I recalled Dr. Kevin Pezzi telling me that while GS is known to be a benign hepatic condition, it may adversely impact estrogen metabolism. Now, it seems to be well accepted that too much estradiol (and perhaps other estrogens) can effectively kill one’s sex drive. I have GS as evidenced by multiple blood works showing consistently mildly off the range total Bilirubin.

Incidentally, can’t elevated Bilirubin cause increased ferritin ? I’m thinking that bilirubin being the breakdown product of RBCs, increased bilirubin might cause ferritin to go up ?

So, I queried Google and found this showing that UGT-1A1 to be indeed connected to estrogen metabolism. Now, what I do not know is whether this can be clinically significant ?

By the way, the pages from which I uncovered this info look interesting with regard to other metabolic matters.

http://www.millipore.com/pathways/pathviewer.do?pathwayId=240

http://74.125.47.132/search?q=cache:tvqX9wGOHzcJ:www.genecards.org/cgi-bin/carddisp.pl%3Fgene%3DUgt1a1+gilbert+syndrome+estrogen+metabolism+ugt+1a1&cd=1&hl=en&ct=clnk&gl=ca

Dr. Mariano,

would you think that a mild case of hemolytic anemia might very adversely affect libido ? I have a mild cas. I recall my primary care physician telling me about this, but she wasn’t concerned at all though. The reason I bring this up is, we’re still talking anemia and while I know of the more severe impact of various anemias, I do not know whether this would have a quite a detrimental impact on sex drive. I’m thinking it might because of overall reduced energy availability.

I’m pasting the following from the links I posted above on UGT-1A1 gene map :

This gene encodes a UDP-glucuronosyltransferase, an enzyme of the glucuronidation pathway that transforms small lipophilic molecules, such as steroids, bilirubin, hormones, and drugs, into water-soluble, excretable metabolites. This gene is part of a complex locus that encodes several UDP-glucuronosyltransferases. The locus includes thirteen unique alternate first exons followed by four common exons. Four of the alternate first exons are considered pseudogenes. Each of the remaining nine 5′ exons may be spliced to the four common exons, resulting in nine proteins with different N-termini and identical C-termini. Each first exon encodes the substrate binding site, and is regulated by its own promoter. The preferred substrate of this enzyme is bilirubin, although it also has moderate activity with simple phenols, flavones, and C18 steroids. Mutations in this gene result in Crigler-Najjar syndromes types I and II and in Gilbert syndrome. [provided by RefSeq]