Hi Friends, I've been trying to figure out a generic model that explains non-segmental vitiligo. I came up to the following drawing so that I'd like to share with you.
The idea is to better understand the cause/trigger combination, which varies from person to person, in order to improve the individual chance to fight this disease.
This model doesn't consider exceptional causes like Hypothyroidism, Hashimoto disease, Adrenal fatigue, Liver toxicity, Lead contamination, etc.
Please feel free to make a comment.
Replies
Hi!
I think in this model lacks another cause that helps to vitiligo growing up: toxic elements like bad alimentation that contains properties which can be toxic, differents substances such as anesthesia,... I think these differents elements can aid in the oxidation of our system and consequently there are a plus for vitiligo's growing up.Maybe there aren't vitiligo's base, but in my opinion there are concepts that we have to take into account.
I agree. In my informative site (www.vitiligomap.com) I refer to these as exceptional secondary causes.
I'm not sure if they cause NSV (non-segmental vitiligo) or other type of vitiligo.
That's why I didn't consider in the generic NSV model.
Chris,
I've been studying NSV only. But the model theory is based on the fact that modern life weakens our natural defenses, so that we just need a trigger to start a new disease. A pulse. A severe event.
Once the disease is triggered, a hysteresis effect comes and doesn't let it go back to normal if you just overcome the trigger event. One needs to recover to a certain level "much" better than when it was triggered, to untrigger it.
I think the model applies to many diseases...
Imagine this inside of your system. Tell me if it can cause all of these problems.
My own highlight.
A. fumigatus is a saprotrophic fungus that only becomes pathogenic for very simple biological reasons:
it is present in high concentrations in the atmosphere, it grows faster than any other airborne fungi at 40 degrees C and it can overcome the defence of the host not because it has developed specific systems but because the host colo- nized has a very weak defence immunity. This should direct future studies towards the host rather than the fungus to understand the pathobiology of A. fumigatus.