One thing which I found when I got better and which made me want to write my article from my own research on this disorder was seeing many people, some more qualified than others, stating that they knew THE cause of this and that they had a better approach. The standard treatment for Pyrrole Disorder had been arrived at through decades of clinical research by treating sufferers, and has been observed to be most beneficial to most people. This treatment consists of vitamin B6 in various forms, zinc, and associated micronutrients.
Some less informed of the research would say this treatment is harmful and promote their own instead. The idea that the HPL (Mauve Factor, erroneously known as kryptopyrrole by many) binds to zinc and B6, causing it to be flushed out in the urine, seems to be an old unproven idea. This idea seems to have persisted due to what looks to be the inability so far to get a proper simple scientific explanation of what exactly is happening. It seems that because kryptopyrrole (but not HPL) was observed to bind to zinc and B6 in the laboratory, this was a better explanation than none at all when it comes to describing this to people.
As of yet, there seems to have been no real observation of HPL binding to zinc and B6 in any great amounts in the urine of those with high HPL excretion. This is why this condition is known as a “functional deficiency”, meaning the amounts are still within ‘normal’ ranges even if low, and would not be recognised by most Health professionals as being a real problem. It seems that it really is necessary, for this disorder to be diagnosed, to look at the HPL levels in urine.
Hydroxyhemopyrrolin-2-one (HPL). “One” as in “ketone”.
There are many ideas of what causes elevated HPL. There is no doubt the famed genetic error of heme metabolism which up until recently has been given as a blanket explanation, probably much in the same vein as the binding one. This explanation is unsatisfactory, as HPL now appears to be a metric for oxidative stress. What exactly is that then? Simply put, it would appear that it is anything which increases the efforts of the body to maintain a balance of electrons, or more simply to keep oxidative free radicals in check. This seems to affect brain function most of all.
Anything can do this, including toxins, heavy metals, glucose, injury, illness, and all varieties of life stresses. Of course there are surely genetic predispositions to all of these, which is most probably why it has been observed to run in families with greater emphasis on lighter-skinned peoples. The fact this disorder leads to even poorer stress response and behavioural disorders of various kinds would seem to be setting up a vicious circle which perhaps promotes and perpetuates the emotional and psychological stresses, as in the last sentence.
It would appear that it is this oxidative stress, through means which have yet to be fully explored, which would cause the problems in processing the B6, zinc, and other micronutrients and which causes this disorder as well as causing havoc in the DNA epigenetic markers leading to methylation problems among many others.
One reason for this view is that proteins are prone to degradation by OS. HPL may then likely be a residue of oxidative heme degradation. Enzymes are proteins which play vital roles such as in the function of B6 and zinc in creating neurotransmitters among other metabolites. Previously mentioned low-normal levels of B6 and zinc needing massive supplementation may be explained by the need to increase the activity of related enzymes depleted by OS.
High supplementation is needed to increase concentrations to get the same metabolic effect when enzyme levels are low (C) as with normal enzyme levels (A) otherwise function is impaired (B).
This means the HPL would be just a symptom or marker (but a useful one) to determine the need for additional micronutrients from this oxidative stress, not the cause. The fact that this has been useful so far is a blessing, and would justify the continued naming of this disorder after the “pyrroles” it seems even if it’s just a shorthand for what would be otherwise a cumbersome “B6 and zinc functional deficiency associated with excessive oxidative stress”.
Just what that oxidative stress is actually doing, and how the treatments can be improved, is the reason why it is imperative that funds are allocated for proper study of this issue which is devastatingly important not just for the people who are unfortunate to be its immediate subjects, but the society they live in.
Better Living Through Biochemistry 