11 replies to this topic

[YOLF]

???

[platypus]

There is no data. What is the role of mitochondria in celiac disease? 

[niner]

It could be positive, negative, or neutral for the health of the gut in a person with Celiac disease-- If anyone has Celiac disease and has used c60oo, let us know.  As for the rest of the body, I'd expect it to behave like it does in everyone else. 

[Turnbuckle]

Judging by the following paper, I'd say it would likely help. And even better might be oral glutathione.

 

The celiac disease is an autoimmune gastrointestinal disorder caused by gluten from wheat, rye or barley. In genetically predisposed persons, gluten induces the immune-mediated inflammation of small intestinal mucosa. Histological lesions include intraepithelial lymphocytosis, crypt hypertrophy and villous atrophy, resulting in malabsorption of micro- and macronutrients. The only treatment for celiac patients is a permanent gluten-free diet (GFD). Reactive oxygen species (ROS) and oxidative stress are strongly associated with the celiac disease. Glutathione (GSH) is a main detoxifier of endogenous and exogenous ROS in the intestine. In order to explain the role of glutathione redox cycle in celiac patients, we examined the activities of GSH-related antioxidant (AO) enzymes glutathione peroxidase (GPx) and glutathione reductase (GR), as well as the concentration of GSH in small intestinal biopsies and peripheral blood of children affected by the celiac disease. The concentration of lipid hydroperoxides (LOOH) as markers of oxidative damage was measured in the same samples. The results clearly demonstrate a significant malfunction of GSH redox cycle with a concomitant decrease in the capacity to regenerate GSH and detoxify LOOH in celiac patients, even after several years of GFD. The oral administration of GSH and a diet rich in natural antioxidants, as well as appropriate dietary supplements, could be of great benefit to the patients.

 

http://www.ncbi.nlm....pubmed/22441607

 

 

Edited by Turnbuckle, 21 June 2015 - 03:16 PM.

[bixbyte]

 

Judging by the following paper, I'd say it would likely help. And even better might be oral glutathione.

 

The celiac disease is an autoimmune gastrointestinal disorder caused by gluten from wheat, rye or barley. In genetically predisposed persons, gluten induces the immune-mediated inflammation of small intestinal mucosa. Histological lesions include intraepithelial lymphocytosis, crypt hypertrophy and villous atrophy, resulting in malabsorption of micro- and macronutrients. The only treatment for celiac patients is a permanent gluten-free diet (GFD). Reactive oxygen species (ROS) and oxidative stress are strongly associated with the celiac disease. Glutathione (GSH) is a main detoxifier of endogenous and exogenous ROS in the intestine. In order to explain the role of glutathione redox cycle in celiac patients, we examined the activities of GSH-related antioxidant (AO) enzymes glutathione peroxidase (GPx) and glutathione reductase (GR), as well as the concentration of GSH in small intestinal biopsies and peripheral blood of children affected by the celiac disease. The concentration of lipid hydroperoxides (LOOH) as markers of oxidative damage was measured in the same samples. The results clearly demonstrate a significant malfunction of GSH redox cycle with a concomitant decrease in the capacity to regenerate GSH and detoxify LOOH in celiac patients, even after several years of GFD. The oral administration of GSH and a diet rich in natural antioxidants, as well as appropriate dietary supplements, could be of great benefit to the patients.

 

http://www.ncbi.nlm....pubmed/22441607

 

 

 

 

IN MY HUMBLE OPINION:

Celiac and the Glutathione relationship may be influenced but this relationship is not statistically significantly if we look at further newer studies.

Appears to be a genetic problem and the  GSSH is only a relationship of this illness?

Supplementing with Glutathione may have no effect on treating CD?

Additionally, Fullerenes may have no benefits to people that suffer from CD unless further studies discover otherwise?

See Abstract below:

 

 

 

• Abstract

Send to:

 

 

 

 

Genet Mol Res. 2014 Feb 20;13(1):1030-7. doi: 10.4238/2014.February.20.4.

Evaluation of glutathione peroxidase and superoxide dismutase enzyme polymorphisms in celiac disease patients.

Katar M1, Ozugurlu AF2, Ozyurt H2, Benli I2.

Author information

 

Abstract

Celiac disease (CD) is a multifactorial, inflammatory small bowel disorder characterized by nutrient malabsorption resulting from mucosal damage, the latter induced by cereal products like barley, oat, and wheat. Oxidative stress has previously been reported to play an important role in the pathogenesis of CD. In the present study, we aimed to evaluate the frequency of polymorphisms that affects the structure of the enzymes superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px), with levels being dependent on the amount of oxidative stress and whether or not there is an association with the mutations DQA1*0501, DQB1*0201, and DRB1*04 that are frequently reported for CD. SOD and GSH-Px polymorphisms were investigated by real-time quantitative polymerase chain reaction in 265 cases. Of the 117 cases that had at least one of DQA1*0501, DQB1*0201, or DRB1*04, 98 (83.75%) also had SOD enzyme polymorphisms and 68 (58.12%) also had GSH-Px polymorphisms. In conclusion, although the etiology of CD is not yet entirely clear, many mechanisms have been suggested. This study supports the notion that SOD and GSH-Px polymorphisms are involved in CD development, even though our findings were not statistically significant, and, furthermore, are influenced at various levels. SOD polymorphisms and activities were more frequently identified than those of GSH-Px.

 

 

[Turnbuckle]

 

 

Judging by the following paper, I'd say it would likely help. And even better might be oral glutathione.

 

The celiac disease is an autoimmune gastrointestinal disorder caused by gluten from wheat, rye or barley. In genetically predisposed persons, gluten induces the immune-mediated inflammation of small intestinal mucosa. Histological lesions include intraepithelial lymphocytosis, crypt hypertrophy and villous atrophy, resulting in malabsorption of micro- and macronutrients. The only treatment for celiac patients is a permanent gluten-free diet (GFD). Reactive oxygen species (ROS) and oxidative stress are strongly associated with the celiac disease. Glutathione (GSH) is a main detoxifier of endogenous and exogenous ROS in the intestine. In order to explain the role of glutathione redox cycle in celiac patients, we examined the activities of GSH-related antioxidant (AO) enzymes glutathione peroxidase (GPx) and glutathione reductase (GR), as well as the concentration of GSH in small intestinal biopsies and peripheral blood of children affected by the celiac disease. The concentration of lipid hydroperoxides (LOOH) as markers of oxidative damage was measured in the same samples. The results clearly demonstrate a significant malfunction of GSH redox cycle with a concomitant decrease in the capacity to regenerate GSH and detoxify LOOH in celiac patients, even after several years of GFD. The oral administration of GSH and a diet rich in natural antioxidants, as well as appropriate dietary supplements, could be of great benefit to the patients.

 

http://www.ncbi.nlm....pubmed/22441607

 

 

 

 

IN MY HUMBLE OPINION:

Celiac and the Glutathione relationship may be influenced but this relationship is not statistically significantly if we look at further newer studies.

Appears to be a genetic problem and the  GSSH is only a relationship of this illness?

Supplementing with Glutathione may have no effect on treating CD?

Additionally, Fullerenes may have no benefits to people that suffer from CD unless further studies discover otherwise?

See Abstract below:

 

 

 

• Abstract

Send to:

 

 

 

 

Genet Mol Res. 2014 Feb 20;13(1):1030-7. doi: 10.4238/2014.February.20.4.

Evaluation of glutathione peroxidase and superoxide dismutase enzyme polymorphisms in celiac disease patients.

Katar M1, Ozugurlu AF2, Ozyurt H2, Benli I2.

Author information

 

Abstract

Celiac disease (CD) is a multifactorial, inflammatory small bowel disorder characterized by nutrient malabsorption resulting from mucosal damage, the latter induced by cereal products like barley, oat, and wheat. Oxidative stress has previously been reported to play an important role in the pathogenesis of CD. In the present study, we aimed to evaluate the frequency of polymorphisms that affects the structure of the enzymes superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px), with levels being dependent on the amount of oxidative stress and whether or not there is an association with the mutations DQA1*0501, DQB1*0201, and DRB1*04 that are frequently reported for CD. SOD and GSH-Px polymorphisms were investigated by real-time quantitative polymerase chain reaction in 265 cases. Of the 117 cases that had at least one of DQA1*0501, DQB1*0201, or DRB1*04, 98 (83.75%) also had SOD enzyme polymorphisms and 68 (58.12%) also had GSH-Px polymorphisms. In conclusion, although the etiology of CD is not yet entirely clear, many mechanisms have been suggested. This study supports the notion that SOD and GSH-Px polymorphisms are involved in CD development, even though our findings were not statistically significant, and, furthermore, are influenced at various levels. SOD polymorphisms and activities were more frequently identified than those of GSH-Px.

 

 

 

 

The looked at genetic variants for GSH, but that doesn't mean some deficiency in GSH redox is not involved, and it doesn't mean that oral GSH and/or other antioxidants won't help.

[bixbyte]

 

 

 

Judging by the following paper, I'd say it would likely help. And even better might be oral glutathione.

 

The celiac disease is an autoimmune gastrointestinal disorder caused by gluten from wheat, rye or barley. In genetically predisposed persons, gluten induces the immune-mediated inflammation of small intestinal mucosa. Histological lesions include intraepithelial lymphocytosis, crypt hypertrophy and villous atrophy, resulting in malabsorption of micro- and macronutrients. The only treatment for celiac patients is a permanent gluten-free diet (GFD). Reactive oxygen species (ROS) and oxidative stress are strongly associated with the celiac disease. Glutathione (GSH) is a main detoxifier of endogenous and exogenous ROS in the intestine. In order to explain the role of glutathione redox cycle in celiac patients, we examined the activities of GSH-related antioxidant (AO) enzymes glutathione peroxidase (GPx) and glutathione reductase (GR), as well as the concentration of GSH in small intestinal biopsies and peripheral blood of children affected by the celiac disease. The concentration of lipid hydroperoxides (LOOH) as markers of oxidative damage was measured in the same samples. The results clearly demonstrate a significant malfunction of GSH redox cycle with a concomitant decrease in the capacity to regenerate GSH and detoxify LOOH in celiac patients, even after several years of GFD. The oral administration of GSH and a diet rich in natural antioxidants, as well as appropriate dietary supplements, could be of great benefit to the patients.

 

http://www.ncbi.nlm....pubmed/22441607

 

 

 

 

IN MY HUMBLE OPINION:

Celiac and the Glutathione relationship may be influenced but this relationship is not statistically significantly if we look at further newer studies.

Appears to be a genetic problem and the  GSSH is only a relationship of this illness?

Supplementing with Glutathione may have no effect on treating CD?

Additionally, Fullerenes may have no benefits to people that suffer from CD unless further studies discover otherwise?

See Abstract below:

 

 

 

• Abstract

Send to:

 

 

 

 

Genet Mol Res. 2014 Feb 20;13(1):1030-7. doi: 10.4238/2014.February.20.4.

Evaluation of glutathione peroxidase and superoxide dismutase enzyme polymorphisms in celiac disease patients.

Katar M1, Ozugurlu AF2, Ozyurt H2, Benli I2.

Author information

 

Abstract

Celiac disease (CD) is a multifactorial, inflammatory small bowel disorder characterized by nutrient malabsorption resulting from mucosal damage, the latter induced by cereal products like barley, oat, and wheat. Oxidative stress has previously been reported to play an important role in the pathogenesis of CD. In the present study, we aimed to evaluate the frequency of polymorphisms that affects the structure of the enzymes superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px), with levels being dependent on the amount of oxidative stress and whether or not there is an association with the mutations DQA1*0501, DQB1*0201, and DRB1*04 that are frequently reported for CD. SOD and GSH-Px polymorphisms were investigated by real-time quantitative polymerase chain reaction in 265 cases. Of the 117 cases that had at least one of DQA1*0501, DQB1*0201, or DRB1*04, 98 (83.75%) also had SOD enzyme polymorphisms and 68 (58.12%) also had GSH-Px polymorphisms. In conclusion, although the etiology of CD is not yet entirely clear, many mechanisms have been suggested. This study supports the notion that SOD and GSH-Px polymorphisms are involved in CD development, even though our findings were not statistically significant, and, furthermore, are influenced at various levels. SOD polymorphisms and activities were more frequently identified than those of GSH-Px.

 

 

 

 

The looked at genetic variants for GSH, but that doesn't mean some deficiency in GSH redox is not involved, and it doesn't mean that oral GSH and/or other antioxidants won't help.

 

 

Results

 

There were no differences in oxidative stress biomarkers between treatment groups at baseline. Thirty-nine (39) participants completed the study per protocol. Changes in creatinine standardized F2-isoP (ng/mg creatinine) (0.0±0.1 versus 0.0±0.1, p=0.38) and 8-OHdG (μg/g creatinine) (-0.2±3.3 versus 1.0±3.2, p=0.27) were nonsignificant between groups at week 4. Total reduced, oxidized, and ratio measures of GSH status were also unchanged.

 

Conclusions

 

No significant changes were observed in biomarkers of oxidative stress, including glutathione status, in this clinical trial of oral glutathione supplementation in healthy adults.

 

 

http://www.ncbi.nlm....les/PMC3162377/

 

 

IMHO: Supplementing with Glutatione does not increase those levels. 

[Turnbuckle]

Another study--

 

Eur J Nutr. 2015 Mar;54(2):251-63. doi: 10.1007/s00394-014-0706-z. Epub 2014 May 5.

Randomized controlled trial of oral glutathione supplementation on body stores of glutathione.

Richie JP Jr1, Nichenametla S, Neidig W, Calcagnotto A, Haley JS, Schell TD, Muscat JE.

Author information

Abstract

PURPOSE:

Glutathione (GSH), the most abundant endogenous antioxidant, is a critical regulator of oxidative stress and immune function. While oral GSH has been shown to be bioavailable in laboratory animal models, its efficacy in humans has not been established. Our objective was to determine the long-term effectiveness of oral GSH supplementation on body stores of GSH in healthy adults.

 

METHODS:

A 6-month randomized, double-blinded, placebo-controlled trial of oral GSH (250 or 1,000 mg/day) on GSH levels in blood, erythrocytes, plasma, lymphocytes and exfoliated buccal mucosal cells was conducted in 54 non-smoking adults. Secondary outcomes on a subset of subjects included a battery of immune markers.

 

RESULTS:

GSH levels in blood increased after 1, 3 and 6 months versus baseline at both doses. At 6 months, mean GSH levels increased 30-35 % in erythrocytes, plasma and lymphocytes and 260 % in buccal cells in the high-dose group (P < 0.05). GSH levels increased 17 and 29 % in blood and erythrocytes, respectively, in the low-dose group (P < 0.05). In most cases, the increases were dose and time dependent, and levels returned to baseline after a 1-month washout period. A reduction in oxidative stress in both GSH dose groups was indicated by decreases in the oxidized to reduced glutathione ratio in whole blood after 6 months. Natural killer cytotoxicity increased >twofold in the high-dose group versus placebo (P < 0.05) at 3 months.

 

CONCLUSIONS:

These findings show, for the first time, that daily consumption of GSH supplements was effective at increasing body compartment stores of GSH.

 

PMID: 24791752 [PubMed - in process]

 

 

This is consistent with my own experience, where 1000 mg is much better than 500 mg and about equal to C60 at eliminating residual alcohol effects.

Edited by Turnbuckle, 21 June 2015 - 10:11 PM.

[bixbyte]

Another study--

 

Eur J Nutr. 2015 Mar;54(2):251-63. doi: 10.1007/s00394-014-0706-z. Epub 2014 May 5.

Randomized controlled trial of oral glutathione supplementation on body stores of glutathione.

Richie JP Jr1, Nichenametla S, Neidig W, Calcagnotto A, Haley JS, Schell TD, Muscat JE.

Author information

Abstract

PURPOSE:

Glutathione (GSH), the most abundant endogenous antioxidant, is a critical regulator of oxidative stress and immune function. While oral GSH has been shown to be bioavailable in laboratory animal models, its efficacy in humans has not been established. Our objective was to determine the long-term effectiveness of oral GSH supplementation on body stores of GSH in healthy adults.

 

METHODS:

A 6-month randomized, double-blinded, placebo-controlled trial of oral GSH (250 or 1,000 mg/day) on GSH levels in blood, erythrocytes, plasma, lymphocytes and exfoliated buccal mucosal cells was conducted in 54 non-smoking adults. Secondary outcomes on a subset of subjects included a battery of immune markers.

 

RESULTS:

GSH levels in blood increased after 1, 3 and 6 months versus baseline at both doses. At 6 months, mean GSH levels increased 30-35 % in erythrocytes, plasma and lymphocytes and 260 % in buccal cells in the high-dose group (P < 0.05). GSH levels increased 17 and 29 % in blood and erythrocytes, respectively, in the low-dose group (P < 0.05). In most cases, the increases were dose and time dependent, and levels returned to baseline after a 1-month washout period. A reduction in oxidative stress in both GSH dose groups was indicated by decreases in the oxidized to reduced glutathione ratio in whole blood after 6 months. Natural killer cytotoxicity increased >twofold in the high-dose group versus placebo (P < 0.05) at 3 months.

 

CONCLUSIONS:

These findings show, for the first time, that daily consumption of GSH supplements was effective at increasing body compartment stores of GSH.

 

PMID: 24791752 [PubMed - in process]

 

 

This is consistent with my own experience, where 1000 mg is much better than 500 mg and about equal to C60 at eliminating residual alcohol effects.

 

 

 

Glutatione in your Blood has no effect in helping your cells.

A novel method of increasing Glutathione is by supplementing with NAC.

You could raise cellular GSSH only if your cells are deficient. This is a self limiting cellular reaction.

There is no way to increase your GSSH level even via IV is a waste of $$$.

But C60 supplementation could be of significant benefit because it possesses lipophillic properties 

and is stored within your cell walls.

I also believe that trying to increase your GSSH levels is a scam invented by vitamin sellers.

[Turnbuckle]

 

I also believe that trying to increase your GSSH levels is a scam invented by vitamin sellers.

 

 

 

With many supplements that is true (and also with many drugs being pushed by big pharma, like statins) but in the case of the Setria glutathione I've been taking for years now, I can definitely say it works.

[kurdishfella]

Well people with diseases like celiac or cancer have good genetics because the ones with bad genes died out not because of making offspring early regardless with cancer it comes at later stage in life cus of good genes . So in short nothing will happen badly. And nothing good either most likely. another example of survival is how hairy people have bodies that are adapted to cavemen time. less hairy people have been technology advanced longer hence less body hair. But also worse genes than people with lots of hair since survival of fittest no longer a rule.

Edited by kurdishfella, 29 March 2021 - 11:53 AM.

[YOLF]

Well people with diseases like celiac or cancer have good genetics because the ones with bad genes died out not because of making offspring early regardless with cancer it comes at later stage in life cus of good genes . So in short nothing will happen badly. And nothing good either most likely. another example of survival is how hairy people have bodies that are adapted to cavemen time. less hairy people have been technology advanced longer hence less body hair. But also worse genes than people with lots of hair since survival of fittest no longer a rule.

 

I wouldn't think it's so much a matter of genetics as it is our understanding of them and our ability to accommodate them, such is the heart of what civilization and human development has been. "Fitness" is complicated, but for the survial reasons that you mentioned, it really just boils down to what you know and what you do with yourself and the level of technology and knowledge available to you.

 

I don't know about the hairy hypothesis, I think Italians, Greeks, Persians etc. can be pretty hairy, but they all made major contributions to the formation of civilization as we know it. Though I personally prefer the absence of body hair.