The Gluten File
"Pyroluria," "Pyrrole Disorder," "Elevated Kryptopyrrole," "High Mauve" and other similar terms are all used to describe variants of the same basic condition most commonly known as Pyroluria. It is not uncommon for those with this condition to have gluten and casein sensitivity. This condition is more prevalent in many of the same populations that we see increased prevalence of gluten sensitivity. It can cause wide ranging symptoms, listed below on the right bar.
Two books that I know of that discuss this condition:
Depression Free, Naturally by Joan Matthews Larsen
The Mood Cure by Julia Ross.
Here are two technical papers that discuss the condition:
For those who appreciate a personal account, here is one woman's story:
Pyroluria and Parasites - A Journey Back to Health
And there is a facebook group:
"Mauve Factor" was once mistaken for kryptopyrrole but is the hydroxylactam of hemopyrrole, hydroxyhemopyrrolin-2-one (HPL). Treatment with nutrients--particularly vitamin B6 and zinc--reduces urinary excretion of HPL and improves diverse neurobehavioral symptoms in subjects with elevated urinary HPL. Heightened HPL excretion classically associates with emotional stress, which in turn is known to associate with oxidative stress. For this review, markers for nutritional status and for oxidative stress were examined in relationship to urinary HPL. In cohorts with mixed diagnoses, 24-hour urinary HPL correlated negatively with vitamin B6 activity and zinc concentration in red cells (P < .0001). Above-normal HPL excretion corresponded to subnormal vitamin B6 activity and subnormal zinc with remarkable consistency. HPL correlated inversely with plasma glutathione and red-cell catalase, and correlated directly with plasma nitric oxide (P < .0001). Thus, besides implying proportionate needs for vitamin B6 and zinc, HPL is a promising biomarker for oxidative stress. HPL is known to cause non-erythroid heme depression, which lowers zinc, increases nitric oxide, and increases oxidative stress. Administration of prednisone reportedly provoked HPL excretion in animals. Since adrenocorticoid (and catecholamine) stress hormones mediate intestinal permeability, urinary HPL examined in relationship to urinary indicans, presumptive marker for intestinal permeability. Urinary HPL associated with higher levels of indicans (P < .0001). Antibiotics reportedly reduce HPL in urine, suggesting an enterobic role in production. Potentially, gut is a reservoir for HPL or its precursor, and stress-related changes in intestinal permeability mediate systemic and urinary concentrations.
So... How does pyroluria relate to gluten sensitivity? Good question.
In our case, we found gluten sensitivity before we found pyroluria, but that was just happenstance. However, it did not go unnoticed by me that the groups more likely to have pyroluria (Autism, ADHD, Alcoholism, Bipolar Disorder, Depression, Dyslexia, Schizophrenia) were the same groups at higher risk for gluten sensitivity (and in some cases celiac disease).
What the exact relationship is, I don't know. Does underlying pyroluria contribute to gluten/casein sensitivity or does underlying food sensitivity contribute to pyroluria? I haven't heard the answer to that. What are the connecting pieces?
Google zinc deficiency leaky gut together. Google zinc deficiency immune system together.
Does this study tell us anything?
Eur J Intern Med. 2008 Mar;19(2):83-91. Epub 2007 Nov 26
In 1997, a German group demonstrated that the antigen of the biomarker EMA (endomysial antibodies) in coeliac disease is a calcium-dependent thiol enzyme, transglutaminase type 2 (TG2). This most important discovery opened up an exciting field of research aimed at a better understanding of the pathogenesis of coeliac disease, a T-cell-driven autoimmune disorder with a prevalence of about 1%. The accidental activation of TG2, possibly caused by a stress-induced local deficiency of zinc in the intestinal wall, might play a key role where the enzyme catalyzes an atypical deamidation of specific glutamine residues of food gliadins. The genetic contribution is HLA DQ2 or DQ8, which can form a complex with the TG2-modified gliadin residues, resulting in an immune response with the formation of antibodies against both gliadin and the enzyme. Indeed, the immunopathogenesis of coeliac disease can now be recognized partly at the molecular level. Progress has already improved the opportunities for laboratory diagnostics and, hopefully, new ways of treating and preventing coeliac disease will become available. These exciting developments might stimulate research within other fields of autoimmune disorders. With its focus on TG2, this review highlights some of the intriguing mechanisms of the pathogenesis of coeliac disease, such as the structure of the neo-antigen, the involvement of calcium and zinc, and the effects of coeliac antibodies on TG2 activity. Moreover, the many pitfalls due to dubious laboratory practice are addressed, as is the potential when a fundamental biological mechanism is understood at the molecular level.
Higher prevalence among these groups:
Chronic Lyme disease and Pyroluria?
Symptoms may include:
poor tolerance of physical and emotional stress
impaired immune function/ frequent infections
memory problems/ brain fog
sensitivity to light, noise, and tactile sensitivities
irritability/ explosive anger
intolerance to some protein foods, drugs or alcohol
cold hands and feet
lack of regular periods in females
impotence in males
stretch marks in skin
poor dream recall
For labs outside the US, see the Nutritional Healing site.
Treatment is centered on zinc and B6 supplements
together with omega-6 essential fatty acids and other supportive
supplements. The dosages must be titrated to individual
requirements overseen by a doctor knowledgeable about this condition.