Taurine Deficiency in Thalassemics

I was reading on the antioxidant taurine because according to this study people with thalassemia beta are low in the antioxidant taurine.

http://tropej.oxfordjournals.org/cgi/pdf_extract/52/3/227

So I did some more search to see if its also good for G6PD deficiency that I have and it looks like it is. It protects the body from oxidation against heavy metals like cadmium, mercury, lead, iron, etc:
http://www.jbmb.or.kr/jbmb/jbmb_files/[41-9]0809300834_(657-663)BMB106(08-114).pdf
http://www.ncbi.nlm.nih.gov/pubmed/11598776
http://www.ncbi.nlm.nih.gov/pubmed/15545001

The contraindicated substances in fava beans that cause hemolysis is G6PD deficient people oxidate cells by unbinding iron from ferritine. Free iron that is not bound to ferritine acts as an oxidant and damages cells:
http://www.ncbi.nlm.nih.gov/pubmed/2730003

So I think for someone like me with both thalassemia and G6PD deficiency it looks like a good supplement. What do you think?

P.S. I was just thinking. Whenever something made of iron touches my skin I get rushes. Like an iron belt buckle, or  necklace with an iron ornament. Could this be the reason? Anyone else has this?

There's a lot to this. I'll be back with more but I want to point out the top link. Taurine of 1000 mg daily provided a "significant amelioration in the activity of liver enzymes (ALT and AST). This is a very important issue for many thal majors, as both Exjade use and hepatitis can raise these levels.
This may be a key to controlling these enzymes.

Thanks karoloydi.

Taurine also protects from the toxicity of iron overload.

http://circ.ahajournals.org/cgi/content/abstract/109/15/1877

Background— Iron overload has an increasing worldwide prevalence and is associated with significant cardiovascular morbidity and mortality. Elevated iron levels in the myocardium lead to impaired systolic and diastolic function and elevated oxidative stress. Taurine accounts for 25% to 50% of the amino acid pool in myocardium, possesses antioxidant properties, and can inhibit L-type Ca2+ channels. Thus, we hypothesized that this agent would reduce the cardiovascular effects of iron overload.

Methods and Results— Iron-overloaded mice were generated by intraperitoneal injection of iron either chronically (5 days per week for 13 weeks) or subacutely (5 days per week for 4 weeks). Iron overload causes increased mortality, elevated oxidative stress, systolic and diastolic dysfunction, hypotension, and bradycardia. Taurine supplementation increased myocardial taurine levels by 45% and led to reductions in mortality and improved cardiac function, heart rate, and blood pressure in iron-overloaded mice. Histological examination of the myocardium revealed reduced apoptosis and interstitial fibrosis in iron-overloaded mice supplemented with taurine. Taurine mediated reduced oxidative stress in iron-overloaded mice along with attenuation of myocardial lipid peroxidation and protection of reduced glutathione level.

Conclusions— These results demonstrate that treatment with taurine reduces iron-mediated myocardial oxidative stress, preserves cardiovascular function, and improves survival in iron-overloaded mice. The role of taurine in protecting reduced glutathione levels provides an important mechanism by which oxidative stress–induced myocardial damage can be curtailed. Taurine, as a dietary supplement, represents a potential new therapeutic agent to reduce the cardiovascular burden from iron-overload conditions.