Drareg
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Study claims vitamin E prevents RBC destruction in G6PDh deficient hemolytic anemia.
Role of vitamin E supplementation on serum levels of copper and zinc in hemolytic anemic patients with G6PD deficiency. - PubMed - NCBI
Vitamin E scavenges free radicals and may prevent destruction of RBC in Glucose6-phosphate dehydrogenase (G6PD) deficient hemolytic anemia, where changes in copper (Cu) and zinc (Zn) may act as additional contributory factors for hemolysis. In the present study changes in serum Cu and Zn and role of vitamin E supplementation on these changes were observed in hemolytic anemic patients with G6PD deficiency. This study was conducted in the Department of Physiology, Bangabandhu Sheikh Mujib Medical University (BSMMU), Dhaka during July 2005-June 2006. For this, 102 subjects with age ranged 5-40 years of both sexes were included in the study. Among them 68 were G6PD deficient patients, of whom 34 were in supplemented group and 34 were non-supplemented group. The supplemented group received vitamin E for 60 consecutive days at a dose of 800 IU/day for adult and 400 IU/day for children < or =12 years (4 times daily). Age and sex matched 34 apparently healthy subjects with normal G6PD level were taken to observe the base line data (healthy control) and also for comparison. All the G6PD deficient patients were selected from the Out Patient Department (OPD) of Hematology, BSMMU, Dhaka, and all the healthy subjects from personal contact. Blood G6PD level was done by spectrophotometric method and serum Cu, Zn levels by atomic absorption spectrophotometric method. To observe the availability of binding proteins serum total protein, albumin, globulin and A:G ratio were done by standard laboratory techniques. All parameters were measured on day 1 of their 1st visit and also on day 60 in deficient groups. Data analysis was done by appropriate statistical method. Serum Cu was significantly (p<0.001) higher but serum Zn, total protein, albumin, A/G ratio were significantly (p<0.001) lower in G6PD deficient groups in comparison to those of healthy control on day 1. After vitamin E supplementation, values of these parameters were comparable with those of healthy control in supplemented group in comparison to those of their pre-supplemented and non-supplemented groups both on day 1 and day 60. So, vitamin E supplementation has got its effective role in restoration of normal serum concentration of Cu and Zn in this group of patients.
This study shows vitamin E helping those with G6PDH deficiency in the Mediterranean ,whats interesting here is that some researches took an angle with Sardinians that their longevity and lack of chronic disease was due to limited G6PDH activity, we know their diets contain a lot of vitamin E,this implies you could speculate differently.
MMS: Error
What's also plausible is that Vitamin E helps create an enzyme that prevents DHEA converting into the less preferred androgens, I think Haidut mentioned this somewhere ? the G6PDH enzyme inhibition could be high estrogen keeping it low, vitamin E stops this?
Role of vitamin E supplementation on serum levels of copper and zinc in hemolytic anemic patients with G6PD deficiency. - PubMed - NCBI
Vitamin E scavenges free radicals and may prevent destruction of RBC in Glucose6-phosphate dehydrogenase (G6PD) deficient hemolytic anemia, where changes in copper (Cu) and zinc (Zn) may act as additional contributory factors for hemolysis. In the present study changes in serum Cu and Zn and role of vitamin E supplementation on these changes were observed in hemolytic anemic patients with G6PD deficiency. This study was conducted in the Department of Physiology, Bangabandhu Sheikh Mujib Medical University (BSMMU), Dhaka during July 2005-June 2006. For this, 102 subjects with age ranged 5-40 years of both sexes were included in the study. Among them 68 were G6PD deficient patients, of whom 34 were in supplemented group and 34 were non-supplemented group. The supplemented group received vitamin E for 60 consecutive days at a dose of 800 IU/day for adult and 400 IU/day for children < or =12 years (4 times daily). Age and sex matched 34 apparently healthy subjects with normal G6PD level were taken to observe the base line data (healthy control) and also for comparison. All the G6PD deficient patients were selected from the Out Patient Department (OPD) of Hematology, BSMMU, Dhaka, and all the healthy subjects from personal contact. Blood G6PD level was done by spectrophotometric method and serum Cu, Zn levels by atomic absorption spectrophotometric method. To observe the availability of binding proteins serum total protein, albumin, globulin and A:G ratio were done by standard laboratory techniques. All parameters were measured on day 1 of their 1st visit and also on day 60 in deficient groups. Data analysis was done by appropriate statistical method. Serum Cu was significantly (p<0.001) higher but serum Zn, total protein, albumin, A/G ratio were significantly (p<0.001) lower in G6PD deficient groups in comparison to those of healthy control on day 1. After vitamin E supplementation, values of these parameters were comparable with those of healthy control in supplemented group in comparison to those of their pre-supplemented and non-supplemented groups both on day 1 and day 60. So, vitamin E supplementation has got its effective role in restoration of normal serum concentration of Cu and Zn in this group of patients.
This study shows vitamin E helping those with G6PDH deficiency in the Mediterranean ,whats interesting here is that some researches took an angle with Sardinians that their longevity and lack of chronic disease was due to limited G6PDH activity, we know their diets contain a lot of vitamin E,this implies you could speculate differently.
MMS: Error
What's also plausible is that Vitamin E helps create an enzyme that prevents DHEA converting into the less preferred androgens, I think Haidut mentioned this somewhere ? the G6PDH enzyme inhibition could be high estrogen keeping it low, vitamin E stops this?
