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 Post subject: LDN & Suboxone together
PostPosted: Sun Feb 25, 2018 4:18 pm 
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Not sure if this is the right forum topic, please move it (moderators) if you feel another place would be better.

I consider my suboxone doctor, "Dr.R", pretty advanced and well-educated in his understanding of addiction and the brain. Like Dr. Junig he believes in patient education and is super compassionate. To keep this clear & short I need to write in sections. As the title suggests this is about the use of Suboxone and Low Dose Naltrexone (LDN) concurrently. A lot of web sites warn people to wait for all opiates to clear their system before taking LDN in order to avoid precipitated withdrwawal. However I've noticed that some places are suggesting the use of LDN along with opiates in order to increase their efficacy. Where I've noticed a lot of "misiniformation" is the use of LDN with the mainteinance opiates, methadone and suboxone, on public forums. People here are writing about their experience or thoughts about using LDN for PAWS and thinking it impossible to use LDN concurrently with suboxone. There is 1 study which I have found, which I will try to link, which is about the use of LDN to get people over from Suboxone to vivotril and which my Dr. D said he thought was a bit brutal in how fast they did it. Other than that there are no studies on the use of a mainteinance opiate concurrently with LDN. Like I said there are many studies on the use of opiates and LDN to highten analgesia... actually there is 1 pharmaceutical designed with this in mind, here's the most current info I could find on "oxytrex" quicly:

https://www.centerwatch.com/drug-inform ... x?CatID=19

Oof I didn't mean to write so much already, but I felt that just for people to understand where I'm coming from I felt it necessary to emphasive the lack of reserach and zero first-person reports available online.

Where it gets interesting is that my addiction doctor, Dr.D, has used LDN to get people off suboxone. His theory is that LDN modulates the stress response by decreasing coritsol levels in the blood (briefly), which helps people better tolerate the discomfort from decreasing/getting off suboxone. The hows and why's are super interesting, and I'll post my account here of it.

LDN has a wide variety of uses. I guess I can ramble forever my own knowledge, but it's best you just do some searcing yourself.
///////////////////


Last edited by beautifuldreams on Mon Feb 26, 2018 10:49 pm, edited 1 time in total.

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PostPosted: Sun Feb 25, 2018 4:44 pm 
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I am not aware that Oxytrex ever came to market?
Any full agonist/naltrexone combinations currently on the market are designed as diversion/misuse formulations so when used properly the naltrexone is not absorbed.
Do you get the benefit of LDN if you swallow the saliva when done dosing with Suboxone? Seems like it should be in the range of what most people are discussing.
How does your doctor prescribe it and what compounding pharmacy are they using? Perhaps you could persuade them to post or allow you to post whatever information they give out at the office?
This is NOT presented as part of the 8 hour waiver course nor have I seen it in numerous presentations since I took the course, so I find the approach intriguing.


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PostPosted: Sun Feb 25, 2018 5:23 pm 
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I wrote a long description here. It's way too rambling even for me to reread. I will edit it. Sorry for whoever might have read it and might be responding. I will go back and edit it today or tomorrow. Or divide it into a few posts.

Thanks for understanding.


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PostPosted: Sun Feb 25, 2018 8:01 pm 
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I had to delete this because I feel it had too much personal info as well, so sorry! I don't have the time right now to go back and edit this post for now which is why I've removed it and will go back and edit it later. I'm probably overly paranoid! It mainly contained the science which you can find online.

THis is an excerpt describing LDN's paradoxical property taken from a Stanford University paper published in 2014 (although this property has been known for much longer I wanted to find an explanation of it from a respectable source)

https://www.ncbi.nlm.nih.gov/pmc/articl ... po=12.8571

Why a low dosage?
Successful treatment of chronic pain with naltrexone may require low dosages. Theoretically, a complete blockade of endogenous opioid systems would not be a desirable outcome with a chronic pain patient. Basic science evidence supports that concept by showing that low- and high-dose opioid antagonists have quite different impacts on the physiologic system [43].

It may initially seem strange that a medication can have an opposite effect when given at a low dosage. However, there is a strong precedent for this concept—and with opioid-related drugs in particular. A paradoxical hyperalgesic effect of low-dose morphine was first widely reported in 1987 [44]. Morphine was administered via the IV route to rats after arthritis was induced using Freund’s adjuvant. A dose of 100 μg/kg produced clear analgesia, 50 μg/kg produced less significant analgesia, and 30 μg/kg showed no difference from saline. At around 10 μg/kg, however, the researchers saw the development of morphine hyperalgesia, which became most pronounced at 6 μg/kg. This finding, which has been replicated several times (e.g., [45]), suggests that there is a small window at which opioid analgesics produce the opposite effects than those typically expected. The dosage of morphine that appears to cause paradoxical hyperalgesia is approximately 1/10th of the dosage typically used to produce analgesia. We note that the dosage of naltrexone that is used to reduce pain is also approximately 1/10th of the dosage used for substance abuse treatment.


Last edited by beautifuldreams on Mon Feb 26, 2018 10:48 pm, edited 1 time in total.

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PostPosted: Sun Feb 25, 2018 9:00 pm 
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I have done no research in this area of pharmacology so I can be of no help. Thank you, though, for delving into it and providing some research that is available. Like Dr. Junig, I don't think that a study that isn't double blind is real evidence, but I haven't followed any of your links. I have too many other things crowding my head! Lol!

I think that your doctor is awesome for trying new things to help his patients. After all, every single suboxone doctor who took the 8 hour course and got their DEA waiver, has adjusted the methods for prescribing, dosing, and tapering after receiving feedback from patients for whom the original Reckitt Benkheiser recommendations didn't work, or could work better. I think that it's good for doctors to try some careful and safe experiments based on their knowledge and experience, as long as the patient is aware of the changes.

What we don't want, is for anyone to copycat what your doctor is trying without the benefit of being a doctor themselves. In other words, it wouldn't be appropriate for anyone on this forum to suggest a course of action involving LDN and suboxone. Even if someone has a protocol that has worked for him/her, we would not want the promotion of a new method of tapering here, unless it has been thoroughly and properly vetted scientifically first.

That being said, we appreciate that you are willing to share your experience with us! If you would omit the exact dosages or protocol, we would appreciate it. At least until I can run it by the other mods and Dr. J. Thanks!

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PostPosted: Mon Feb 26, 2018 3:31 pm 
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Quote:
LDN not only helps with chronic pain but with regulating the immune system, and also with depression and anxiety. There are no FDA approved trials on LDN though!!! The first time I took it I felt like my brain had been 'turned on" and my personality started coming through again. I was laughing and making jokes and experienced an overall sense of well0being. I took it for 2 months, and deciced to stop because I had some pressing health issues that needed to be addressed and I didn't want LDN to be a possible negative influencer.. Even though there are few side effects from it... I wish I hadn't stopped it but I freaked out and stopped all supplements


Yep, I had an almost identical experience. Then, I tried suboxone and I consider it one of the biggest mistakes of my life. Insidious side effects presented from both Naloxone and bupe, and I had to stop. I am in preparation to start my beloved LDN again.

So much info out there, I wonder if these docs have actually tried it themselves? Not snarky. Genuine question!

Agree, we may not have the exact protocol, but how are we to get there without thinking outside the box. Applause for the docs who have and who are exploring the different combinations. True pioneers in my book.

Remember the difference with LDN: You are not taking another powerful drug, you are prompting your body to heal itself. I would think this could be a valuable ALTERNATIVE for addicts who have made the personal decision to be done with chemicals instead of encouraging prolonged use with suboxone. Don't get me wrong, I believe Sub has its place for sure.

Isn't it worth a consideration for the RIGHT CANDIDATE? I don't expect it the be effective for everyone, but it's not right for no one either.

I've just become aware of using it for withdrawal instead of just PAWS and all the other illnesses. I hope the research continues.


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PostPosted: Mon Feb 26, 2018 3:55 pm 
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Certainly anyone can PM the OP and get more specific information. I am just trying to prevent anyone from being able to blame this forum for a protocol that may not work for them because we know very little about the science behind it.

If Dr. J wants to chime in on this, whatever he says goes. If he thinks that discussing specific dosages, etc, is fine, then I withdraw my request that it not be discussed on this forum. But until then, please refrain from giving more than a general outline of this treatment experiment. Thanks!

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PostPosted: Mon Feb 26, 2018 9:10 pm 
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Just noticed this FASCINATING discussion. I don't have time to read it in detail right now, unfortunately-- but I want to get a couple points out very quickly, and then I'll share more later.

I assume people have seen the NIH Public Access study that I shared recently: http://www.suboxforum.com/ldn.pdf I haven't reviewed the thread closely, but please always try to differentiate between peer-reviewed studies, extrapolations from animal studies, and the worst-- anecdotes or theories of doctors (including me!). I'm not saying that wasn't done here, because I haven't read the thread yet. Just try to do that to keep the discussion as accurate as possible.

Finally, I just noted the comments of Amy, one of our moderators-- and she is spot-on. We cannot have any specific dosing instructions here, so if they are somewhere in the text, please delete them. Just put an 'X' over any number and leave the rest of the text alone. I'll look at things tomorrow night, and if I see them I'll have to delete them or, if written in words, I'll have to remove the post. That would not be good because there appears to be an interesting discussion at hand. Please, take out numbers, and moderators please do so if you are wandering through and have the time.

I've prescribed combinations of agonists and partial agonists (buprenorphine and butorphanol) and found interesting effects, that I believe could revolutionize pain control. I see an easy path to production of a deterrent-proof, addiction-proof narcotic pain reliever. So I'm always interested in agonist/antagonist combinations-- and when I read about the combination of naloxone and oxycodone I saw a connection with what I see with oxycodone combined with buprenorphine.

Remember people, the 'n' is naltrexone, not naloxone. The naloxone in Suboxone is metabolized within an hour, but naltrexone has a much longer half-life (and oral bioavailability).


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PostPosted: Mon Feb 26, 2018 9:43 pm 
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i deleted this because i wrote down too much about the dosage and it was too rambling and i revealed too much personal details. i need to try to be more succint! i'll go back and edit my other posts too since they are too rambly and long.


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PostPosted: Tue Feb 27, 2018 7:53 am 
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Side note:

The docs probably already know this, but the newish FDA approved weight loss drug Contrave is a combo of Wellbutrin and naltrexone. Some of their studies could be of interest with regard to how naltrexone affected the brain, IDK.


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PostPosted: Tue Feb 27, 2018 1:41 pm 
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Per the OP's suggestion I did move this topic into the Freestyle section where it belongs.

Looking at the original link posted I found nothing Suboxone related with it only reporting the use of drugs containing Oxycodone. Why we need this here on a forum for Suboxone therapy I can't say.

We do encourage discussion about new treatments but please be very careful in your wording. As the doctor stated, no dosage numbers or anything related to medical advice unless posted by one of our resident physicians.

Like some others I still have no opinion on LDN therapy yet. Whether or I'll do some research remains to be seen. Why? Because that is not what this forum is about.

Let's just do a wait and see approach with this subject matter.

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PostPosted: Tue Feb 27, 2018 3:20 pm 
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rule62 wrote:
Because that is not what this forum is about.

I don't get it, I thought it was about this:

SuboxForum provides buprenorphine and Suboxone information and is a place for addicts and those who love them to discuss opioid, pain pill, heroin, and other addictions. Join us to discuss your personal reasons to taper off Suboxone or your reasons to stay on Suboxone. Recognizing that opiate dependence is a potentially fatal disease, we respect all effective treatments for opiate dependence, whether or not the treatment includes buprenorphine or Suboxone. We recognize that Suboxone is the first iteration of a new approach to opioid dependence, and we use the forum to stay informed about the latest forms of buprenorphine and other opiate analogs.

I'd like to thank the OP for the information.


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PostPosted: Wed Feb 28, 2018 12:43 am 
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Your point is well taken and it does say that on the first page of this forum. But still, the subject matter walks a fine line and that's why it was moved to Freestyle. This site has never condoned using full agonist opiates as part of a recovery program although it may work with this one. We just need more facts.

This new therapy may be a good one but it still needs more research done. We tend to side with our doctors here for supplying the correct information on new addiction treatments.

Until then, let's hope we get more good studies about this one.

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PostPosted: Wed Feb 28, 2018 2:56 am 
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I'm confused as naltrexone is an opiate antagonist what full agonist are you refering to?


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PostPosted: Wed Feb 28, 2018 5:22 pm 
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The very first post had a link to Oxytrex, oxycodone paired with low dose Naltrexone.


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PostPosted: Wed Feb 28, 2018 8:04 pm 
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Char wrote:

I'd like to thank the OP for the information.


Thank you Char! This does take a lot of time (yikes! much more than I thought! but i think it's worth it) so I appreciate any encouragement/appreciation. Thanks to everyone else too for your feedback! Thanks for mentioning that 1 drug for weightloss, I noticed an ad for it in a magazine because it had naltrexone. I can't remember if it used LDN or ULDN. That's so interesting. Thanks for linking that study Dr. Junig, those are the only types of studies I could find for the use of LDN with a long-term opiate, to use temporarily to help get off suboxone/methadone. I'll try to find this one my Dad e-mailed me where they used LDN to transition people on suboxone (using it simultaneously with suboxone) over to Vivitrol, he asked my Doc about it and he said he thought that the transition from Suboxone to Vivitrol was too fast, or "brutal" lol as he put it. It's sort of the same idea my doctor has (to use LDN to helps suboxone patients transition over to naltrexone and then nothing (or continue naltrexone if the patient wants to). I'll have to ask my doc but I think I'm the first patient using LDN as an adjunct to suboxone (initially started it because of my autoimmune issues). Otherwise he uses it to help patients with getting off but I need to ask. I'm really interested to hear your thoughts on this!

-----------------------------------------------------

I’m not going to post my own dosing protocol (unless Dr. Junig says otherwise) but it’s worth defining what LDN is here by mentioning that LDN “Low Dose Naltrexone” is the use of naltrexone in “low” doses. I think most people take around X mg. The naltrexone pill for addiction comes in X mg. Then there’s ULDN “Ultra Low Dose Naltrexone” which is much lower dosing into the mcg level. I think ULDN is usually taken by people who want to improve the analgesia from their opiate pain medications. Oxytrex has ULDN and oxycodone together since the addition of ULDN makes Oxytrex a better drug for what it’s intended for, analgesia. Thanks for asking Rule61 about that because it made me realze that I just flew into talking about LDN without giving much of an intro. I figured there would be skepticism (as I was) which is why I included Oxytrex for credibility pruposes. Even though the drug isn’t on the market yet I wanted to mention how if a pharmaceutiful company attempted to make a drug from this then there must be something there. Maybe not the best approach lol. Not trying to convince anyone of anything either. Just wanted to inspire some initial curiosity without bogging people in the boring details. The second post with the link to the Stanford University Study and quote below I think offers a pretty good introduction. I hope that anyone who wants to pitch in about opiate antagonists, LDN, and the science behind it does so, I’ll try my best to include info from sources or links or share my own knowledge and try to source it as mine whenever possible.

I want to keep an experience log for no other reason than to shed light on my experience because there are no experiences online on the use of LDN with Suboxone. Not trying to be antagonistic (pun intended lol) or inspire a debate here. This is time consuming but if it helps anyone then awesome! Having looked through the “suobxone and mood” area and noticing people talk about suboxone plus other medications(antidepressants) I think it should go there rather than “freestyle”. Here’s why I’m taking it:

..................while on suboxone (currently)..............................
-autoimmune disease reduction of antibodies
-to help my ADD symptoms (apparently it's good for ADD/focus)
-help with depression and anxiety "mood" (whether or not related to suboxone)
-help with possible suboxone side-effects [color=#BF0080]++++++I'm going to include another post below that I wrote a couple days ago to explain this "mood" better+++++

......................................to help get off suboxone.........................
to aid in tapering off suboxone when i am ready to get off suboxone, using LDN to mitigate the stress response of decreasing suboxone levels in blood. like i mentioned at some point i will switch to nalrexone
-------------------------------after I no longer take suboxone....................
-to aid with PAWS (once off the subs)
-to aid with addiction (once off the subs, apparently LDN also also helps with addictive urges?)[/color]

I wrote this yesterday but had to change the dosages since I had included them. It’s a bit rambling, sorry!

Description:
I've been on suboxone for 4.5 years averaging 2-8mg/day. Since November, December, and January I've been on 2mg. At the end of January I had surgery and went back up to 4mg suboxone.

2 weeks ago I started LDN1. A week ago I doubled the LDN (I’ll call this LDN2). Hope it’s ok to mention the increase in amount of LDN? That way I can more easily refer to my dosage and know myself which one I’m talking about? Also, if anyone wants to know how much LDN I’m actually taking they can PM and calculate it by just multiplying it by the number at the end of LDN by the number I give them? Otherwise, it will be impossible to share unless I give a log, but then they won’t know what Im’ referring to here in the actual description. Also, it helps me talk about my current LDN dosage without saying “the one I took 2 weeks ago” and lets people know at least the proportions? Not to mention for my own reference it’s nice to know, that way I don’t have to keep a separate one on MSWord and fill it in each time. If this an issue just X it out or I can do it myself when I see the response. It’s just less work to “swap” it now than delete it and fill it in later once I get the OK. Anyone who wants to try LDN and PM’s me for my dosing needs to understand LDN doesn’t work like that although it will be helpful since they won’t have anywhere to look at. The dosing for LDN is different for each condition not to mention individual brain. In addition, my doc doesn’t have a “strict” way of using it, but a “lets see approach, this is what’s worked generally on my patients”. It’s extremely individualized that way. My Doc has used it more with suboxone tapering, not suboxone mainteinance (from what I understand) so I’m kind of a guinea pig for him too. Right now I’m using the LDN concurrently with suboxone and am not actively looking to get off of it (in my opinion for myself I can start considering if I want to when I am stabilized at 2mgsuboxnoe) just decrease my dosage and other reasons I mentioned. With LDN everything is about dosing (time, amount), so it would be a shame to leave it out. If it’s an issue maybe I can just use the numbers to refer to which dosage increase instead of the actual proportion? Then if someone wants it they can just PM for what each number refers to? So LDN3 would be dosage increase number 3?

Friday, February 23rd I started 3mg suboxone.
Currently taking the LDN2 at night on an empty stomach. Taking 1mg suboxone when I wake up (strips, so half a strip) and 2mg mid-day.

I am not having severe withdrawals when I wake up in the morning. The intermittent withdrwals for me begin at 2mg, and once I stabalize on 2mg they are almost non-existent. Back when I was on 2mg (after being on 2mg for 2 months my interdose withdrawal were virtually non-existant) and I started the LDN1 I had no interdose withdrwawals. I did experience them when I started the LDN2. It kinda sucked because I had the slight runs, sneezy, not feeeling well, and the annoying "need" to take the suboxone to get my day started. At the time I was taking 2mg subs, and would take the entire 2mg in the am. It's my 3rd day on 3mg subs, and I am not having bad withdrawal in the morning... actually just the shivers. Based on my last LDN trial (and only previous trial to date) I expect my morning interdose withdrawal to return once I get to 2mg. Interestingly enough, my suboxone doctor (who also prescribes the LDN... like I said he's the one who uses LDN to help people get off suboxone more smoothly) predicted that not only would I risk "feeling" my suboxone more when dosing by takig such a high dose of suboxone (4mg) concurrently with LDN, but that I would have more withdrawal in the morning. Neither have occured. It is an unfortunate truth that for some people they can "feel" their suboxone. For me this is DEFINITELY not a euphoria, perhaps a mood-lift at times, it's just a physical sensation of having increasing opiate levels. My pupils sometimes even get smaller. But nothing to write home about. This “euphoria” effect, which my doc is aware happens in me, was actually non-existant when I was on 2mg subs and LDN2.
Now on 3mg subs and LDN2 I'm feeling the "normal" opiate-effect that I get when I take subxoone (I think I have a very fast metabolism and am very sensitive to drugs which makes me one of those who fortuantely/unfortunately "feels" their meds). I only mention this out of interest/curiosity. The difference with 4mg and 3mg is very little in terms of interdose withdrwal,

Since back when I was one 2mg subs and LDN2 the morning withdrawal sucked (though worht the mental effects!) so we will be trying a different dosing strategy this time. I'm taking 1mg suboxone in the AM just to "fill" my receptors (get myself out of whatever withdrawal) so I can eat comofortably and the rest of my dose in the midday of 2mg.

Afterwards I will go down on the suboxone to 2.5mg by taking 1mg in the morning and 1.5mg in the middy while concorruently LDN2.

Then I will do 1mg subs in the AM and 1mg subs in the Midday, while taking LDN2 in the PM.

I won't increase the LDN till I am down to 2mg suboxone. I have to discuss this with my doc.

OOf I wrote so much more than I thought! I wanted to write more on my experience currently with LDN but breifly here it is (thus far):

Usually when reducing my suboxone (I've only been on 4mg for about 3 weeks) I get a "craving" or uncomfortable sensation for suboxone even though it doesn't get me high. Now when reducing from 4mg to 3mg I'm not really concerning myself with the suboxone. I mean sometimes I'll even obsess over it even when I am fully stabilized. I noticed this happening when taking 2mg subs especially (can't remember if this happened also when I was taking LDN2 during my first trial with LDN).
Other than that I haven't experienced the dramatic mood lift I had the first time when I increased to LDN2 after being on LDN1 for 1 month. Indeed, I actually feel some agitation! But I had the agitation before the LDN which I experienced severly a couple weeks after my surgery. I have a lot of things going on with me right now, my body getting used to a synthetic hormone after a surgery, and also taking 3mg suboxone when before I was taking less. I feel much better mentally when taking less suboxone, espeically starting at 2mg the cognitive fog really improves. But I really don't want the morning withdrawals that I had when taking 2mg of suboxone and LDn2. I'm hoping that together with my suboxone Doc that we can come up with a plan to prevent this level of discomfort. I'm thinking that doing LDN2 in the evening (maintaining the same dosing in other words LDN-wise) but doing 1mg suboxone in the AM and 1mg subxoone in the PM will mitigate that morning withdrawal. Perhaps having higher sub levels at night while I also take the LDN will help the morning withdrawal. Instead of having the LDN "Ride the back" of my suboxone dosing as I did last time. DOes this make any sense?? I'm sorry if it doesnt. Please let me know if you want me to clarify.

I will go back and edit. And keep updating with my experiences. Sorry for the discursive raambling style here.

Anyways, I think it's interesting because one would think that the higher dose of suboxone one is one the more of a withdrawal one will get when taking LDN. In my case this is not true. Taking 3mg of suboxone results in less of withdrawals from LDN2 than 2mg of suboxone. I suppose the suboxone is so strong that it "covers" your receptors well enough to keep the LND from really penetrating through? Who the hell knows! Then again, I'm SURE that if someone is one .5mg buprenorphine and another someone on 8mg suboxone daily were to take X mg naltrexone that the one on 8mg suboxone would suffer MUCH greater withdrawals from the X mg naltrexone. But if you give them LDN2 the one taking .5mg buprenorphine daily will suffer more than the one taking 8mg suboxone.

Ok, now I'm just conjecturing!

Thank you everyone!!

+++++++++++++++I wrote this a couple days ago, sorry it may not be the clearest, I'll try to edit it when I can+++++++++++++++++++++++++++++++++++++++++

I hope this doesn't offend anyone as I know that some people get annoyed when people lay blame on suboxone for mood/cognitive issues but personally suboxone makes me feel a bit numb, artistically mute, but that's MY personal experience, and last time i was on LDN after 1 month it really "woke" my brain up. And I'm quite sure it's suboxone related. If this side-effect (that I'm sure other suboxone patients experience as well) can be alleviated if not eradicated as a side-effect (that shouldn't be the reason people want to stop suboxone) then i feel LDN can actually help with keeping people on opiate maintenance medication by mitigating unwanted side effects! stopping should always be because one is ready to stop! my doctor is constantly warning me about the dangers of quitting suboxone but he recognizes that when I'm ready he'll help me with that. Stopping should always be because one is ready to stop! not because of side-effects! these side-effects are better than the risk of death/overdose/incarceration anyday! Perhaps, just maybe, if suboxone helps patients who experience these possibly suboxone-related side-effects, then maybe those patients will stop wanting to "get off suboxone". If it indeed does improve their emotional range then these patients won't be wanting to get off suboxone anymore and instead have more energy to focus on recovery while on suboxone in addition to improved mood. There are some drugs designed specifically to alleviate drug-related side-effects (ok, i'm off on a tangent, sorry, can't resist, what about the hilarious-named condition "Opiate Induced Constipation" that sounds like "Oh I See" when you say the acronym? This one the pharmaceutical industry got right!! hahahaha. pretty sure they created it just to sell the drug "Symproic" (I'm not going to link it or I'll really confuse people but it is an opiate antagonist!). Buprenorphine affects everyone differently. For some it works as an antidepressant! Apparently even some people have used it for that reason, off-label. Personally I think it's made my emotions more "level". On suboxone my mood is more “level”. I feel that the highs and lows are never quite so high or low. Also the intermediate emotions are less intense. Since I got on suboxone my mood has been EXTRAORDINARILY level. Also, it helps my anxiety TREMENDOUSLY!! Not sure I could have achieved and done some of the things I have without the anxiety squelching properties of suboxone. However, my appreciation for art has been squelched I feel. I am also content with being alone, like a hermit and have to “force” myself to socialize. Not sure if that unsociability is related to the emotionally muting-effects of suboxone. I will elaborate on this more later but when I did my first trial with LDN I felt this “muting” effect lessen tremendously! Like I said, it’s like my brain “turned-on”. Sometimes before I take my dose I will feel emotional, like my brain is “free” to go where it wants, and will cry much easier and can if I let myself, I also find things funnier and can laugh easily. My sense of empathy feel greater as I feel this connection to things. And that is why I think perhaps I don’t have such a need to “socialize” while on suboxone? Because it decreases my need for connection? What’s the point when the “reward” of socializing isn’t as strong. I’m 30 and since I’ve been on subxoone, for 5 years, except for recently I finally had one!, I haven’t had a single boyfriend or sexual experience or even wanted a boyfriend or needed one. Prior to being on subxoone if I didn’t have a bf I was actively seeking and wanting one (except for the 1 year I was using prior to being on suboxone). Although I did find 1 guy recently to whom I was attracted to and felt something for (unfortunately due to logistical reasons I broke it off… sigh… after 5 years you start to wonder if there’s something wrong with you when during the sexual prime of your life you have little to no desire for a relationship or sex and that experience helped disprove that!! oops sorry if TMI). He once said when we were in an argument that I seemed “dead” and like I had no soul. This was so bizarre to me because I’m the “funny, crazily creative and spontaneous, unpredictable” … at least that’s how I identified myself for the longest time. Perhaps it’s aging, perhaps my autoimmune illness, perhaps suboxone? Certainly the depths of these “numb” feelings aren’t all due to suboxone but depression.

I get the kind of depression that is energyless, tired, no appetite, and blah as opposed to the one that is negative and anxiety-ridden and like everything is black (though I experienced it in my teens). For this kind of depression (my type, the “blah” curse I feel…) LDN is especially good for, I read in the book, “The LDN Book” by Linda Elsegood that LDN is great for my kind of depression, which is though to be induced by a lack of opiates or something. Which makes sense, because the first time I ever took Vicodin I will NEVER forget the feeling, moment, time of day. I was walking so I didn’t feel the body high, but mentally I suddenly felt “all is alright with the world”. Not wow! I feel High!! Just a sense that “I am OK, this is OK, the world is a FINE place to be in”…. of course, then when I made it to my dorm room and laid down I was HIT by the euphoria... and I was no longer a “cucumber” (but a pickle! I shouldn’t laugh but couldn’t help it with the cucumber to pickle metaphor we’ve all head in IOP) Anyways, for people like me antidepressants don’t work as well because what they needs is something to work on their opiate receptors. Right before I take my suboxone I theorize that my receptors are more “open”, which is why I am more emotional, things have this exhilarating feel to them so it’s not a negative thing entirely. Then afterwards it’s like the lights in my brain “turn off”. This sounds so horrible!! And I’m not going to lie, it does make me sad. I’m not blaming it on suboxone, but saying that I’m quite sure that it has “some” play in this. And when I took the LDN I was for the first time in years, laughing daily and finding things funny but without that “mania” or “obnoxious feel-goodness” that positive feelings can bring. I just felt this sense of stability and most of all SENSE OF WELLBEING unlike ANY drug. Because like Char said, LDN “helps the brain heal itself” (not sure if that’s exactly how it works, but this description is spot on I think). to illustrate… it helps to modulate the immune system, in other words helps YOUR immune system “modulate” itself… and you have to find the “right” dose for your body. My point is, if you’re one of those who may have the emotional blunting effect from suboxone and if LDN can help alleviate if not ERADICATE it, then this is a method to help people stay on suboxone and aid them in their recovery! Suboxone has perhaps saved my life. Definitely kept me from turning into an IV user (I’m quite sure!) I live in a town where the opiate epidemic hit REALLY hard and I LITERALLY ONCE HAD SOMEONE ASKE ME AT A PARKING LOT “WHAT DO YOU WANT” took me a few seconds to realize he was asking me if I wanted drugs!! I was coming out of the gym so I wasn’t dressed too nicely and maybe that called his attention, and it wasn’t in the nice part of town. But still, unbelievable!! Nowadays, I would have wanted to punch that asshole for offering me drugs. Had I not been on suboxone at the time (this was 1 year into my suboxnoe) I would have who knows?? Said yes??? Or maybe gone back to that place knowing it was a hot spot for drug deals?? Gives me the chills. Sorry for rambling like this but I feel it so important to explain this! Like I keep saying, I’ll go back and edit this for clarity without removing anything that someone may have directly commented to so as not to get confusing.
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Your post is very dense and I'm not saying that's a bad thing, but there are a couple of numbers that I am going to edit. Even giving people ballpark numbers is not going to work on this forum for the very reasons that Dr. Junig mentions below. LDN is not yet even a theory; it's at the very beginning of being a hypothesis. We have no problem with you and your doctor embarking on an experiment at your own risk, but you may only give general anecdotal evidence, and no suggestion of specific numbers. You will see where I have edited above. -Amy


Last edited by beautifuldreams on Wed Feb 28, 2018 11:07 pm, edited 1 time in total.

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PostPosted: Wed Feb 28, 2018 8:34 pm 
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February 27 & 28:

Both days I took suboxone 3mg (1mg in the am and 2mg at midday).

I forgot to take the LDN the night of the 26th. I had a harder time getting up in the morning (it's like I didn't have that "ooompf") and I found my mind a little foggy. Though I did find my sleep a bit deeper? I didn't think I had less dreams than usual (and because of the LDN2 they're very intense).

Nothing much else to report for now!


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PostPosted: Wed Feb 28, 2018 9:21 pm 
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I suppose I'll comment....

The most frustrating thing about the forum is that sometimes people come and 'talk science', but then talk with terms and claims that nobody involved in research would respect, or even recognize. It is also frustrating when people describe vague symptoms that can't be impeached, because doing so opens the door to accusations of insensitivity, or worse-- something like 'all I know is this is how I feel'. You'll never read THAT in a peer-reviewed publication!

Science progresses very inefficiently, with accuracy far more important than rapidity. Single studies are virtually meaningless. No methods or treatment approaches occur after one study or publication-- not even close. A single article is a drop in an ocean, when it comes to medical science. The opiniions being formed about low dose naltrexone measure up to about two or three drops. But reporters and laypeople (and charlatans like Dr. Oz) live in a world where new things suddenly get invented. It just doesn't work that way. Take the idea of treating opioid addiction with buprenorphine-- where decades of French experience led to several large clinical trials.... all that before the studies that were used for FDA approval. And of course we have FDA resporting for the past 15 years too, all showing that buprenorphine is one of the safest medications prescribed.

But I digress... my point is that nobody knows if ldn does anything at all. Individual stories, I'm sorry, are just not reliable. I suppose that a good placebo effect holds value, but I really hope this forum knows the difference between anecdotes and science, and between placebo and real effects.

Naltrexone is interesting, but nobody has provided any evidence about the effects of a weak antagonist, combined with the much-more-potent antagonist, buprenorphine. Does a weaker antagonist even bind to the mu receptor in a person who has buprenorphine in the vicinity of the receptor? Probably not--- but we just don't know.

And finally, people suggest negative subjective effects from buprenorphine, but don't seem concerned about the hepatotoxicity of naltrexone. The liver damage is dose related, so the pushers of Vivitrol and ldn claim it isn't relevant. But think of this-- how would you feel about buprenorphine, if there was known liver damage from doses twice what you're taking? Would you tolerate that risk? maybe-- but people on naltrexone ignore that risk altogether.

Gotta go--


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PostPosted: Wed Feb 28, 2018 11:17 pm 
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docm2 wrote:
The very first post had a link to Oxytrex, oxycodone paired with low dose Naltrexone.

Ah thankyou i think? that concept confuses me as thought there was an issue with ldn whilst on a full agonist triggering precipitated withdrawl.
I'll stick with straightup oxycodone hold the ldn and consider it after that phase is done.
There is some great personal experience comment re using ldn whilst still on full agonist meds but it emphasizes starting with tiny tiny doses and working up to find the right dose and offcourse if too big a dose precipitated withdrawl is triggered. Too scary for me as i am doing what i am to lessen the pain load.
NB i pressume i cant link a sight that sells ldn as that is where i read the commentary and yes i always have salt at hand for any commentary that might have a vested interest.
None the less very interesting and potentionally important for the millions worldwide ( too many?)


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PostPosted: Thu Mar 01, 2018 10:23 am 
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Quote:
And finally, people suggest negative subjective effects from buprenorphine, but don't seem concerned about the hepatotoxicity of naltrexone. The liver damage is dose related, so the pushers of Vivitrol and ldn claim it isn't relevant. But think of this-- how would you feel about buprenorphine, if there was known liver damage from doses twice what you're taking? Would you tolerate that risk? maybe-- but people on naltrexone ignore that risk altogether.


No, I don't think they ignore it at all. I think they take the time to do the research, and make an informed decision. They also do the math.


Low Dose Naltrexone – Can it hurt the liver?

The FDA Warning for liver when taking very large doses (300 mg) of Naltrexone
& Clinical Trials about it safety in the liver

Unfortunately, the FDA Naltrexone ‘black box’ warning about the possibility of liver issues can be very misleading when investigating Naltrexone or Low Dose Naltrexone because it does not provide the scope or dosage on which the warning is based. The below is information about the Black Box warning – it is based on a clinical study where patients were taking extremely high dosages of Naltrexone (300 mg a day) and a sub-set of obese patients developed some liver anomalies. Additionally, included below are 4 subsequent National Institutes of Health / National Library of Medicine Clinical Studies or Articles that specifically discuss the safety of Naltrexone to the liver, when used below 300 mg a day.

Therefore, according to the below studies, the dosages of Low Dose Naltrexone (LDN), which are a very small fraction of either a regular or high dosage of Naltrexone, could be presumed to have no negative affect of the liver. Note: The normal LDN dosage for adults is 4.5 mg or less per day, which is 1/66th of the maximum safe dosage level. For children the normal dose is between 1 mg (1/300th of the maximum safe dosage) to 3 mg (1/100th of the maximum safe dosage).

Also, the immune modulating affect of the opioid antagonist, Naltrexone, have been shown to improve the liver’s condition, including reducing ALT/AST levels, cholestasis-induced liver injury, liver fibrosis, and hepatitis. Those clinical trails will be posted separately.

The following is an excerpt from the National Institutes of Health/National Library of Medicine/Daily Med Website (http://dailymed.nlm.nih.gov/dailymed/dr ... fm?id=4682)

“Evidence of the hepatotoxic potential of naltrexone is derived primarily from a placebo controlled study in which naltrexone hydrochloride was administered to obese subjects at a dose approximately five-fold that recommended for the blockade of opiate receptors (300 mg per day)..”

*Note: Patients with end-stage liver disease, severe cirrhosis, or in an acute hepatic state, should carefully consider with their doctor which drugs (including LDN) will adversely affect their liver given its extremely distressed state.*

The below four (4) clinical studies are quoted from the National Institutes of Health / National Library of Medicine/Pub Med Website: (http://www.ncbi.nlm.nih.gov/sites/entrez?db=pubmed).

Study 1 –

Study of hepatotoxicity of naltrexone in the treatment of alcoholism.

Alcohol. 2006 Feb;38(2):117-20. Links

Yen MH, Ko HC, Tang FI, Lu RB, Hong JS.
Department of Pharmacology, National Defense Medical Center, Taipei, Taiwan.

Since a black box warning was issued by the Food and Drug Administration regarding the use of the opiate antagonist naltrexone (NTX), many clinicians have been concerned about current labeling of the potential hepatotoxicity risk of NTX in the treatment of opiate dependence and alcoholism. Despite many reports that demonstrated that the use of NTX did not cause elevation of liver enzymes, controversy concerning whether NTX is hepatotoxic continues. The current study monitored 74 alcoholic patients who received 25mg of NTX daily in the first week and then 50mg of NTX daily for the rest of the 12-week period. After the 12-week treatment, levels of the hepatic enzymes alanine aminotransferase (ALT) and aspartate aminotransferase (AST) did not show any elevation, except in one subject, and the results strongly support that NTX did not induce abnormalities in liver function tests or elevate the liver enzymes. Instead, a statistical significance of decreasing levels of ALT and AST in the liver was shown throughout the study. These findings provide further support that NTX is not hepatotoxic at the recommended daily dose and may be beneficial for patients with elevated liver enzymes.

PMID: 16839858 [PubMed – indexed for MEDLINE]

Study 2 –

High-dose naltrexone and liver function safety.

Am J Addict. 1997 Winter;6(1):21-9.Links

Marrazzi MA, Wroblewski JM, Kinzie J, Luby ED.
Department of Psychiatry, Harper-Grace Hospitals, Detroit, MI, USA.

Studies have found naltrexone useful in the treatment of diseases other than opiate addiction in which endogenous opioids presumably play a role, such as alcoholism and eating disorders. Some of these studies involve high doses (100-200 mg bid). Because investigational studies with high doses (300 mg/day) reported clinically significant increases in liver enzyme levels, the authors measured a spectrum of liver function parameters in response to high doses of naltrexone in a double-blind, crossover trial (100 mg bid) followed by an open-label period (200 mg bid). They observed no adverse clinical or laboratory changes in liver function in association with high-dose naltrexone therapy in eating disorders.

PMID: 9097868 [PubMed – indexed for MEDLINE]
Study 3 –

Naltrexone: report of lack of hepatotoxicity in acute viral hepatitis, with a review of the literature.

Addict Biol. 2004 Mar;9(1):81-7. Links

Brewer C, Wong VS.
The Stapleford Centre, London, UK. cbrewer@doctors.net.uk

Many clinicians appear to be concerned about the potential hepatotoxicity of the opiate antagonist naltrexone (NTX) and this may be one reason why it is not used more widely in treating both heroin and alcohol abusers. Some much-quoted early studies noted abnormalities in liver function tests (LFTs) in very obese patients taking high doses, although there was no evidence of clinically significant liver dysfunction. These concerns may be reinforced by advice in the UK product information sheet to perform LFTs before and during treatment, by high infection rates with hepatitis C virus (HCV) among injecting heroin addicts and by the frequency of abnormal LFTs in alcohol abusers. We describe a heroin abuser in whom clinical and laboratory manifestations of acute hepatitis B and C appeared a few days after the insertion of a subcutaneous naltrexone implant. A decision was made not to remove the implant but the hepatitis resolved completely and uneventfully well within the normal time-scale. A review of the literature indicates that even when given at much higher doses than are needed for treating heroin or alcohol abusers, there is no evidence that NTX causes clinically significant liver disease or exacerbates, even at high doses, serious pre-existing liver disease. During the past decade, NTX has been shown to be safe and effective in the treatment of pruritus associated with severe jaundice caused by severe and sometimes life-threatening cirrhosis and other liver diseases. Its safety, even in these extreme conditions, is particularly reassuring. We suggest that it may be more appropriate and economical to advise patients to report promptly any suspected side effects than to perform regular LFTs, which may be misleading.

PMID: 15203443 [PubMed – indexed for MEDLINE]
Study 4 –

Safety of high-dose naltrexone treatment: hepatic transaminase profiles among outpatients.

Clin Neuropharmacol. 2006 Mar-Apr;29(2):77-9. Links

Kim SW, Grant JE, Yoon G, Williams KA, Remmel RP.
Department of Psychiatry, Medical School, University of Minnesota, Minneapolis, 55454-1495, USA. kimxx003@umn.edu

OBJECTIVES: This study was carried out to test the hypothesis that the hepatic safety profile of prolonged high-dose oral naltrexone (150 mg/d) is acceptable if over-the-counter analgesic use is restricted.

METHODS: Data from 41 consecutive outpatients with impulse-control disorder receiving naltrexone therapy were analyzed.

RESULTS: The mean treatment duration was 328 days and the mean naltrexone dose was 142 mg/d. Pretherapy/posttherapy mean aspartate transaminase and alanine transaminase levels in the naltrexone-alone group were 21.79/22.54 and 21.74/21.49 U, respectively (all within reference range).

CONCLUSIONS: Although limited in scope, these findings support the hypothesis that long-term use of high-dose oral naltrexone is safe in otherwise healthy patients with impulse-control disorders who restrict their intake of acetaminophen, aspirin, or nonaspirin nonsteroidal anti-inflammatory drugs (NSAID). However, confirming studies are needed.

PMID: 16614539 [PubMed – indexed for MEDLINE]
https://www.skipspharmacy.com/wplog/pha ... altrexone-–-can-it-hurt-the-liver/


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Fond Du Lac Psychiatry
Dr. Jeffrey Junig, M.D., Ph.D.

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