LDN for Psoriasis: Good Treatment But Still Not a Cure

Low Dose Naltrexone (LDN) is a popular alternative treatment not only for psoriasis. Still the most people do not get it and are clueless about the reasons why and how Naltrexone in low dosages works for so many chronic inflammatory and degenerative diseases.

Many doctors, chiropractors and naturopaths agree that LDN is quite an effective and relatively very safe treatment for many diseases.

Since I am absolutely sure that psoriasis is an Autonomic Nervous System dysfunction rather than autoimmune disease (or some form of immune disease) I do agree that potent drug like Naltrexone may improve or even completely clear up psoriasis.

Naltrexone affects the neurons substantially so there is a chance of improvement of psoriasis.

I say a chance because it is relatively easy to guess the biochemistry outcomes of the immune system compared to guessing the biochemistry outcomes of nervous system.

But what if the secret power of Naltrexone lies somewhere else?

What if it is not about its direct effects on the nervous system?

How does naltrexone exactly contribute to improvement of psoriasis?

One theory is that taking this drug which blocks the opioid receptors makes the brain produce own endorphins because it “thinks” that there is an endorphin deficiency.

But if you think about this theory it sounds kind of weird.

If the opioid receptors were blocked with Naltrexone then what purpose would the endorphins serve?

And are they (endorphins) even anti-inflammatory? Maybe and maybe not!

The researchers found out that one of the endogenous endorphins – beta-endorphin – affected the inflammation differently in two inbred rat strains.[8]

The another group of researchers proved that beta-endorphins in cultured human articular chondrocytes (knee cartilage) increased the levels of two strongly pro-inflammatory messengers: IL-1 Beta and TNF-Alpha.[9]


In order to investigate if beta-endorphins anti-inflammatory effect in cartilage-damaging states is mediated via tumor necrosis factor-alpha (TNF-alpha) and interleukin-1 beta (IL-1 beta), we examined its influence on these two cytokines in vitro. Human articular chondrocytes were obtained from patients undergoing total knee arthroplasty and stimulated with beta-endorphin (60-6000 ng/ml). Protein levels of TNF-alpha and IL-1 beta were measured by ELISA in supernatants from articular chondrocyte cultures. beta-Endorphin significantly increased the levels of IL-1 beta for all concentrations used after 15 min incubation, and when stimulated with 600 and 6000 ng/ml after 24 h incubation. The opioid-induced increase in IL-1 beta was blocked by naltrexone in the group tested. TNF-alpha expression was also significantly stimulated by 60 and 600 ng/ml beta-endorphin after 15 min, an effect blocked by naltrexone in the group tested. These findings indicate that the mechanism of beta-endorphins anti-inflammatory influence in cartilage-damaging states is not apparently mediated via these two cytokines modulation.

Abstract Source: Andjelkov N, Elvenes J, Martin J, Johansen O. Opiate regulation of IL-1beta and TNF-alpha in cultured human articular chondrocytes. Biochem Biophys Res Commun. 2005 Aug 12;333(4):1295-9.


So, maybe the answer is that endorphins are generally pro-inflammatory and it is just our feeling that they should be anti-inflammatory because they attenuate the pain.

They do attenuate the pain but as this study proved, beta-endorphin application increased the nasal congestion which “is mediated through direct neuroendocrine receptor activation independent of mast cell activation and that during the allergic reaction there is a beta-endorphin/mast cell interaction that enhances the mediator response to nasal allergen challenge.” [10]

So, attenuation of pain is not the same thing as elimination of the inflammation.

This is also the case of the opiate king – Morphine.

This drug is strongly pro-inflammatory even though we might get an impression that the exact opposite is true.

It is a well known fact that opiate receptors agonists induce the histamine release as you can see in the picture below where the veins are clearly visible due to morphine induced histamine release.

Author: James Heilman, MD for Wikipedia

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