnic groups such as the Han, and in some european group like the Askanzai jews), then we have already accepted that there is some genetic basis. If 30-75% of SUD susceptibility is due to genetics, it is just plain MEAN to try to get people to give another explanation. However, if individuals want to ignore the genetic basis of response, then they need to also ignore other genetically based responses.


3) Some people have some susceptibility to specific substances that appears to be mediated via genetics and environment. It is likely that some individuals are susceptible to the effects of a specific class of substances. It is also likely that there is a range of problematic behaviors that vary from physiological dependence to engaging in completely socially unacceptable behaviors while under the influence. We are AWFUL at describing these variations.

This susceptibility likely has little to do with any other mental disorders, aside from common sense implications (e.g., maybe it is not a great idea to drink a ton of 4Loko with a someone with bipolar disorder). .

Exceptions are obvious, like how smoking cigarettes in over medicated schizophrenics reduces oversedation of FGAs through CYP induction via cigarettes.

4) People who abuse substances are obviously going to reach out to use substances when there are good times, bad times, and boring times. This isn’t self medicating anything. Treating some mood stuff isn't going to do a damn thing for these people. Giving people false promises, and letting them feel as if it is their fault that said promises don't work.... that is awful. No better than telling them that their SUD is hurting baby jesus, or whatever.

5) People can have 2+ problems. Professionals should be able to deal with this. The reductionist idea of that every problem can be explained by something is just dumb.

6) If the literature shows that treating an underlying mood disorder has little effect on substance use.... this entire theory is wrong. If the literature predominantly shows that the only pharmacological treatments that work are naltrexone and such ... it's not a self medication anything. It's a SUD.

7) There are many many many social, financial, legal, religious, moral, relational, etc implications for SUDs. The SMH offers people a socially accepted excuse from this stuff. There is no science to this idea. It takes real character to not collude with people.

8) People are not accurate in what they say, across the board. It is unclear as to whether this is straight up lying, or some human tendency. It doesn't matter. The literature shows that substance abuse typically comes BEFORE mood problems. We know that treating mood problems does not stop substance abuse. Therefore, we should treat the substance abuse, and ignore any patient attributions. Anyone who has treated a delusional person knows how this works.

9) Which is preferable:

a. Telling a patient that he/she has a substance use problem, and that their mood problems will get better when that is under control. When asked, telling that patient, "We don't know why some people use drugs. It looks like there's some genetics, some environment, and some personal choice. What matters is that we treat that, and get you better."

b. Telling a patient that his/her substance abuse is caused by some underlying thing that may or may not be present. Getting them to believe that their SUD is caused by this mood thing. Getting them to believe that if this mood thing is treated, that they will get sober. Treating the mood thing, and then having them believe that any resulting SUD is a matter of personal choice?
I'm not going to address each of your bullets. Am I understanding correctly that you're arguing that there's no value to addressing the role of craving management, emotion regulation, distress tolerance, and/or coping skills broadly in the management and treatment of SUDs? Are you also claiming that it is "collusion" to suggest to people experiencing SUDs that psychosocial treatment to reduce psychological distress might be helpful for them in treating their SUD?

If I'm off-base I'd appreciate it if you could try to summarize your specific claims in a way that is more concise.

I'll throw in this graph for discussion, which I think is illustrative of the role distress plays in substance use behavior, and also demonstrates the importance of the research method to address this question. This example is from a study investigating momentary reports of affect and tobacco use among patients committed to abstinence. Analysis of the EMA data demonstrated that when respondents reported that stress was what triggered their return to use there was an hour-by-hour escalation of negative affect in the ~5 hour period leading up to the use event (black dots). Meanwhile, when respondents reported that it was another type of trigger that led to use (e.g., exposure to smoking cues) there was not the same escalation of negative affect (white dots). Interestingly, when you only look at this question using daily-averaged data the effect disappears (left side of graph). Dynamic influences on smoking relapse process - PubMed

1600320162745.png

It's simply not consistent with the growing body of evidence coming from these studies with greater temporal resolution to claim that negative affect/distress don't play a role in substance use disorders, problematic use, or the chronicity of these presentations. We can point to genetic risk factors all we want, but that does not account for even close to 100% of the variance...so why would you suggest it's "collusion" to address the role of psychosocial factors that clearly play a role?
 
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I'm not going to address each of your bullets. Am I understanding correctly that you're arguing that there's no value to addressing the role of craving management, emotion regulation, distress tolerance, and/or coping skills broadly in the management and treatment of SUDs? Are you also claiming that it is "collusion" to suggest to people experiencing SUDs that psychosocial treatment to reduce psychological distress might be helpful for them in treating their SUD?

If I'm off-base I'd appreciate it if you could try to summarize your specific claims in a way that is more concise.

I'll throw in this graph for discussion, which I think is illustrative of the role distress plays in substance use behavior, and also demonstrates the importance of the research method to address this question. This example is from a study investigating momentary reports of affect and tobacco use among patients committed to abstinence. Analysis of the EMA data demonstrated that when respondents reported that stress was what triggered their return to use there was an hour-by-hour escalation of negative affect in the ~5 hour period leading up to the use event (black dots). Meanwhile, when respondents reported that it was another type of trigger that led to use (e.g., exposure to smoking cues) there was not the same escalation of negative affect (white dots). Interestingly, when you only look at this question using daily-averaged data the effect disappears (left side of graph). Dynamic influences on smoking relapse process - PubMed

View attachment 318458

It's simply not consistent with the growing body of evidence coming from these studies with greater temporal resolution to claim that negative affect/distress don't play a role in substance use disorders, problematic use, or the chronicity of these presentations. We can point to genetic risk factors all we want, but that does not account for even close to 100% of the variance...so why would you suggest it's "collusion" to address the role of psychosocial factors that clearly play a role?
1) This is the problem. People don't know what the SMH is, they are not looking up the term, they are making up definitions, acting like they know what the definition is and then getting all upset when presented with a technical argument.


2) I NEVER said "that there's no value to addressing the role of craving management, emotion regulation, distress tolerance, and/or coping skills broadly in the management and treatment of SUDs". Watch the misquotes. To address your issues:

a. Pharmacological management of cravings has been empirically validated as a method of successful intervention in SUD, independent of any mood disorder.
b. Interventions for SUD that focus upon emotional regulation have failed to show efficacy in SUDs.
c. Interventions for SUDs that focus upon distress tolerance have shown equivocal efficacy for SUDs. I am extremely skeptical about the social skills improvement stuff in SUDs, as obtaining illegal substances requires some social savy.
d. Interventions for distress tolerance and/or coping skills have shown equivocal efficacy. And coping skills are not a predictive variable for substance use across the board.


3) What I AM saying:

a. If someone is using a term, they sure as hell should know what that term means.
b. If someone wants to talk about some other idea, they should acknowledge the standard body of literature, and explain their deviations.
c. The SMH indicates that the CAUSE of SUD is an underlying mental disorder (i.e., affective disorders and ADHD), that the nature of the disorder will dictate which substance is used, and that this substance use will improve the person's functioning. THIS HAS BEEN REPEATEDLY DISPROVEN ON MANY LEVELS FOR 35 YEARS!
d. People don't bother to read the literature, and have NO IDEA what that term means. This doesn't stop them from using it. That is bad.
e. Self report is inaccurate across multiple areas, including SUDs. But that doesn't even matter, because...
f. Treating a mood disorder has almost no effect on SUDs. Which presents a challenge to the idea that SUDs are an attempt to self medicate.
g. If the SMH, and the treatments thereof, are not supported, then we should drop that crap and pursue what science tells us.
 
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1) Substances are pleasurable. Anyone that fails to acknowledge that fact is paternalistic at best, and an aggressively idiotic person otherwise. People use substances because they feel good. The simplicity of that explanation can be very uncomfortable for some people due to a myriad of social, moral, ethical, financial, legal, and relational implications. However, it is pure collusion to ignore the hedonistic explanation. One calls to mind the southpark episode featuring tiger wood's infidelity. If the pleasure is NOT a factor, then show me anyone who has binge ate cabbage, or self medicated using the things we know work against mental disorders.
People severely underestimate this. This is thought 1 when someone with an SUD sits in the chair in front of me.

1) This is the problem. People don't know what the SMH is, they are not looking up the term, they are making up definitions, acting like they know what the definition is and then getting all upset when presented with a technical argument.
Agreed - problem is the definitions have been so distorted and modified and then assumptions are made.

c. The SMH indicates that the CAUSE of SUD is an underlying mental disorder (i.e., affective disorders and ADHD), that the nature of the disorder will dictate which substance is used, and that this substance use will improve the person's functioning. THIS HAS BEEN REPEATEDLY DISPROVEN ON MANY LEVELS FOR 35 YEARS!
Following the point above. Honestly, this literature is a hot mess. I have spent years deep into this stuff and sometimes get so frustrated. Honestly, this just leads me back to the first quote above in most instances - occams razor - Drugs are fun. The chemicals can lead to bad stuff happening to a minority of people, a minority of the time. There are a variety of people, variety of chemicals, and variety of contexts - thus the diversity in presentation, problems, and resulting scattershot of treatment approaches and explanations.
 

Ollie123

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@Ollie123 I see things differently. The SMH is a myth that is not supported. Since that time, people have been scrambling to try to find something, anything, about this idea that can be supported. It is rare that this type of frantic behavior pans out in favor of science. It sure as hell didn't work out for Reik. As for the the amount of money invested... See: well... the presidential campaign...all of 2020... certain politicians....climate change deniers...

My read on the situation:

1) Substances are pleasurable. Anyone that fails to acknowledge that fact is paternalistic at best, and an aggressively idiotic person otherwise. People use substances because they feel good. The simplicity of that explanation can be very uncomfortable for some people due to a myriad of social, moral, ethical, financial, legal, and relational implications. However, it is pure collusion to ignore the hedonistic explanation. One calls to mind the southpark episode featuring tiger wood's infidelity. If the pleasure is NOT a factor, then show me anyone who has binge ate cabbage, or self medicated using the things we know work against mental disorders.

2) There are clearly genetics at play. It is intellectually dishonest to ignore this fact. Anyone who remember the Minnesota Twin study knows that substance abuse is highly heritbale. Further twin studies show about 30-60% heritability of substance abuse (depending on substance and population...looking at you, the Irish), which demonstrates the entire penetrance vs expressivity vs pleiotrophy stuff (Goldman, 2006; Ducci,& Goldman, 2012; etc). Those numbers will look familiar to anyone who has looked that the literature about the heritability of FSIQ stuff where heritablilty is like 75% (mediated by environment), the heritbality of achievement stuff which pegs heritability at around 60% (obkay, 2016), heritbaility of 5 factor models, or whatever Cloninger is up to nowadays. Kinda weird those numbers are circling each other.

If we can address differential responses to substances in some ethnic groups (e.g., flush reactions in alcohol secondary to AD1HB-2 polymorphisms in some asian ethnic groups such as the Han, and in some european group like the Askanzai jews), then we have already accepted that there is some genetic basis. If 30-75% of SUD susceptibility is due to genetics, it is just plain MEAN to try to get people to give another explanation. However, if individuals want to ignore the genetic basis of response, then they need to also ignore other genetically based responses.


3) Some people have some susceptibility to specific substances that appears to be mediated via genetics and environment. It is likely that some individuals are susceptible to the effects of a specific class of substances. It is also likely that there is a range of problematic behaviors that vary from physiological dependence to engaging in completely socially unacceptable behaviors while under the influence. We are AWFUL at describing these variations.

This susceptibility likely has little to do with any other mental disorders, aside from common sense implications (e.g., maybe it is not a great idea to drink a ton of 4Loko with a someone with bipolar disorder). .

Exceptions are obvious, like how smoking cigarettes in over medicated schizophrenics reduces oversedation of FGAs through CYP induction via cigarettes.

4) People who abuse substances are obviously going to reach out to use substances when there are good times, bad times, and boring times. This isn’t self medicating anything. Treating some mood stuff isn't going to do a damn thing for these people. Giving people false promises, and letting them feel as if it is their fault that said promises don't work.... that is awful. No better than telling them that their SUD is hurting baby jesus, or whatever.

5) People can have 2+ problems. Professionals should be able to deal with this. The reductionist idea of that every problem can be explained by something is just dumb.

6) If the literature shows that treating an underlying mood disorder has little effect on substance use.... this entire theory is wrong. If the literature predominantly shows that the only pharmacological treatments that work are naltrexone and such ... it's not a self medication anything. It's a SUD.

7) There are many many many social, financial, legal, religious, moral, relational, etc implications for SUDs. The SMH offers people a socially accepted excuse from this stuff. There is no science to this idea. It takes real character to not collude with people.

8) People are not accurate in what they say, across the board. It is unclear as to whether this is straight up lying, or some human tendency. It doesn't matter. The literature shows that substance abuse typically comes BEFORE mood problems. We know that treating mood problems does not stop substance abuse. Therefore, we should treat the substance abuse, and ignore any patient attributions. Anyone who has treated a delusional person knows how this works.

9) Which is preferable:

a. Telling a patient that he/she has a substance use problem, and that their mood problems will get better when that is under control. When asked, telling that patient, "We don't know why some people use drugs. It looks like there's some genetics, some environment, and some personal choice. What matters is that we treat that, and get you better."

b. Telling a patient that his/her substance abuse is caused by some underlying thing that may or may not be present. Getting them to believe that their SUD is caused by this mood thing. Getting them to believe that if this mood thing is treated, that they will get sober. Treating the mood thing, and then having them believe that any resulting SUD is a matter of personal choice?
Again, don't disagree with really anything you said related to SMH. "Substances are pleasurable and this is the main reason why people use them" is arguably the central tenet of my entire research program at the moment. I'd push back slightly on a few points (the extent to which people are "scrambling" versus just the normal process of revising theories, whether 50% of variance is the best we can hope to do and its "mean" to aim higher) but that is mostly nit-picking.

I'm guessing we're just used to talking about this in different circles. Some of the things it sounds like you have encountered are literally ridiculous and it is sad these even need to be said at this point (SUDs often precede mood problems, you need to treat both, etc.). Even 25 years ago these really weren't up for debate in academic circles. I mean, people were still publishing on it because you can still build at least a moderately successful scientific career by pounding bigger/better nails into coffins already covered in them, but that is besides the point. Let's not throw the baby out with the bathwater though. Your example of an "obvious exception" is a good one and one that would not necessarily have been as obvious 20-30 years ago. Talking about how X hypothesis is not supported is one thing, but turning all contradictory evidence back around to "That's not the hypothesis laid out 40 years ago" is just...odd. At least in the academic circles I associate with, everyone moved on decades ago and no one cares what the original hypothesis was at this point - re: self-medication or virtually anything else. No one talking about self-medication is trying to prove or disprove the original hypothesis anymore....it is long dead. The literature remains a confusing mess, but some basic concepts were carried forward and led to new theories and this will likely continue for the forseeable future like it does for everything in academia. I don't think we are anywhere near the point where I would be comfortable categorically ruling out the possibility that certain subgroups (not necessarily subgroups that align with DSM criteria) of people experience differential reinforcement from drug use (not necessarily due to drug-specific pharmacological actions). That's a pretty damn soft theory - and still something I would argue doesn't have great support - but its a thread some people are following and I think is worth exploring. I suspect you will argue that isn't the SMH from 40 year ago. It isn't. And that's the point.
 
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beginner2011

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Talking about how X hypothesis is not supported is one thing, but turning all contradictory evidence back around to "That's not the hypothesis laid out 40 years ago" is just...odd. At least in the academic circles I associate with, everyone moved on decades ago and no one cares what the original hypothesis was at this point - re: self-medication or virtually anything else. No one talking about self-medication is trying to prove or disprove the original hypothesis anymore....it is long dead.
Says it better than I will. I'd rather not continue arguing about this particular issue.

b. Interventions for SUD that focus upon emotional regulation have failed to show efficacy in SUDs.



c. Interventions for SUDs that focus upon distress tolerance have shown equivocal efficacy for SUDs. I am extremely skeptical about the social skills improvement stuff in SUDs, as obtaining illegal substances requires some social savy.
d. Interventions for distress tolerance and/or coping skills have shown equivocal efficacy. And coping skills are not a predictive variable for substance use across the board.
Also, this is just not accurate. Here are some examples:

And here's a theory paper describing the theoretical models and hypothesized mechanisms of action -- which include emotion regulation/distress tolerance/coping skills:

3) What I AM saying:

a. If someone is using a term, they sure as hell should know what that term means.
See the 1997 formulation, which is what people these days cite.

f. Treating a mood disorder has almost no effect on SUDs. Which presents a challenge to the idea that SUDs are an attempt to self medicate.
Source?
 

PsyDr

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@beginner2011


1) Those articles do not show that these treatments stop substance abuse, or even reduce substance use to non-problematic levels. If you think that improvement on 1/11 of the symptoms of a disorder is anything other than equivocal results, we will fundamentally disagree. If you think that it is acceptable for a study to measure mood and pain, while simultaneously failing to take into account the substance's depressogenic effects, hyperalgia effects, sleep effects, induction of hypogonadism and the resulting effects thereof, etc... we will fundamentally disagree. If you consider improvement on distress tolerance measures, without substantial changes in substance use, to be anything more than equivocal results, we will disagree. If you are able to reconcile statements from papers you cited previously that indicate that coping is not related to increased alcohol use, with your disagreement of my reiteration of those statements, I'd love to hear it.

2) Tell me how you are able to reconcile an opinion that authors have read that definition citations with : the removal of the specificity component of the hypothesis which is very clearly defined in that paper, the failure to address which affective state is being studied (which is addressed in the paper by symptom cluster of disorder with attribution to specific substances), the absence of the temporal sequences of onsets which the 1997 paper discusses for about a full page, or the absence of pretty much any other key components of the 1997 paper.

3) As I see it, you are making statements about the SMH before you have read the article, you are saying you will argue about this/not that, have severely characterized what I say, stating that you won't address some things while addressing other things, asking for citations already provided, changing definitions back and forth, and changing focuses only to return to previous ones.

a. The most innocuous explanation for this behavior that I can imagine is an interaction between my writing style, a unique reading style, some disorganization, different levels of educational achievement, and some time constraints. If this is the case, maybe looking at the references, before demanding they be provided, would be the cool thing to do. And maybe it would be cool to apologize when you accidentally mischaracterize something. Alternatively, if there is some other reason and I am embarrassing you, please feel free to PM me, and I'm happy to apologize.

b. However, it is also possible that you are being unfair. I'm happy to interact with that set of standards too, I just need to know if that is what we are doing.


@Ollie123

To be fair, I'm mostly a clinician, who is not involved in the assessment, treatment, or research of SUDs. The chances of me knowing more than you about this topic approach nil. And the chances of me talking to the same type of people, in the same type of way is even worse. (Unless you include pathological gambling as it relates to neuro disorders).

On the street level, it would seem that few have any idea what the term self medication means. It seems to be a highly overused justification that allows therapist to explain away bad behavior, while completely ignoring personal agency, even when there is no underlying mental disorder, and/or no SUDs. I have issue with that.

@AbnormalPsych

I don't get it. People rarely look for a "deep" explanation as to why someone would want to eat pizza. They tend to understand it is delicious. They tend to understand that this "deliciousness" is caused by a few billion years of evolution that refined cellular metabolism to use the of carbs/fats/salts, and that a few thousand years of human history has really favored the people who got as many calories as possible. They tend to understand that there are variations in these preferences, mediated by genetic factors like lactose tolerance, and mediated by personal experience, etc. So why can't we do that with substances of abuse?!
 
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beginner2011

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1) Those articles do not show that these treatments stop substance abuse, or even reduce substance use to non-problematic levels. If you think that improvement on 1/11 of the symptoms of a disorder is anything other than equivocal results, we will fundamentally disagree. If you think that it is acceptable for a study to measure mood and pain, while simultaneously failing to take into account the substance's depressogenic effects, hyperalgia effects, sleep effects, induction of hypogonadism and the resulting effects thereof, etc... we will fundamentally disagree. If you consider improvement on distress tolerance measures, without substantial changes in substance use, to be anything more than equivocal results, we will disagree. If you are able to reconcile statements from papers you cited previously that indicate that coping is not related to increased alcohol use, with your disagreement of my reiteration of those statements, I'd love to hear it.
The MBRP study published in JAMA demonstrated significant reductions in binge drinking and probability of return to substance use during follow up. I pointed out that these interventions are effective at reducing substance use. I'm not sure what more to say.

2) Tell me how you are able to reconcile an opinion that authors have read that definition citations with : the removal of the specificity component of the hypothesis which is very clearly defined in that paper, the failure to address which affective state is being studied (which is addressed in the paper by symptom cluster of disorder with attribution to specific substances), the absence of the temporal sequences of onsets which the 1997 paper discusses for about a full page, or the absence of pretty much any other key components of the 1997 paper.
Here is the direct quote that I mentioned earlier from the 1997 Khantzian article:
1600367806377.png

3) As I see it, you are making statements about the SMH before you have read the article, you are saying you will argue about this/not that, have severely characterized what I say, stating that you won't address some things while addressing other things, asking for citations already provided, changing definitions back and forth, and changing focuses only to return to previous ones.
I requested access to the article, and then mentioned that I found it. Then I quoted it. See the image above. You mentioned about half a dozen different authors but have not yet linked a single specific citation for this claim: " Treating a mood disorder has almost no effect on SUDs. Which presents a challenge to the idea that SUDs are an attempt to self medicate." I'm sure they exist, and you seem to be stating so with a great deal of certainty and confidence, so I simply requested it for my own reference.

a. The most innocuous explanation for this behavior that I can imagine is an interaction between my writing style, a unique reading style, some disorganization, different levels of educational achievement, and some time constraints. If this is the case, maybe looking at the references, before demanding they be provided, would be the cool thing to do. And maybe it would be cool to apologize when you accidentally mischaracterize something. Alternatively, if there is some other reason and I am embarrassing you, please feel free to PM me, and I'm happy to apologize.
I did not mean to mischaracterize your argument. I asked repeatedly for you to clarify and then quoted you and attempted to address your specific statements directly. I believe I've done this in a fair way, and I'm also aware that online I have a tendency to be more argumentative than is useful. I take issue with your characterization of discussing self-medication of negative affect among people experience substance use disorders as "colluding" with them. I'm not asking you to apologize, but I'll acknowledge that characterization made me feel defensive. Also, I think it's pretty absurd and disrespectful to point to "different levels of educational achievement" as an explanation for disagreement on a board filled with psychologists (with presumably extremely similar levels of educational achievement).

b. However, it is also possible that you are being unfair. I'm happy to interact with that set of standards too, I just need to know if that is what we are doing.
Not sure what you're talking about here.

@Ollie123

To be fair, I'm mostly a clinician, who is not involved in the assessment, treatment, or research of SUDs. The chances of me knowing more than you about this topic approach nil. And the chances of me talking to the same type of people, in the same type of way is even worse. (Unless you include pathological gambling as it relates to neuro disorders).

On the street level, it would seem that few have any idea what the term self medication means. It seems to be a highly overused justification that allows therapist to explain away bad behavior, while completely ignoring personal agency, even when there is no underlying mental disorder, and/or no SUDs. I have issue with that.
Self-medication-related theories for the development/maintenance of substance use problems do not ignore personal agency.

@AbnormalPsych

I don't get it. People rarely look for a "deep" explanation as to why someone would want to eat pizza. They tend to understand it is delicious. They tend to understand that this "deliciousness" is caused by a few billion years of evolution that refined cellular metabolism to use the of carbs/fats/salts, and that a few thousand years of human history has really favored the people who got as many calories as possible. They tend to understand that there are variations in these preferences, mediated by genetic factors like lactose tolerance, and mediated by personal experience, etc. So why can't we do that with substances of abuse?!
I'm not up on the eating disorders literature or field, but my understanding is that there is more to the etiology, maintenance, and remission of eating disorders than you're implying.

Edit: I see that I originally linked a MORE study that was not my intended citation, which is probably part of the reason you were confused. I don't currently have access to my citation manager, so I apologize for that. A better cite would be this one: APA PsycNet
 
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PsyDr

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The MBRP study published in JAMA demonstrated significant reductions in binge drinking and probability of return to substance use during follow up. I pointed out that these interventions are effective at reducing substance use. I'm not sure what more to say.


Here is the direct quote that I mentioned earlier from the 1997 Khantzian article:
View attachment 318476


I requested access to the article, and then mentioned that I found it. Then I quoted it. See the image above. You mentioned about half a dozen different authors but have not yet linked a single specific citation for this claim: " Treating a mood disorder has almost no effect on SUDs. Which presents a challenge to the idea that SUDs are an attempt to self medicate." I'm sure they exist, and you seem to be stating so with a great deal of certainty and confidence, so I simply requested it for my own reference.


I did not mean to mischaracterize your argument. I asked repeatedly for you to clarify and then quoted you and attempted to address your specific statements directly. I believe I've done this in a fair way, and I'm also aware that online I have a tendency to be more argumentative than is useful. I take issue with your characterization of discussing self-medication of negative affect among people experience substance use disorders as "colluding" with them. I'm not asking you to apologize, but I'll acknowledge that characterization made me feel defensive. Also, I think it's pretty absurd and disrespectful to point to "different levels of educational achievement" as an explanation for disagreement on a board filled with psychologists (with presumably extremely similar levels of educational achievement).


Not sure what you're talking about here.


Self-medication-related theories for the development/maintenance of substance use problems do not ignore personal agency.


I'm not up on the eating disorders literature or field, but my understanding is that there is more to the etiology, maintenance, and remission of eating disorders than you're implying.

Edit: I see that I originally linked a MORE study that was not my intended citation, which is probably part of the reason you were confused. I don't currently have access to my citation manager, so I apologize for that.

1) Happy to treat you as an equal. I apologize. I just assumed that anyone who saw that the FIRST WORD in the title of this website is STUDENT, might recognize that posters have potential student status, and therefore different educational status. And I guess reading that someone's status of "post-doc" , would be a pretty good indication of a difference in educational achievement. I never considered that seeing a student status on a student website, and offering that maybe there is a difference in education would be considered "absurd" or disrespectful".

2) As you noticed in my posting, SMH is a very specific thing. And as you can see in the FIRST SENTENCE of the image of the 1997 that you posted, there are TWO PARTS to the SMH, and that the second part has 3 components. Therefore, can you reconcile Dr. Hawn's description of the SMH as limited to alcohol as defined in statements of:

" Fourth, and one of the most widely accepted explanations for high comorbidity rates between PTSD and AUD, is the self-medication hypothesis, a causal model that postulates that individuals with PTSD are more prone to developing problematic drinking behaviors due to a tendency to drink to cope with negative internal experiences (Khantzian, 1997). Consistent with learning theory, the use of alcohol to temporarily alleviate PTSD symptoms acts as a cogent short-term negative reinforcer. "


With the statements in the 1997 article which indicate,

" For example, Vietnam .veterans with whom I worked gave compelling evidence of how opiates calmed and contained their rage. (It is. worth
commenting, parenthetically, that rage and anger are constant companions and concomitants of trauma and violence of any kind.) In the case of alcohol abuse, the alcohol can offset or reverse psychic numbing, feelings of estrangement, and detachment in low to moderate doses, and it can dampen emotional flooding in high, "hypnotic" doses. In these latter cases my patients .have referred to the "obliterating" effects of alcohol and other drugs. Finally, it should not be surprising that stimulants such as cocaine are often used by PTSD patients, as Kosten and Krystal have suggested, to offset the anhedonia and deactivation commonly seen in this disorder. "

Did the fundamental properties of alcohol change to cover the properties of cocaine and opiates? Did mood states of PTSD become homogeneous?

3) That is NOT what I said about collusion. You are AGAIN making stuff up.

4) If you know more about the topic of collusion in SMH, you might want to contact the Stanford psychiatrist, Dr. Lembke, who introduced that term into that literature by stating, "But the risks of colluding in a narrative which is poorly founded outweigh the risk of making our patients angry."(Lembke, 2012). Tell her that you know more than someone with a few dozen publications, a Ted talk, and a consultancy to federal government. Let me know how that goes.

5) Can you reconcile your statement,

a. "You mentioned about half a dozen different authors but have not yet linked a single specific citation for this claim: " Treating a mood disorder has almost no effect on SUDs. Which presents a challenge to the idea that SUDs are an attempt to self medicate."

b. with my posts that offered the citations of ( Nunes, 1991; Nunes, 2004; Cornelius, 2001; Conrnelius, 1997; Pennitti, 2004; McHugh, 2015; etc)? Because I can't, other than a misspelling of one name.

c. In individuals with co-morbid MDD and SUDs, does treatment with SSRIs/TCAs stop substance use? No. (Nunes, 2004). In individuals with MDD and co-morbid SUD, does substance use stop after SSRI response such that BDI scores are in the minimal range? No (Cornelius, 1997). Does antidepressant treatment of individuals with MDD and co-morbid SUD,show efficacy for substance use? No (Pettinati, 2004). In co-occurring anxiety/SUDs, does psychotherapy, or pharmacotherapy of the anxiety disorder alone result in reliable change in SUDs? No (McHugh, 2015).

6) There you go again, making stuff up, saying I made an argument that I never had, and then offering a counter argument about something I never mentioned. Show me where I said ANYTHING about eating disorders, or admit you are making stuff up.
 
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beginner2011

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1) Happy to treat you as an equal. I apologize. I just assumed that anyone who saw that the FIRST WORD in the title of this website is STUDENT, might recognize that posters have potential student status, and therefore different educational status. And I guess reading that someone's status of "post-doc" , would be a pretty good indication of a difference in educational achievement. I never considered that seeing a student status on a student website, and offering that maybe there is a difference in education would be considered "absurd" or disrespectful".
Cool. Thanks.

2) As you noticed in my posting, SMH is a very specific thing.
Yes, I'm aware of that. Also, citing the 1997 article and identifying a specific element of it is not an endorsement of the entirety of the article. I'll also note that when I first quoted that specific sentence from the article you responded by saying:
@beginner2011
NONE OF WHAT YOU ARE CALLING THE SMH IS THE SMH!!!!
And as you can see in the FIRST SENTENCE of the image of the 1997 that you posted, there are TWO PARTS to the SMH, and that the second part has 3 components. Therefore, can you reconcile Dr. Hawn's description of the SMH as limited to alcohol as defined in statements of:
" Fourth, and one of the most widely accepted explanations for high comorbidity rates between PTSD and AUD, is the self-medication hypothesis, a causal model that postulates that individuals with PTSD are more prone to developing problematic drinking behaviors due to a tendency to drink to cope with negative internal experiences (Khantzian, 1997). Consistent with learning theory, the use of alcohol to temporarily alleviate PTSD symptoms acts as a cogent short-term negative reinforcer. "

With the statements in the 1997 article which indicate,

" For example, Vietnam .veterans with whom I worked gave compelling evidence of how opiates calmed and contained their rage. (It is. worth
commenting, parenthetically, that rage and anger are constant companions and concomitants of trauma and violence of any kind.) In the case of alcohol abuse, the alcohol can offset or reverse psychic numbing, feelings of estrangement, and detachment in low to moderate doses, and it can dampen emotional flooding in high, "hypnotic" doses. In these latter cases my patients .have referred to the "obliterating" effects of alcohol and other drugs. Finally, it should not be surprising that stimulants such as cocaine are often used by PTSD patients, as Kosten and Krystal have suggested, to offset the anhedonia and deactivation commonly seen in this disorder. "

Did the fundamental properties of alcohol change to cover the properties of cocaine and opiates? Did mood states of PTSD become homogeneous?
Yea, I mean, I see what you're saying that this particular element of the original 1997 proposal has clearly been re-interpreted. As Ollie has mentioned, that definitely doesn't mean it's time to throw out the whole idea.

3) That is NOT what I said about collusion. You are AGAIN making stuff up.
You're welcome to clarify what you meant. Perhaps I misunderstood.

4) If you know more about the topic of collusion in SMH, you might want to contact the Stanford psychiatrist, Dr. Lembke, who introduced that term into that literature by stating, "But the risks of colluding in a narrative which is poorly founded outweigh the risk of making our patients angry."(Lembke, 2012). Tell her that you know more than someone with a few dozen publications, a Ted talk, and a consultancy to federal government. Let me know how that goes.
Are we making arguments from authority now? No thanks.

5) Can you reconcile your statement,

a. "You mentioned about half a dozen different authors but have not yet linked a single specific citation for this claim: " Treating a mood disorder has almost no effect on SUDs. Which presents a challenge to the idea that SUDs are an attempt to self medicate."

b. with my posts that offered the citations of ( Nunes, 1991; Nunes, 2004; Cornelius, 2001; Conrnelius, 1997; Pennitti, 2004; McHugh, 2015; etc)? Because I can't, other than a misspelling of one name.
Right, I asked for a link, or at least a more complete citation than simply names and dates which are helpful, but a more complete citation is what I requested. There's a reason APA style includes all the info it does, and I try to provide the doi links to citations since it takes me about 10s, but it would take anyone else quite a while to figure out exactly what I'm citing. I wish I had more time to look into this stuff, but I don't. If you don't want to share more info that's your prerogative, but that's what I'm hoping you'll share.

c. In individuals with co-morbid MDD and SUDs, does treatment with SSRIs/TCAs stop substance use? No. (Nunes, 2004). In individuals with MDD and co-morbid SUD, does substance use stop after SSRI response such that BDI scores are in the minimal range? No (Cornelius, 1997). Does antidepressant treatment of individuals with MDD and co-morbid SUD,show efficacy for substance use? No (Pettinati, 2004). In co-occurring anxiety/SUDs, does psychotherapy, or pharmacotherapy of the anxiety disorder alone result in reliable change in SUDs? No (McHugh, 2015).
Awesome. Thank you. I'll look into these more. It does look like they're mostly restricted to pharmacotherapy, which is definitely outside of my knowledgebase. I will say that my understanding is that there is a fair bit of evidence that the treatment of PTSD in the context of co-ocurring SUD/PTSD does reduce SUD symptoms. I was literally just looking at a slide this afternoon from an as yet unpublished national VA presentation stating that SUD outcomes were mediated by reductions in PTSD symptoms. Again, my understanding is also that the validity of the self-medication model (as it is typically applied these days) is not nearly so broad as to say that the SUD is a product of the co-occurring disorder -- it's much more limited and acknowledges that the NA and SU behaviors are mutually reinforcing (but neither is necessarily sufficient to produce the other).

6) There you go again, making stuff up, saying I made an argument that I never had, and then offering a counter argument about something I never mentioned. Show me where I said ANYTHING about eating disorders, or admit you are making stuff up.
You made an analogy between SUD and eating pizza. No one wonders why people casually drink alcohol or recreationally use substances. Tons of people do use substances (just like tons of people eat pizza) and that doesn't necessarily mean the self-medication model is relevant to their use. My example was intended to illustrate how silly that analogy is, which is why I brought up eating disorders, which would be the more appropriate analogy in the context of eating.

I'd much prefer this was a conversation as opposed to an argument. I've appreciated you challenging my thinking in this area, and I've also appreciated Ollie's weighing in. I will say that I'm currently surrounded by clinical and research folks that are fairly prominent in this area who all endorse some elements of the self-medication model. Just today I attended a presentation with two separate presenters who cited the self medication model (I noted that they specifically referred to it is as a model) as informing their research agenda. There are many more examples than I can fully draw on, and my primary disappointment with our discussion here is that I think I've failed to convince you that this is a legitimate consideration when working with patients experiencing SUDs. I think your patients would benefit if I had done a better job of advocating for the validity of the model, but c'est la vie.
 
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Emotional regulation has been established to reduce substance abuse, see page 58 of this meta-analysis as a starting point to explore further. Nothing outside of medically assisted treatment has had great results, but emotional regulation has been more positive than many things. As for AA, I knew a guy who practiced in and taught addictions for 30 years; he had a contract with the state and was a former alcoholic himself. He was a fan of AA. The reason you might not be convinced may be you overestimate the success rates of other forms of non medical treatment.
 
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Cool. Thanks.


Yes, I'm aware of that. Also, citing the 1997 article and identifying a specific element of it is not an endorsement of the entirety of the article. I'll also note that when I first quoted that specific sentence from the article you responded by saying:



Yea, I mean, I see what you're saying that this particular element of the original 1997 proposal has clearly been re-interpreted. As Ollie has mentioned, that definitely doesn't mean it's time to throw out the whole idea.


You're welcome to clarify what you meant. Perhaps I misunderstood.


Are we making arguments from authority now? No thanks.



Right, I asked for a link, or at least a more complete citation than simply names and dates which are helpful, but a more complete citation is what I requested. There's a reason APA style includes all the info it does, and I try to provide the doi links to citations since it takes me about 10s, but it would take anyone else quite a while to figure out exactly what I'm citing. I wish I had more time to look into this stuff, but I don't. If you don't want to share more info that's your prerogative, but that's what I'm hoping you'll share.


Awesome. Thank you. I'll look into these more. It does look like they're mostly restricted to pharmacotherapy, which is definitely outside of my knowledgebase. I will say that my understanding is that there is a fair bit of evidence that the treatment of PTSD in the context of co-ocurring SUD/PTSD does reduce SUD symptoms. I was literally just looking at a slide this afternoon from an as yet unpublished national VA presentation stating that SUD outcomes were mediated by reductions in PTSD symptoms. Again, my understanding is also that the validity of the self-medication model (as it is typically applied these days) is not nearly so broad as to say that the SUD is a product of the co-occurring disorder -- it's much more limited and acknowledges that the NA and SU behaviors are mutually reinforcing (but neither is necessarily sufficient to produce the other).


You made an analogy between SUD and eating pizza. No one wonders why people casually drink alcohol or recreationally use substances. Tons of people do use substances (just like tons of people eat pizza) and that doesn't necessarily mean the self-medication model is relevant to their use. My example was intended to illustrate how silly that analogy is, which is why I brought up eating disorders, which would be the more appropriate analogy in the context of eating.

I'd much prefer this was a conversation as opposed to an argument. I've appreciated you challenging my thinking in this area, and I've also appreciated Ollie's weighing in. I will say that I'm currently surrounded by clinical and research folks that are fairly prominent in this area who all endorse some elements of the self-medication model. Just today I attended a presentation with two separate presenters who cited the self medication model (I noted that they specifically referred to it is as a model) as informing their research agenda. There are many more examples than I can fully draw on, and my primary disappointment with our discussion here is that I think I've failed to convince you that this is a legitimate consideration when working with patients experiencing SUDs. I think your patients would benefit if I had done a better job of advocating for the validity of the model, but c'est la vie.
You have chosen to misquote me about things I never said, changed definitions to definitions, created rules for my behavior that do not apply to you (eg, saying an appeal to authority is not okay for me, and then saying that your position is supporting by people you work with), acted as if repeated information was new without admitting it wasn’t, and are now using ad hominems. You’re welcome to clarify if I misunderstood. These observations create substantial barriers to my acceptance of the respectability of your general character, the credibility of your clinical opinions about my patients, and the utility of further interaction. I would wish you well, if I could.
 
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PsyDr

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Ah, the old, "I feel sorry for your patients" ad hominem, I was wondering when that would rear its lazy head.
Right up there with completely changing the content, then attributing that false content to a person, then arguing against the false content, and when called out, using the apology, “I’m sorry if I misunderstood you.”.

It’s not an apology, and it’s not a misunderstanding. But it is a tactic.
 
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beginner2011

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You have chosen to misquote me about things I never said, changed definitions to definitions,
Nope. I quoted the definition provided in the paper you cited. Then you told me I was making things up and misunderstanding the paper.

created rules for my behavior that do not apply to you (eg, saying an appeal to authority is not okay for me, and then saying that your position is supporting by people you work with)
From my perspective the difference is I have no expectation that it will convince you, merely sharing information, not shouting you down and saying "WHY DON'T YOU GO TALK TO THIS AUTHORITY IF YOU'RE SO SMART!?"

acted as if repeated information was new without admitting it wasn’t,
You're right that I didn't spend 10 minutes for each of your vague references to find the actual content of the evidence. I asked you to clarify and provide more detailed citations than (Doe, 1982)

and are now using ad hominems. You’re welcome to clarify if I misunderstood. These observations create substantial barriers to my acceptance of the respectability of your general character, the credibility of your clinical opinions about my patients, and the utility of further interaction. I would wish you well, if I could.
Sorry to hear that. I did not intend for that statement to be an attack of your character. Explaining my take away. I see how you would take offense to that -- similar to how I took offense to you implying the same thing ("collusion").

You continue to not respond to the substantive evidence supporting the self-medication model. I agree this is no longer a fruitful interaction (if it ever was). I do wish you well.

For reference, here is the slide I mentioned:
1600441157897.png
 

Fan_of_Meehl

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QUOTE="WisNeuro, post: 22151416, member: 248083"]
Ah, the old, "I feel sorry for your patients" ad hominem, I was wondering when that would rear its lazy head.
Yeah...I hate that one too. It's extremely patronizing. And it's like a slur wrapped/diaguised as virtue ('"I'm very concerned for the safety of your patients" [e.g., 'I'm ethical/competent and you are not']) with the added vicious (though subtle) implication of a threat that such an insinuation implies (e.g., 'If I knew your identity I might be duty-bound to report your lack of ethics/competence to your licensing board or your employer') all embedded in the absurd context that the person making the slur has never met or observed you, your patients, or you interacting with your patients in a clinical context.
 
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beginner2011

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Yeah...I hate that one too. It's extremely patronizing. And it's like a slur wrapped/diaguised as virtue ('"I'm very concerned for the safety of your patients" [e.g., 'I'm ethical/competent and you are not']) with the added vicious (though subtle) implication of a threat that such an insinuation implies (e.g., 'If I knew your identity I might be duty-bound to report your lack of ethics/competence to your licensing board or your employer') all embedded in the absurd context that the person making the slur has never met or observed you, your patients, or you interacting with your patients in a clinical context.
...This is all because I said I regretted not making a more compelling argument? Now I'm impugning someone else's professional practice? Are you kidding me?
 

Fan_of_Meehl

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Nah
...This is all because I said I regretted not making a more compelling argument? Now I'm impugning someone else's professional practice? Are you kidding me?
Nah...I wasn't saying that you, specifically, have engaged in this behavior in the current thread. I was agreeing with WisNeuro about the general topic of hating that tactic (if employed). Thanks for the opportunity to clarify. Reading everything in this thread would be WAY too labor-intensive.
 

AbnormalPsych

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1)It's a sneaky trick. AA treats "Alcoholism", NOT the DSM5 or ICD10 alcohol disorders. AA defines alcoholism as a spiritual disease, mixed in with some physical cravings, and some mental stuff.
2) They don't define success like you'd think. Hint: it's not sobriety.
3) AA's early publications claimed success for 50-75%. But no data.
4)In the early 2000s, AA made some national news because someone obtained their data. Long story short, AA excluded the fact that the majority of people drop out after one meeting, and even more drop out within a few meetings. Throw those people in, and their combined success rate was like 5-10%. Not that great. And their version of "success" is not necessarily life time sobriety.
5) There was some conflict stuff with the legality of the courts mandating religious treatment.
6) And the self medication hypothesis isn't supported.
7) But all of this is a cheap way for society to deal with a problem, kinda.
@PsyDr You happen to know off hand any articles that sum up this stuff and other review and critiques of the existing AA model and limited literature? Looking for something to pass along to some one and not be 'the bad guy.'
 
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My patients who have serious mental health conditions get worse when they use substances and it is my recollection that this is supported in the literature. I also recall that for co-occurring disorders, treating both disorders predicts better outcomes. Patients also tend to report that they use substances to deal with symptoms, but that often seems like a justification to continue use despite negative consequences. My concern about the thinking about self-medication (referring more broadly to what I see in clinical practice as opposed to research on the SMH) is that it feeds into a problem of the disorder that we are trying to treat and that it reflects a type of fuzzy logic regarding the above mentioned findings. The danger with fuzzy logic when dealing with substance use is that those tend to be the types of patients most likely to drive a hole through the logic to their own detriment. I find it vital to be solidly grounded when working with people with substance abuse.
 
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