1. Deborah Barr Deborah Barr United States says:

    Chris Griffiths OBE MD FRCP, are you aware of these two suggested models of different types of psoriasis?

    The first is where there is a slight problem with an excess nutrient (copper has been suggested) where for some genetic reason (such as a minor problem with the ceruplasimin where the gene having set the point at which it scavenges excess copper from the body a bit higher than normal, similar to the wrong zener diode being placed in a circuit, so instead of 5 volts being maintained on one side of it, 5.1 volts are being maintained on one side of it.)

    The excess nutrient can be used up by the body doing more of a process that uses a lot of that nutrient, the way a farm wife before refrigeration would use excess milk to make cheese and extra milk and eggs to make pudding.

    But just as if she could only get rid of the extra pudding by force-feeding the farm workers until they got fat, the body forcing overgrowth of certain cells has side effects.

    Keritanoid cells are supposed to be part of psoriasis overgrowth. If my older medical understanding is still correct, they are high producers of interlukin1, and an excess of interlukin1 would result in immune system disorders, such as psoriatic arthritis.

    Other types of cell overgrowth, possibly correlating with callus psoriasis on feet and fingers, versus the plaque psoriasis might be different cell overgrowth, with different ramifications, but patients with the same type of cell overgrowth should follow a similar pattern, although where the body chooses to aim the excess will vary.

    The other model is a shortage. If keritanoid cells put out more interlukin1, then a body might stimulate the creation of psoriasis to  increase interlukin1, possibly but not necessarily causing a depletion of that same nutrient as was in excess above - due to dietary cravings or genetics having created that higher set point for this very purpose. So two variations, for diagnostic purposes: the healthy and the depleted forms of low interlukin1 psoriasis.

    (As genetic types interbreed, that higher set point might have been inherited without the lower natural amount of interlukin1, creating the first model of psoriasis, above.)

    These two variations of psoriasis can be differentiated by whether their psoriasis infects when scratched. Some people's infects very easily - the low interlukin1 model. The excess nutrient form does not seem to ever infect, as would other causes of keritanoid cell overgrowth not postulated here; I always assume there is an "other," because there almost always is.

    For the first model, if the excess of nutrient, the suggested copper, is being used up through this usage and others, such as the dopamine to norepinephrin conversion, causing anxiety, then the excess of copper would not show on lab tests, the body having sufficiently protected itself from the oxidative and other damages of extra copper.

    What would be demonstrated in the first model could be a large amount of one use of that nutrient via one body function excess, or variable amounts of a variety of body functions that over use that same nutrient, according to genetics, diet, history, and other environmental exposures.

    The second model would include people whose psoriasis developed during a severe illness (or smaller germ exposures when younger, depending on shortage of interlukin1 from other sources, and so many other variables.) This could be tested by injecting extra interlukin1 when the psoriasis starts to develop, when they are ill. The body may or may not keep creating psoriasis out of inertia or "habit" in some people once psoriasis has started.

    These two models would explain why treatment of psoriasis using biologicals cause a risk of illness in some people but less in others.

    The first model would explain how genes can directly cause psoriasis and other conditions, so treatment could be targeted at the root cause instead of a symptom which causes further symptoms up the line, and not only deal with the psoriasis, but potentially other illness which might seem unrelated without this model of dysfunction.

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