Psoriasis Is A Hypersensitive Response
You probably never heard this term in relation to psoriasis or any other chronic disease.
I don’t know because in other words I have been mentioning psoriasis being a hypersensitive protective mechanism for years on this blog.
The science acknowledges the “hypersensitive response” exists in plants but why in the heck they don’t consider that there might be a chance that immune system in human body works the same way?
Sorry, I did not tell you what a hypersensitive response is yet.
Hypersensitivity and Psoriasis
Here is an abstract of scientific paper published in 1997.
The hypersensitive response, or HR, is a form of cell death often associated with plant resistance to pathogen infection. Reactive oxygen intermediates and ion fluxes are proximal responses probably required for the HR. Apoptosis as defined in animal systems is, thus far, not a strict paradigm for the HR. The diversity observed in plant cell death morphologies suggests that there may be multiple pathways through which the HR can be triggered. Signals from pathogens appear to interfere with these pathways. HR may play in plants the same role as certain programmed cell deaths in animals with respect to restricting pathogen growth. In addition, the HR could regulate the defense responses of the plant in both local and distant tissues.
And here is an explanation of hypersensitive response as it is described on Wikipedia:
The hypersensitive response (HR) is a mechanism, used by plants, to prevent the spread of infection by microbial pathogens. The HR is characterized by the rapid death of cells in the local region surrounding an infection. The HR serves to restrict the growth and spread of pathogens to other parts of the plant. The HR is analogous to the innate immune system found in animals, and commonly precedes a slower systemic (whole plant) response, which ultimately leads to systemic acquired resistance (SAR).
We shouldn’t go down the molecular biochemistry pathway here…and questioning the biochemical processes behind the fast growth and replacement of skin cells in psoriasis.
That does not make any sense.
I already stated more than 4 years ago that iodine tincture applied to psoriasis plaques ultimately clears up the plaques.
Because iodine is an antiseptic and kills the microbes present on the skin and in the hair follicles (like Malassezia species).
Malassezia yeasts cause chronic recurrent dermatoses like PV, seborrhoeic dermatitis (SD), and Malassezia folliculitis. Recently, it has been proven that they play a role in the pathogenesis of atopic dermatitis and psoriasis, especially in cases involving the scalp.
And here is another scientific paper – Scalp psoriasis: synergy between the Malassezia yeasts and skin irritation due to calcipotriol – that suspected Malassezia yeast to be a possible sensitizer of immune system:
To investigate if there is a synergy between the presence of the Malassezia yeasts and the adverse reaction during treatment of scalp psoriasis with calcipotriol scalp solution, patients were treated with itraconazole to reduce the number of Malassezia yeasts. This study was a double-blind, placebo-controlled parallel group study between oral itraconazole or placebo for 8 weeks in patients with scalp psoriasis. After 2 weeks, calcipotriol scalp solution was applied twice daily for 6 weeks. Altogether 137 patients, 67 in the itraconazole group and 70 in the placebo group, comprised the intention-to-treat population. There were 13 (19.4%) patients with local skin irritation in the itraconazole group compared to 33 (47.1%) in the placebo group (p < 0.001). The skin irritation was significantly lower in patients with a low number of cultured Malassezia yeasts (p = 0.017). Thus, when Malassezia was eliminated or the numbers reduced, the irritation produced by calcipotriol was significantly diminished.
However, the design of this study didn’t eliminate other possible causes of decreased sensitivity to calcipotriol.
So, we can not be 100% sure that itraconazole treatment induced lower numbers of Malassezia yeast is really what decreased the sensitivity to calcipotriol.
It is possible that killing the yeast in the digestive tract or anywhere else in the body decreased the inflammation thus desensitized the inflammatory reaction to dermal application of calcipotriol.
Another possible option is that itraconazole induced inhibition of liver detoxification enzymes (CYP450) attenuated the inflammation.
You know when your body is inflamed your immune system may and usually will react even to slightest immunostimulatory events (ingested food, yeast in the hair follicle, stainless steel – nickel, pollen you breath = asthma…)
You can read more about the inflammation and what causes it in my previous post “Allergy