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Senior Member
United Kingdom
I found out a few months ago that dextro naltrexone is available privately from a Scottish pharmacy. I read in the article on health rising that dextro is way better than ldn as it acts directly instead of indirectly.

Some info on dextro naltrexone:


1. Antagonist effect at Toll-like receptors (TLR)
2. TLR-4 receptors exist on microglial cells, other macrophages, mast cells
3. Activated microglial cells produce proinflammatory cytokines, substance P, nitric oxide
4. Inhibition leads to a decreased proinflammatory cascade

From Corts article:


(For some reason the site won't let me choose qoute to wrap this in)

Younger’s studies basically started the LDN fibromyalgia craze. He gloomed onto LDN in the same way he’s did with dextromethorphan and the botanicals he’s been testing – by painstakingly searching through the medical literature to look for anything that might tamp down neuroinflammation.

Dextro-naltrexone may be better than LDN at taming the microglia.

Now he’s focused on a different form of naltrexone called dextro-naltrexone. (There are at least three forms of naltrexone; the higher dose form used to treat opioid addiction; the lower dose form used in FM, ME/CFS and other diseases to reduce pain and neuroinflammation and dextro-naltrexone – a different form of the drug altogether.

Both naltrexone and dextro-naltrexone block the TLR4 receptors from activating the microglia. Dextro-naltrexone probably never made to commercial development because naltrexone was first conceived as an anti-abuse opioid drug. Naltrexone’s ability to interact with the opioid receptors made it an enticing possibility for an anti-opioid drug.

When it became clear that low dose naltrexone causes an increase in an endogenous opioid called the opioid growth factor (OGF, [Met5]-enkephalin) and other parts of the opioid system the stage was set for LDN’s introduction as an anti-pain drug.

Younger always thought, though, that LDN’s usefulness in FM/ME/CFS is due to its ability to calm the microglia – not it’s interaction with the opioid receptors.

Plus LDN’s interaction with the opioid system may, however, have come with a cost. LDN”s interaction with opioid receptors may be causing side-effects and limiting the dose and therefore the effectiveness of the drug in FM and ME/CFS.

Enter dextro-naltrexone. It has the same potent microglia inhibiting properties as LDN but without the opioid hit.

Dextro-naltrexone presents the decidedly enticing possibility of being able to use a potent microglial inhibiting in far higher doses than is possible with LDN. We won’t know until the trial is finished but that should translate into more microglia suppression, greater pain suppression and more people who tolerate the drug.

Plus unlike LDN which cannot be used with opioids, dextro-naltrexone should be able to be used with them and might even – by removing the TL4R activation problem – remove the side-effects often found with opioid pain-killer’s. (Studies also suggest dextro-naltrexone might also be able to ameliorate the side-effects of stimulants.)


Senior Member
Promising research for those CFS/ME patients with fibromyalgia. But I guess for the others, LDN is the straightforward option for now because it has a larger evidence base, wider availability, and trust and experience from physicians. The opioid interaction is completely overrated anyways. The effect of LDN on opioid receptors manifests differently to the one known from normal doses of Naltrexone for the use of opioid addiction (10.1007/s10067-014-2517-2).

By the way, here is an article discussing Dextro-Naltrexone as well for the treatment of CFS/ME.
Chronic Fatigue Syndrome: Naltrexone as an Alternative Treatment

From their discussion:
The concept of having a paradoxical hyperalgesia effect produced at significantly reduced doses of medications has been demonstrated before. The most notable example is that of morphine. The hyperalgesia effect can be seen at roughly one-tenth of the dose than that would typically produce reduced pain. This suggests that there is a small window at which opioid analgesics produce the opposite effects than those typically expected.12 Therefore, this same principle may explain the effects as seen with the hyperalgesia nature of greatly reduced doses of naltrexone.