Since taking this stuff I have only had one bout of dystonia...and that wass on the day I ran out. I normally have excrutiating pain with dystonia for at least nhalf an hour every morning,about 10 minutes after waking...and late at night...and that lasts about the same. To be free of just one symptom os great by me.
Hugs and kisses galore to the person who lightbulbed this .thank you
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So glad to hear that news

Very interesting discussion about dextromethorphan. My husband has been taking 4.5 mg of LDN (low dose naltrexone) for his PD for a couple years now (along with a couple 25/100 car/lev, 5 mg selegeline, and various supplements). We are wondering if there could be further beneficial effect from taking the dextromethorphan while taking the LDN or is it one or the other, but not both, because they have possibly similar modes of action?? Anyone have any thoughts?

in my opinion, Kathie. The published work on DM and suppression of inflammation in animal studies shows that dextromethorphan and naltrexone have the same effect at the same, very low, concentrations. Using both at the same time could result in a total concentration of the two that would be less effective than either one alone.
There is apparently something very unusual about the way this class of drugs produce this anti-inflammatory effect, and keeping the total dose in that 4.5 to 7.5 mg range may be critical to whatever efficacy they may have, i.e., more may not be better.

Robert

I have read a lot on LDN and dextromethorphan being used to slow progression of neurological diseases. Not that I understand it all but there seems to be a difference of opinion between the Dr. Bihari people and the NIH group on how these opioid antagonists work. The NIH group seems to believe these drugs work by suppressing neuroinflammation caused by over activated microglial (killer) cells which destroy dopamine producing neurons. In any event, they all seem to believe that these drugs work at very low doses. The research doctor in the email below says not to exceed 10mg a day on naltrexone. If we assume DM and LDN dosages are equivalent, to combine LDN and DM at a combined dose below 10mg may not be risky but no one knows. From what I've seen here, DM seems to have the added benefit of reducing PD symptoms by boosting dopamine production. Maybe LDN has the same effect but there are so few taking LDN for PD, I've never seen that mentioned as a plus.
It seems the drug companies are doing a lot of research on very expensive new drug thearpies that we may or may not see anytime soon. It's a shame that they don't pick up on old established drugs like DM and naltrexone and look at the the work that has come out of Dr. Hong's group at the NIH.
Ashley

Below is an email exchange with one of the developers of LDN. I don't know if it's appropriate to name him, so I guess I shouldn't:
Jan 06
If I could ask you, do you accept the basic claims of Dr. Bihari on the method of action and (probable) effectiveness of LDN?

Response: Low dose naltrexone may have a variety of actions. One certainly is that it works through the Opioid Growth Factor (OGF)- OGF receptor (OGFr) axis. OGF is an inhibitory growth peptide that appears to stablize cells/tissues. This can occur in tissue culture (cells are grown outside the body) and in animals/humans. When we discovered all of this about 25 years ago, the basis for the action naltrexone at low doses is that it acts for 6-8 hours. During this time the naltrexone does not allow the enkephalins/endorphins (opioids) of the body to interact with the opioid receptors on cells/tissues. The cells/tissues compensate for the deprivation of natural endorphins/enkephalins by making more of these opioids, and also making more opioid receptors. Now the trick - if you only block with naltrexone for 6-8 hours, for the remaining 18 hours or so you have high levels of opioids interacting with the opioid receptors and you get a supersensitive reaction. OGF is probably the best example of how naltrexone does its thing. OGF can repress cells, but most probably has effects on the immune system under in vivo (entire animal/human) situations.

Would you recommend LDN to a friend if they had a disease in which LDN could stop progression?
Response: The only legitimate study that I have (we are talking about statistics, etc) for low dose naltrexone is one that I know about - this is concerning Crohn's disease. And even this is a preliminary report. The internet is filled with claims about LDN - including some from doctors. Please be aware that science is not serving as underpinnings for these claims.

Now, in saying this, please let me say that LDN has many potentially terrific effects. But all of this should be done under a physician's supervision. Take the LDN once a day - in our patent on this we recommended dosages of 3-10 mg of naltrexone/daily. I believe many now are using 4.5 mg/day - that is fine and was derived from our claims. Do not take this more than once a day. Do not take this if you are using opioid-based pain medications. Have a doctor examine the patient prior to beginning medication, making special assessment of the signs/symptoms that you want to treat. Have a follow-up visit in one month, and again in the 2nd month. Compare the outcomes to the original data. If nothing changes - or things decline - try a new medication.

I've viewed your many publications (not that I can really understand them) and noticed that most of your work now is in Opioid Growth Factor. Is that in any way related to how LDN works? Have you given up on naltrexone (LDN) as a disease treatment?
Response: Our discovery of LDN (we call it intermittent opioid receptor blockade) was made in a serendipity fashion, while looking for agents to alter growth (e.g., cancer, development). In actuality, LDN is really not doing anything to growth/biological activity. It is really interrupting the body with its natural chemicals - the enkephalins/endorphins. Therefore, our mission has to identify the precise opioid in the body that influences biological activities - this is methionine enkephalin - what is called opioid growth factor (OGF) to distinguish it from methionine enkephalin's role as a neurotransmitter in the nervous sytem. We then went on to identify the receptor for OGF - this is now called the OGF receptor (OGFr). We then went on to clone and sequence the gene for OGFr - it is one of the 20,000 genes in humans, and we know its chromosomal location. In fact, OGF is now being used in phase II clinical trials (we already passed phase I and have a publication in a journal on this) by our group to treat pancreatic cancer. How the OGF-OGFr axis does its thing - the mechanisms - as well as using this now to help patients, really is our focus.

... but is nevertheless very useful.
Please read this
http://www.continuingeducation.com/p...han/dextro.pdf

I know it's a bit tough for non-scientists, but I think that it's so well written and up to date that just about anybody can gather the pertinent points as it relates to the pharmacology of DM (Dextromethorphan)

Now for my interpretation and comments. DM is a strange duck in it's pharmacology. It is said not to be an opiod mu agonist (narcotic, dependancy, increasingly tolerant so one tends to up the dose to get the same effects); but it either is a low affinity mu, kappa, delta or sigma ligand (the subsets of opioid receptors, that have different modes of action as opioids) because it DOES act like an opioid agonist in many respects. The bodies ability to metabolically "racemize" DM and produce the known opioid mu agonist "Levorphan" (simply, the mirror image of DM, but with totally diffferent action in the body; a narcotic with all the "bugs" associated with a strong narcotic) must be considered in it's overall effects in humans.
What I find interesting and possibly at the heart of what we are observing is that DM is an antagonist to the "Excitatory amino acids" specifically NMDA. When the brain is flooded with excitatory amino acid neurotransmitter release, that is likely the cause of dyskinesia. Antagonizing these neurotransmitters quells their effects and so for PWP it calms us down releasing us from the muscular contractions that are associated with dystonia and dyskinesia. Another good thing is that is develops tolerance apparently very slowly, if at all.
Please take the time to read this article, even if you get bored at times , you will perk up at certain paragraphs.
DM has long been known to cause some pretty spacey trips in the 1000-1300mg range (i mean like a powerful hallucinogen, and by no means "fun" at all).
That it has weak serotonergic reuptake inhibitatory properties shouldn't be a mystery, it appears that DM "hits" a lot of neurotransmitter systems in various ways. Last, since naltrexone is a pure opioid antagonist, I would think that you would simply cancel out the effects of both drugs , cs

How are those of you testing this one doing now?

As far as symptomatic relief, I have become so physically busy with fishing, yard work, and daily chores etc, that it has become impossible to measure syptomatic relief..The good news is that I have been able to what I have set out to do

As far as neuro protection/progression..Its still too early to tell

I personally can can honestly say that my dystonia was somewhat reduced whilst on Dextra thingy ..sorry..can` t write it all.I was taking it in Covonia cough medicine...and decided to stop whilst taking Metatone.The dystonia returned but not as aggressively.I am still just on Metatone,wondering whether I could take both this and the Covonia at the same time.I should,at my last neuro apptment be increasing my ropinarole but decided not to.Instead I am looking to drop one of my daily tablets..not complete doses.I take 8 a day so will start by dropping one for a week or so,then be brave and drop another.
Dextra...doo da...DEFINATELY suppressed the dystonia.
My energy level is fantastic which I put down to the Metatone.
Would appreciate advice as to if I can take them both
Oh...I am also detoxing at the minute.

Sorry./..can` t wade through the lengthy scientific posts so could some brainy person just say YES or NO. I will be happy with "simple"
Suits me to a T
Thank you for bringing this knowledge to light.It has been great to be free of the agony of a twisted foot and lower leg for a while.
I can stand a great deal of pain but dystonia is something else.

x

I asked my GP if I could obtain Dextra.....in a tablet form,hence doing away with the alcohol content.It doesn`t affect me but I know some folk here are intolerant of alcohol in formula`s.I was surprised at his answer...that it is not on the UK drug registry and he thought could be addictive.I haven`t found the cough medicine addictive..but would be interested as to how you guys take it/..Again sorry...can`t go wading through the posts....too much else to do