15 Comments

  1. dah_sab

    I experience a slight but noticeable elevation of mood for around 90 minutes to two hours after taking suboxone. In addition, I also get a burst of energy lasting about the same time. So I usually take suboxone, let it take effect, then do my ‘chores’ around the house. Suboxone seems to make it possible for me to do things that otherwise I wouldn’t have the will or energy to tackle. Nothing big, just washing dishes, cleaning toilets, stuff like that which I might otherwise put off for days on end.
    But like I said, it only lasts two hours max. I can’t imagine seriously taking it for depression. I take effexor for that (!) Maybe suboxone affects others for a longer period of time, but if we’ve learned anything, it’s what goes up must come down. I’d have to take about 48mgs of suboxone if I were taking it for depression.

  2. Matt2

    I’ve noticed a big change from taking Suboxone. I think I wrote in another response about the little over 4 months I spent being “abstinent” after my last detox from using. I was horribly, horribly depressed and anxious which was obviously in big part from withdrawals but even before I started using opiates I’d been diagnosed with both depression and an anxiety disorder. Dr tried all kinds of anti depressants all made me feel like a zombie and raised my blood pressure. I loved opiates because I honestly thought they made me feel normal, as in social phobias were gone thought I was a halfway decent human being etc. After my last relapse when I started Suboxone I literally felt better instantly, not any kind of euphoria or anything like that but human or level :). The last 2 years while taking it I’ve felt balanced, I guess that’s the best way to put it. I still obviously experience the whole range of emotions and as such can get a little down sometimes but it’s very rare and nothing like it used to be. Great topic I’ve often wondered about this 🙂

  3. jamez70

    According to Wikipedia:
    “A clinical trial conducted at Harvard Medical School in the mid-1990s demonstrated that a majority of unipolar non-psychotic patients with major depression refractory to conventional thymoleptic antidepressants could be successfully treated with buprenorphine.[13] See opioids for other (predominantly favorable) experiments with buprenorphine and other opioids for psychological relief. However, psychological distress is currently not an approved indication for the use of any opioid, and legally it falls in to a “gray zone”.[14][15] In the United States, the doctor still needs the proper DEA licensing under the Drug Addiction Treatment Act of 2000 to prescribe Subutex or Suboxone for opioid addiction/dependence. Treatment of clinical depression is not indicated either but some doctors are realising its potential as an antidepressant in cases where the patient cannot tolerate or is resistant to conventional thymoleptic antidepressants. Psychological relief differs from depression and psychological distress is not usually an indication for prescribing any type of drug especially opiates.”
    When I was on Suboxone, its hard to be subjective about that effect because at the time there was a lot going on in my life. One thing is for sure is that it really made me sleep normally, which is RARE. Probably too much because I’d fall asleep alot when I was taking Suboxone.
    I really think there is something to its antidepressive effects. I wonder if that would be ‘off label’ use and not covered under the 100 patient limit, as when a physician would prescribe it ‘for pain’? That might be interesting if so.

  4. mattyr9

    I’ve struggled also with depression and social anxiety well before abusing drugs. When I found opiates (Oxycontin/heroin), I thought I had found “the cure” to my depression. However any anti-depressive benefits gained from opiate misuse were very short term and as tolerance rose exponentially, all the negative aspects of an opiate dependent lifestyle outweighed any sort of “mood-lift”.
    I have seen several studies looking into the question of whether Suboxone can be used for depression and have heard many anecdotal reports that include an “anti-depression” effect from using Suboxone.
    From personal experience, being treated with Suboxone for 15 months, I can say first hand that there is a definite positive effect the drug has on my mood in general. Whether this is a placebo effect or simply the presence of a low level of opiate in my brain, not sure. While Suboxone hasn’t been a “cure-all” for my mental state, I do find myself in very depressed states every so often, I believe it would be many times worse if I was off the medication totally.
    I am currently in the process of weaning off Suboxone, and this is one of the biggest fears I have besides the obvious acute withdrawal that comes along with my body getting through life without any opiate. I am down to 4 mg/day and I’m trying to prepare the best I can to cope with life in the absence of my safety net, Suboxone.

  5. angelo212

    I think doctors can and do perscribe Suboxone for deppression. I definitely feel better. Took the cravings away and I feel in a better mood (upbeat). I can work a 12 hour day go to the gym and still have energy on 8mg. Only problem is it takes me 1 and a half hours to fall asleep. There was a guy (don’t remember if he was a doctor but he was pushing suboxone to be used for depression. I think he had is own forum just for this topic. I will find this but need a few days. It was very interesting the things he had to say about suboxone and depression.

  6. johnpal716

    Hello,
    It’s difficult for me to hone in on whether being on Suboxone is what’s improved my depression, or all of the other changes in my life that came along with getting clean, or just getting clean in general.
    My first dose of Suboxone brought me out of a week of very hard withdrawal and into a state not unlike that touchy-feely opiate buzz for a day or two, and then a few days later I remember feeling so low and so spent, crying for no reason, sobbing to my folks: “I don’t know what’s wrong… I just don’t have any seratonin in my brain anymore!”.
    Somewhere over the past year I started having hobbies, interests, and friends again, and realized my life was coming together. Sleeping normal, rising early in the morning, exercising… all these things as a result of feeling good, but also contributing to feeling good.
    Twice I have had no Suboxone since I started taking it: once I left it at a campsite bathroom, another time I missed a doctor appointment; both times dealt with withdrawal. And the first symptom I noticed was depression and anxiety.
    Seems that if we take it, let ourselves feel better, use the time constructively, and do things that go hand in hand with wellness and happiness (and sobriety.. like meetings and working the program) it hold depression at bay. But Suboxone alone… not so sure.
    Be Well,
    jp

  7. Jack Russel

    I was never addicted to pain meds (meth and alcohol and GHB). After being sober for around 9 months my doctor put me on Suboxone for depression. It made me feel “something other than bad” for a while. Now i just take it because i am addicted to it. I believe it was less effective than regular anti-depressants.
    I was addicted to exercise, driving fast, anything that gave me a natural high. I was like that before, during, and after my drug addiction, thats why my doctor thought Suboxone might be a good choice. I DO NOT BELIEVE IT WAS. Now im just addicted to Suboxone and have another withdrawal to look forward too.
    PS; My dose is 16 mg a day. This is my first post online ever.

  8. brokencompass

    just curious if it really works for depression and/or anxiety. been on nearly every antidepressant and anti-anxiety med since 1996, newest antidepressant is ritalin (which I HATE). None have worked…. have had issues with opiates in the past, after 3 surgeries in 2 years, ready to try anything. docs have told me some people just have no response of any kind to antidepressants, which only made me feel more depressed.lol
    any thoughts??

    • A recent study in JAMA shows you are not alone– antidepressants are probably less effective than people believe. As for bupe and depression, I wouldn’t consider it for anyone not already opioid-dependent, as that is just too great a burden to give to someone– regardless of whether the drug treats depression.
      I believe that in some people, low mood comes from an imbalance in the endogenous opioid systems, and buprenorphine ‘stabilizes’ and restores that balance by providing constant opioid stimulation. Then there are people who are having low mood as part of a constellation of ‘cravings’ for opioids, and again, buprenorphine is helpful for those symptoms. I would guess that responding to buprenorphine would be perhaps a 50/50 proposition at best, but if you are using something as lousy as ritalin, you wouldn’t do any worse by trying buprenorphine.
      JJ

  9. ArcRendition

    Opiod’s intrinsically effect and manipulate a multitude of neurotransmitters despite their high affinity for primary opioid receptors, mu, kappa and delta. Obviously the type of opioid, (full agonist, semi-synthetic, synthetic, partial agonist) have as much to do with the pharmacodynamics as they do clinical applications and abuse ramifications. With that said, patients tend to experience a significant drop in opioid induced mood-elevation after cessation of the substance and during withdrawal primarily due to a cascade of psychophysiological effects, however I will only be focusing on a single facet of that deluge of bodily disruption since its highly applicable to the topic.
    As state earlier, opioids affect a number of neurotransmitters and their concentrations; potentiating some with inhibiting others. Relevant to mood however are well known group of you’ve all heard about, the Trimonoamine neurotransmitters, serotonin, norepinephrine and dopamine. Opioids, including the semi-synthetic, partial opioid agonist, buprenorphrine tend to manipulate regulatory neurotransmitters, of which are the Trimonoamine’s. The manipulation of these transmitters consequently affect the patient’s mood. However, with cessation of opioid usage, resulting in withdrawal, there is a sudden an significant drop in the concentration these critical mood regulating Monoamines which is why depression often results after cessation; in juxtaposition however, continuance typically results in remission of depression and even general mood elevation. Unfortunately, the revocation of beneficial side effects are inextricably correlated, if not causally linked to bodily habituation, or tolerance, to opioids.
    Although the precise differences in pharmacokinetics of buprenorphrine in contrast to other opioids are unknown, there seems to be an overwhelming degree of correlative anecdotal evidence that notes its prolonged mood-enhancing qualities unlike that of any other opioid.
    Lastly and most relevant to the mood discussion is the link between opioids, depression, folic acid and folate. For example, a skilled clinician will prescribe L-methylfolate (brand name: Deplin, generic folate) as part of an opioid withdrawal and maintenance regimen to address the adverse effects of opioid withdrawal on serotonin, norepinephrine and dopamine. Why, and how does this concern my mood? L-methylfolate is the final metabolite of folic acid, as such it is immediately able to penetrate the blood-brain barrier as it is the precursor of the trimonaime neurotransmitter synthesis, as such critical to balanced concentrations of mood stabilizing neurotransmitters primarily the trimonoamine’s thereby avoid withdrawal depression.
    Under regular circumstances, normal people without depression or who are receptive to antidepressants can simply consume and properly metabolize folic-acid, however up to 50% of people suffer from what is known as Polymorphism of the MTHFR gene which among other maladies, inhibits the body’s ability to metabolize folic-acid resulting in low folate (short for L-methylfolate) plasma levels and consequently low trimonoamine concentrations which leads to depression and antidepressant resistance. L-methylfolate cannot be substituted with any dietary supplement than prescription strength L-methylfolate in affected patients because only L-methylfolate can cross the blood brain barrier and only L-methylfolate can be used to synthesize trimonoaimes. More precisely, polymorphism of the MTHFR gene (as well as other etiologies) may leave the patient resistant to traditional antidepressants such as, but not limited to SSRIs simply because there isn’t enough serotonin to inhibit the reuptake of said serotonin. So, if you’re depressed and antidepressants are not working, it may be due to a folate deficiency caused by an inability to metabolize folic acid into it’s final metabolite, L-methylfolate (folate) for one of many reason (not just Polymorphism of the MTHFR gene). You may want to consider Deplin in conjunction with an antidepressant and continue buprenorphrine if needed for mood-enhancement.
    Feel free to message me for ANY reason or if you have any questions about anything I have explained above or if you would like to discuss your personal case in confidence!

    • I’m on the fence about approving these comments. I take no issue with them– but I recognize that they are, in essence, marketing for a product. I have not examined the product, nor have I reviewed evidence supporting the product’s efficacy. As with all of the things out there, people should research any product thoroughly before putting it into their bodies.

  10. ArcRendition

    SuboxDoc makes and excellent point preceding my words.
    My statements are offered as a complementary scientifically based POSTULATION, and under no circumstances should the information therewithin influence a medical decision without careful consideration, consultation and assessment of the risks and benefits under the supervision of licensed Psychiatric Medical Doctor.

  11. ArcRendition

    @brokencompass – How do we contact one another personally on this forum SuboxDoc?
    You should ask your clinician about a food supplement called DEPLIN (L-METHLFOLATE) and ask about having your Folate levels check to determine if you might be one of the few people unable to metabolize Folic Acid to create the final metabolite L-METHYLFOLATE (or just Folate) which as state about is the precursor to trimonoamine neurotransmitter synthesis. You can visit the DEPLIN website for more information or to print the supplement insert jacket for your Physician’s convenience. Anyone can contact me on AIM: arcrendition or at hotmail at the same name.*
    *I am not your doctor and therefor can only make suggestions and present theories which should be properly considered and evaluated by your own Licensed Physician.

  12. ArcRendition

    I understand your reservations regarding the comments I left, especially that of Deplin. But I have no affiliation with the manufacturers of Deplin, its marketing firms, distribution, general sale, or promotion of.
    I’m just a pharmacologically inclined individual who happens to take L-methylfolate. As a reflection with my daily struggle with GAD and depression, it would be a disservice to hear about someone’s battle with depression and not offer potentially life changing information based on both pharmacodynamic empiricism as well as my own anecdotal success with L-methylfolate. I know what I wrote looked suspiciously like a promotion, but I wanted to make sure anyone with an AD resistance had accurate and precise information regarding L-methylfolate and the brand name supplement in which in can be prescribed. So I do apologize for the manner in which the information was presented however your own follow-up statement validates an unfortunate truth about depression and patients who do not adequately respond to traditional antidepressant therapies and an alarming number of physicians who are unaware of the beneficial effects of L-methylfolate supplementation in SSRI/SNRI resistant patients who might concurrently have a partial or entire inability to metabolize Folic Acid. Patients that experience low Folate plasma levels and/or AD resistance are highly correlated to numerous possible etiologies of which include, but not limited to polymorphism of MTHFR. That is to say polymorphism of MTHFR is not the only etiology that should be investigated when a patient suffers from low Folate or AD resistance. As to the efficacy of properly diagnosed patients, L-methylfolate shows a significant improvement in efficacy over placebo in controlled double-blind studies. I should also mention that it is intended to be used as an augmentation to an antidepressant regimen and NOT a substitute for professional advised therapy. Like I said though, it helps me everyday, and I feel strongly about the epidemic of depression and the manner in which clinicians address it without first investigating addressable deficiencies at the root of some patients depression. Although the problem is, the etiology of chemical imbalance that is the cause of depression is not fully understood, but the relationship between folic-acid, L-methylfolate and it’s connection with trimonomine neurotransmitters in one facet of the issue that is undeniable; thus why I am such an advocate and wish to spread the word so to speak. Please don’t interpret this passage as psychiatric criticism as I owe my existence to the doctor in my life, but ironically I was the one who introduced him to the Polymorphism of MTHFR and Deplin! I appreciate you letting me post this as I hope it helps someone on in need.*
    *I am not your doctor and therefor can only make suggestions and present theories which should be properly considered and evaluated by your own Licensed Physician.

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