Bilirubin is widely known as an end product of heme metabolism. Very high levels of serum bilirubin lead to its accumulation in the brain, causing kernicterus.1,2 Almost all newborns display some level of jaundice, and some display high enough serum bilirubin levels that phototherapy or exchange transfusion is considered.
What most of the medical profession has not appreciated is that, from a teleologic perspective, biosynthesis of bilirubin as the key catabolite of heme does not seem to make sense. Bilirubin is a secondary degradation product of heme. Heme is best known as a constituent of hemoglobin, which is released in association with the breakdown of aging red blood cells. Heme also is contained in a wide range of enzymes whose turnover also leads to free heme release. Free heme can be toxic, so nature evolved a family of heme oxygenase enzymes to degrade heme,3,4...
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