This 2008 German research from Muller and Schnakenberg makes a link between Gilbert’s Syndrome and other forms of  hyperbilirubinemia and Environmental Illness.

Gilbert’s syndrome is a relatively common condition occurring in approximately 5% of the population, in which there is a consistently mild elevation in unconjugated bilirubin, “the yellow breakdown product of normal heme catabolism.”  Prior to this, the syndrome was considered completely ‘benign,’ although patients often describe fatigue and abdominal problems to their doctors.  Anecdotal reports have also indicated that a subset of people with Gilbert’s appear to develop Multiple Chemical Sensitivity, Chronic Fatigue Syndrome, and Hypothyroidism.

Having this genetic tendency does not mean you will ever develop Gilbert’s Syndrome in your lifetime.  Having Gilbert’s Syndrome or the other forms of hyperbilirubinemia does not necessarily mean you will develop chemical sensitivity either, but it does indicate an increased susceptibility to chemical sensitivity and environmental illness.

The government of Germany was the first in the world to officially recognized Multiple Chemical Sensitivity as a physiological illness in its National Health Care System and to have the disease classified in the International Classification of Disease, in the World Health Organization (WHO) under ICD -10-GM Code T78.4, in the sections of chapter 19, (injuries, poisoning and certain consequences of toxic causes).  As such, we will probably continue to see interesting research like the work of Muller and Schnakenberg emerging from German universities in the years to come.

Here’s the abstract:

Müller KE, Schnakenberg E (2008) Die Bedeutung der Glukuronidierung bei
umweltmedizinischen Erkrankungen am Beispiel der UDP-Glukuronosyltransferase
Umwelt Medizin Gesellschaft 21(4): 295-300


Glucuronidation represents an important metabolic pathway enhancing the elimination of many lipophilic xenobiotics and endobiotics to more water-soluble compounds. Several UGT1A enzymes including UGT1A1 are encoded by the UGT1A gene complex on chromosome 2q37. The reduced expression of UGT1A1 is cause of unconjugated hyperbilirubinemia of some types of neonatal jaundice, breastfeeding jaundice, Gilbert syndrome, and Crigler-Najjar syndrome type I and Type II.
In spite of the fact, that UDP-glucuronosyl metabolize a number of lipophilic chemicals and drugs, as phenols, hydrocarbons, coumarin, Anthraquinones and the anticancer drug irinotecan, little attention is paid to their importance for the development of environmental diseases. The prevalence of reduced activity of UDP-glucuronidation was significantly elevated (OR: 8,0; p < 0,0001) among patients of a practices for environmental medicine in southern Germany suffering from environmental diseases.

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