Medical Marijuana, PTSD, and VA?

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Empirical support on efficacy of medications in PTSD, for the most part, is limited.

I would say absolutely, there could be an expectancy effect. There are also social features ("Billy Bob said that marijuana really works for this. The docs don't know what they're talking about. [bunch of dudes chime in "Yeah!"] . . . call it the idiot guru effect). In addition, people like to use marijuana. It's a recreational drug. People will rationalize a lot to use it. Further, PTSD often reflects underlying changes in brain systems that regulate stress response including medial prefrontal cortex. What else is impacted by medial prefrontal cortex disruption? Decision making, impulse control. People bad at decision making and that lack impulse control are more likely too . . . . use drugs recreationally.

The self-medication hypothesis. Very popular philosophy amongst professionals. Doesn't jibe with what the recovering addicts always tell me. They say that even when they had psychological problems, which we all know many or even most do, the basic underlying reason for them was that they wanted to get high and that they would use the problems as a justification to continued use.
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The self-medication hypothesis doesn't hold up for a lot of conditions and is more of a way for people to describe their use in a less stigmatizing way or to not acknowledge their problems with substance use. However, there are some conditions where the explanation is more legitimate and certain anxiety disorders and PTSD seem to fit the bill (not all cases but in many cases) - based on longitudinal studies that look at onset, etc.

Regarding whether marijuana is helpful for PTSD - the study PsyDr mentioned earlier suggests that it is NOT helpful. I'll post it again:
http://www.ncbi.nlm.nih.gov/pubmed/26455669

But there is subjectivity to all of this. Moreover, when you are talking about cannabis you are talking about a variety of different types - some more stimulating and some more helpful with sleep. Reasons for using, perception of use, premorbid history, etc., are all important to account for.

But the data suggest that it does not help PTSD symptoms on average, and might make them worse.

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I think that is what Cheetah is saying too. I imagine there are programs with limited resources who are excluding patients in active substance use and I would support their ability to make those choices.
I'd agree with you so long as the choices aren't justified based on clinical presentation - and if instead they are justified by the lack of resources. I've seen them excluded based on "clinical judgment" when this is not supported by the literature. I think that is wrong.
I completely agree with flexibility in this area, but I think that we neglect one of the most important aspects of these treatment studies and that is that they have strict treatment protocols, aka rules. Too often, the real world translation, takes findings like that and ends up with a chaotic poorly implemented treatment without firm guidelines.
An EBT is an EBT. Sure protocols get modified to fit your clinic/population at times but are you basically saying that in your situation you are not able to deliver EBTs for PTSD? Because implementing protocols is a challenge in just about any community. A lot of the data we are discussing comes from community samples and the CTN - not necessarily tightly controlled labs like you are making this sound like. Attendance isn't always perfect and occasionally you will have clients that this does not work for, but that isn't a reason to not do it in general.
 
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Okay, Pragma, when you say:
I'd agree with you so long as the choices aren't justified based on clinical presentation - and if instead they are justified by the lack of resources.

I'm still stuck on clinical presentation. So I'm kind of stating the obvious but when we say 'PTSD tx should concurrently run in the presence of SUD,' I return to what cara susanna noted:

Generally the rules I've seen are that current SUD is okay as long as 1) they aren't high during session 2) they aren't high while completing homework.

This is a golden rule. PE, for example, will not be effective if your Veteran is 1) nodding off from heroin use in session, 2) has many substance-related therapy-interfering behaviors (such as shooting up before time to listen to his/her PE tapes, being late to 90-minute PE session, forgetting homework materials or what content specific-information needed to retain, like SUD ratings), 3) using drugs before in vivos, etc. The research may show that concurrent treatment is effective in reducing both PTSD- and SUD-sxs, but what about stabilization?

If patient presents to the ED with psychotic sxs (hearing voices, thought disorders, paranoia), supportive therapy and psychopharm may be the way to go until we can get a handle on what is happening for this individual (i.e., stabilization). Someone please help me understand that if a patient's SUD is limiting their functioning (in addition to PTSD), isn't treatment of the SUD the lesser of two evils if we think the patient will not adhere to trauma-focused treatment (clinical presentation > lack of resources)?

This is precisely why I like Seeking Safety because the tools are taught and the patient learns to ready themselves for the next stage of treatment, which the patient learns through the initial psychoeducation sessions that the 'next stage of treatment' will be rough and not easy...especially if you are thinking about imaginals from combat trauma.
 
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Smalltown, you are dead wrong about PTSD and ETOH. The most current literature has not found any efficacy for PTSD or causal relationship. The trait vulnerability hypothesis is gaining support over the self medication hypothesis due to advances in SEM in PTSD. Likewise, the DoD/AMA study found that heavy or binge drinking alcohol related problems had an increased attributable risk of suicide.
 
Smalltown, you are dead wrong about PTSD and ETOH. The most current literature has not found any efficacy for PTSD or causal relationship. The trait vulnerability hypothesis is gaining support over the self medication hypothesis due to advances in SEM in PTSD. Likewise, the DoD/AMA study found that heavy or binge drinking alcohol related problems had an increased attributable risk of suicide.
Aren't you saying the same thing I was? I'm confused now. :unsure: Maybe I wasn't clear enough that I disagreed with the hypothesis?
 
Okay, Pragma, when you say:


I'm still stuck on clinical presentation. So I'm kind of stating the obvious but when we say 'PTSD tx should concurrently run in the presence of SUD,' I return to what cara susanna noted:



This is a golden rule. PE, for example, will not be effective if your Veteran is 1) nodding off from heroin use in session, 2) has many substance-related therapy-interfering behaviors (such as shooting up before time to listen to his/her PE tapes, being late to 90-minute PE session, forgetting homework materials or what content specific-information needed to retain, like SUD ratings), 3) using drugs before in vivos, etc. The research may show that concurrent treatment is effective in reducing both PTSD- and SUD-sxs, but what about stabilization?

If patient presents to the ED with psychotic sxs (hearing voices, thought disorders, paranoia), supportive therapy and psychopharm may be the way to go until we can get a handle on what is happening for this individual (i.e., stabilization). Someone please help me understand that if a patient's SUD is limiting their functioning (in addition to PTSD), isn't treatment of the SUD the lesser of two evils if we think the patient will not adhere to trauma-focused treatment (clinical presentation > lack of resources)?

This is precisely why I like Seeking Safety because the tools are taught and the patient learns to ready themselves for the next stage of treatment, which the patient learns through the initial psychoeducation sessions that the 'next stage of treatment' will be rough and not easy...especially if you are thinking about imaginals from combat trauma.
I'm sort of discussing clinics in general and aside from my question for smalltown am not really targeting anyone specifically here. My own experiences have included some really frustrating interactions with clinicians who DO purposely exclude people with PTSD and substance use disorder - they won't take anyone with an active diagnosis. They say this because they say PTSD treatment will make them worse, or that use will interfere with PTSD treatment but there is no data to support that. That's the drum I'm beating.

Of course you can't do PE if someone is using right before session. But it doesn't mean that you can't do it if they are someone who is just an active user that doesn't show up intoxicated to session. Check out the Foa JAMA article I posted. Moreover, that's great that you use Seeking Safety - it has empirical support for people that use substances and have PTSD.

ETA: Here is the JAMA abstract (http://jama.jamanetwork.com/article.aspx?articleid=1724275)

Importance Alcohol dependence comorbid with posttraumatic stress disorder (PTSD) has been found to be resistant to treatment. In addition, there is a concern that prolonged exposure therapy for PTSD may exacerbate alcohol use.

Objective To compare the efficacy of an evidence-based treatment for alcohol dependence (naltrexone) plus an evidence-based treatment for PTSD (prolonged exposure therapy), their combination, and supportive counseling.

Design, Setting, and Participants A single-blind, randomized clinical trial of 165 participants with PTSD and alcohol dependence conducted at the University of Pennsylvania and the Philadelphia Veterans Administration. Participant enrollment began on February 8, 2001, and ended on June 25, 2009. Data collection was completed on August 12, 2010.

Interventions Participants were randomly assigned to (1) prolonged exposure therapy plus naltrexone (100 mg/d), (2) prolonged exposure therapy plus pill placebo, (3) supportive counseling plus naltrexone (100 mg/d), or (4) supportive counseling plus pill placebo. Prolonged exposure therapy was composed of 12 weekly 90-minute sessions followed by 6 biweekly sessions. All participants received supportive counseling.

Main Outcomes and Measures The Timeline Follow-Back Interview and the PTSD Symptom Severity Interview were used to assess the percentage of days drinking alcohol and PTSD severity, respectively, and the Penn Alcohol Craving Scale was used to assess alcohol craving. Independent evaluations occurred prior to treatment (week 0), at posttreatment (week 24), and at 6 months after treatment discontinuation (week 52).

Results Participants in all 4 treatment groups had large reductions in the percentage of days drinking (mean change, −63.9% [95% CI, −73.6% to −54.2%] for prolonged exposure therapy plus naltrexone; −63.9% [95% CI, −73.9% to −53.8%] for prolonged exposure therapy plus placebo; −69.9% [95% CI, −78.7% to −61.2%] for supportive counseling plus naltrexone; and −61.0% [95% CI, −68.9% to −53.0%] for supportive counseling plus placebo). However, those who received naltrexone had lower percentages of days drinking than those who received placebo (mean difference, 7.93%; P = .008). There was also a reduction in PTSD symptoms in all 4 groups, but the main effect of prolonged exposure therapy was not statistically significant. Six months after the end of treatment, participants in all 4 groups had increases in percentage of days drinking. However, those in the prolonged exposure therapy plus naltrexone group had the smallest increases.

Conclusions and Relevance In this study of patients with alcohol dependence and PTSD, naltrexone treatment resulted in a decrease in the percentage of days drinking. Prolonged exposure therapy was not associated with an exacerbation of alcohol use disorder.
 
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Marijuana is not a placebo. I'm pretty sure that most people use it because it makes them feel better. Probably not as effective in PTSD as ETOH, but some people tolerate it better and if it makes them feel better, then it works.

I was pointing out that ETOH does not demonstrate efficacy in PTSD populations. Maybe I misunderstood what you were trying to say here, but it looked like you were saying ETOH is effective in PTSD pops.
 
I was pointing out that ETOH does not demonstrate efficacy in PTSD populations. Maybe I misunderstood what you were trying to say here, but it looked like you were saying ETOH is effective in PTSD pops.
Sorry. I was being a bit tongue in cheek about how and why many patients perceive it as being efficacious because of the immediate effects. I am crystal clear that in the long run, reliance on ETOH as a medication will make the PTSD worse and can also lead to a myriad of other problems.
 
Of course you can't do PE if someone is using right before session. But it doesn't mean that you can't do it if they are someone who is just an active user that doesn't show up intoxicated to session. Check out the Foa JAMA article I posted. Moreover, that's great that you use Seeking Safety - it has empirical support for people that use substances and have PTSD.

Great. We're all in agreement here then. And I'm learning these things from folks who were trained by Foa's former postdocs. (Can we count how many degrees of separation that is from Foa?!? Ha.)

My own experiences have included some really frustrating interactions with clinicians who DO purposely exclude people with PTSD and substance use disorder - they won't take anyone with an active diagnosis

This also pisses me off. These are systemic issues that need to be considered as a whole. Thanks for the articles and discussion, Pragma.
 
Whether patients perceive it to be self medicating is one question. Whether it is, is another.

For example, I think it's pretty clear that alcohol has a major impact on sleep. Is avoiding nightmares sufficient to say it works from a self medicating perspective? I dunno.

Outcome measures become important here. Beating yourself unconscious would also prevent a host of symptoms for any number of disorders. Probably not going to improve your life. You don't see anyone asking for this.

Read has indicated that alcohol use is not caused by ptsd.
 
Read has indicated that alcohol use is not caused by ptsd.

Can you link me somewhere to this info?

I'm not firmly in any camp when it comes to self-medication - I usually spend most of my time educating people about how self-medication does not hold up most of the time. However, the reason it doesn't usually hold up has to do with basic levels of analysis (drug effects that match symptom relief vs. ones that make them worse) as well as unsupportive findings when you look at things longitudinally (e.g., onset of X does not come before onset of Z). But obviously, things are more complicated than that. In the case of PTSD, sometimes the onset of X does come before Z but of course not all the time.

I just think that self-perceived reasons for using, premorbid factors, ongoing symptoms, interacting symptoms (e.g., ETOH and sleep is a vicious cycle), and the timeline can be difficult to tease apart. In the case of PTSD, if there was no premorbid history of severe AUD, then there is severe AUD later, what study design out there has made it definitive that there is no causality there? Has it been replicated?

Thanks for humoring my questions. The sad part is that I think a lot of us know better than to jump on the self-medication bandwagon a lot of the time. But I still want to have good reasoning behind it when I deal with the cases where it might actually be sound.
 
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I have never been in the "you have to be sober before I will treat you" camp. I try not to set up any type of requirement that would be a setup for increased dishonesty or any control dynamics. Talk about enactments. "I haven't really been using much at all since last week." "I see here that you have a positive drug screen from the NP." "I can explain that doc." If I find myself getting into conversations like that I might want to address my own countertransference issues. I also don't tell my patients to stop cutting, stop smoking, start dieting or exercising, or stop having sex. I am even careful not to get too far ahead of them when they say they want to do these healthy behaviors. Walking that line is actually the hardest part. Patient is trying to initiate changes and I want to be supportive, but when they "fail" don't want them to feel that they need to hide it or they let me down, etc.
 
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Read, J.P., Merrill, J.E.*, Griffin, M.E.*, Bachrach, R.*, & Kahn, S.* (2014). Post-traumatic stress and alcohol problems: Self medication or trait vulnerability? The
American Journal on the Addictions, 23, 108-116.
 
The abtract is interesting but the methodology and sampling leave a bit to be desired.

http://onlinelibrary.wiley.com/doi/10.1111/j.1521-0391.2013.12075.x/abstract

Background and Objectives
Posttraumatic stress symptoms (PTSD) and problem alcohol use (ALC) commonly co-occur, but the nature of this co-occurrence is unclear. Self-medication explanations have been forwarded, yet traits such as tendency toward negative emotionality and behavioral disconstraint also have been implicated. In this study we test three competing models (Self-Medication, Trait Vulnerability, Combined Dual Pathway) of PTSD–ALC prospectively in a college sample.

Method
Participants (N = 659; 73% female, M age = 18) provided data at college matriculation (Time 1) and 1 year later (Time 2).

Results
Structural equation models showed disconstraint to meditate the path from PTSD symptoms to alcohol problems, supporting a trait vulnerability conceptualization. Findings regarding negative emotionality and self-medication were more mixed. Negative emotionality played a stronger role in cross-sectional than in prospective analyses, suggesting the importance of temporal proximity.

Conclusions and Scientific Significance
Self-regulation skills may be an important focus for clinicians treating PTSD symptoms and alcohol misuse disorders concurrently. (Am J Addict 2014;23:108–116)
 
Read, J.P., Merrill, J.E.*, Griffin, M.E.*, Bachrach, R.*, & Kahn, S.* (2014). Post-traumatic stress and alcohol problems: Self medication or trait vulnerability? The
American Journal on the Addictions, 23, 108-116.

Very exceedingly far from the final word. I know 3/5 authors and am quite certain they'd say the same. Like most things in psychology, I suspect the ultimate answer will be "it depends" and "a little of both". Best case scenario "Maybe a little more of one than the other."

That said, I largely 2nd everything Pragma has said in this thread. Far too much clinical lore in the substance use field. Heck, there is even significant debate about whether having complete abstinence as the goal (at all) is appropriate. Yet I've met many clinicians who won't treat anyone unless that's the case.
 
I never said it was the final word. Just used it as an example. Obviously, there are other articles supporting the trait vulnerability hypothesis. As with any line of research, there are controversies.

IMO, most have just claimed self medication based on theory. Most of the research has used comorbidity to support the self medication hypothesis, which IMO does not support the theory. When the theory has not been held up, people have revised it (i.e., Khanzitian's 1990s revision of his original theory after empirical studies disproved his original assertion). Not the best way to handle things.
 
Very exceedingly far from the final word. I know 3/5 authors and am quite certain they'd say the same. Like most things in psychology, I suspect the ultimate answer will be "it depends" and "a little of both". Best case scenario "Maybe a little more of one than the other."

That said, I largely 2nd everything Pragma has said in this thread. Far too much clinical lore in the substance use field. Heck, there is even significant debate about whether having complete abstinence as the goal (at all) is appropriate. Yet I've met many clinicians who won't treat anyone unless that's the case.
As far as the debate on whether complete abstinence should be the goal. Anyone that says otherwise is just wrong. We are talking fatal illnesses here and abstinence is the best strategy. How to get to that point we might have different methodologies, but it would be like saying someone with COPD should just smoke less or try to learn to become a "chipper". That's my two cents. :p
 
As far as the debate on whether complete abstinence should be the goal. Anyone that says otherwise is just wrong. We are talking fatal illnesses here and abstinence is the best strategy. How to get to that point we might have different methodologies, but it would be like saying someone with COPD should just smoke less or try to learn to become a "chipper". That's my two cents. :p

You cannot work on a goal that the patient does not buy into or want. When there is resistance there, harm reduction model and methods are in order.
 
As far as the debate on whether complete abstinence should be the goal. Anyone that says otherwise is just wrong. We are talking fatal illnesses here and abstinence is the best strategy. How to get to that point we might have different methodologies, but it would be like saying someone with COPD should just smoke less or try to learn to become a "chipper". That's my two cents. :p

This would be precisely the attitude that an ever-increasing number of addictions specialists are coming to view as one of the biggest barriers to effective care for that population. That's not to say there are never situations where it makes sense to advocate for complete abstinence, its perfectly appropriate in a large number of cases. However, it also sets up a wall that need not be there that keeps people from pursuing treatment and seems largely driven by black & white thinking on our part.
 
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I did not say that I make that the patient's goal. I have my own goals for all of my patients and that is for the optimum. They set their own goals. I don't need to tell them that drugs, smoking, overeating are bad for them, I think they already know that. My goal is to help them get to a point of psychological functioning where they don't need to use self-destructive or maladaptive coping. I'm still working on getting to that point with caffeine myself. For now, I use it to help cope with fatigue and stress, some day my functioning will be to the point where I don't "need" it. Until then, I make a reasoned choice, weigh risks and benefits, and choose to have another latte.
 
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Ironically, the big name in Harm Reduction was second author on the original Self Medication Hypothesis article.
 
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Meh, I don't use it, but this report still doesn't make it look "devastating" by any means. I only briefly glanced at some things on it, but it seems you'd need about 20 years of use to be a half a standard deviation lower than the control group. And that was pretty much the only difference found. Still looks far less dangerous than regular, heavy alcohol use.
 
Meh, I don't use it, but this report still doesn't make it look "devastating" by any means. I only briefly glanced at some things on it, but it seems you'd need about 20 years of use to be a half a standard deviation lower than the control group. And that was pretty much the only difference found. Still looks far less dangerous than regular, heavy alcohol use.
Even with chronic long-term ETOH use (in absence of Korsakoff's or hepatic encephalopathy), aren't the general findngs a return to normal function for most people after six months of abstinence? If I recall correctly, processing speed was one area that doesn't always improve.
 
Even with chronic long-term ETOH use (in absence of Korsakoff's or hepatic encephalopathy), aren't the general findngs a return to normal function for most people after six months of abstinence? If I recall correctly, processing speed was one area that doesn't always improve.

Some things return to normal function. Those pesky, white matter lesions, not as much. And, thiamine deficiency has wide-ranging effects.

We need better data, but from what is out there, in chronic alcoholics, the damage is fairly widespread in terms of bodily systems damage.
 
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Some things return to normal function. Those pesky, white matter lesions, not as much. And, thiamine deficiency has wide-ranging effects.

We need better data, but from what is out there, in chronic alcoholics, the damage is fairly widespread in terms of bodily systems damage.
Increased risk of pretty much any cancer is another biggie, especially when you combine with risk from tobacco which is often co-occurring.
 
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