Tarmander
Member
- Joined
- Apr 30, 2015
- Messages
- 3,772
This study was interesting:
http://www.medwelljournals.com/fulltext ... .1512.1515
If I remember correctly, Peat has said Boron is estrogenic, or that we do not really need it. Basically they induced obesity in rabbits and then through the use of Boron reduced fatty liver. I would be interested to hear what people think of this.
"Abstract: The aim of this study is to provide insight into boron metabolism and to identify metabolic pathways which may explain the presumed increased susceptibility of livers. Boron was administrated in rabbits at three different doses and 96 h intervals for 7 months. Metabolomic profile based on NMR analysis was performed. The most pronounced findings were significant changes in alanine, methionine, pyruvate and creatine. Boron seems to be effective in the prevention of obesity and fatty liver. Metabolic end-points obtained by NMR can be easily assessed and interpreted alone or in combination each other and with classical biochemical parameters for better understanding obesity and boron and liver metabolism."
"Wei et al. (2008) reviewed evidence that implicates mitochondrial dysfunction as a primary mechanism for development of NAFLD. Mitochondrial dysfunction may not only cause fat accumulation but also may lead to the generation of reactive oxygen species and cytokine production contributing to progression of NAFLD. Lipid peroxidation is linked with the excess generation of reactive oxygen species which may be contributed by the exogenous or the endogenous sources. Glutathione is a unique cellular tripeptide that plays a vital role in maintaining the oxidant/antioxidant balance in the tissue that is essential for normal cellular function. Severe depletion of glutathione is considered as the consequence or the cause of oxidative stress. Boron supplementation could replenish the depleted hepatic glutathione level. It should be noted that oxidative stress is often counteracted by glutathione, resulting in its depletion. Borax partly normalizes the liver and offsets the deleterious effects observed in fulminant hepatic failure by modulating the oxidative stress parameters (Pawa and Ali, 2006). In the present study a high level of lipid peroxidation associated with glutathione depletion was exhibited in group not receiving boron and lipid peroxidation inhibited significantly in experimental groups"
http://www.medwelljournals.com/fulltext ... .1512.1515
If I remember correctly, Peat has said Boron is estrogenic, or that we do not really need it. Basically they induced obesity in rabbits and then through the use of Boron reduced fatty liver. I would be interested to hear what people think of this.
"Abstract: The aim of this study is to provide insight into boron metabolism and to identify metabolic pathways which may explain the presumed increased susceptibility of livers. Boron was administrated in rabbits at three different doses and 96 h intervals for 7 months. Metabolomic profile based on NMR analysis was performed. The most pronounced findings were significant changes in alanine, methionine, pyruvate and creatine. Boron seems to be effective in the prevention of obesity and fatty liver. Metabolic end-points obtained by NMR can be easily assessed and interpreted alone or in combination each other and with classical biochemical parameters for better understanding obesity and boron and liver metabolism."
"Wei et al. (2008) reviewed evidence that implicates mitochondrial dysfunction as a primary mechanism for development of NAFLD. Mitochondrial dysfunction may not only cause fat accumulation but also may lead to the generation of reactive oxygen species and cytokine production contributing to progression of NAFLD. Lipid peroxidation is linked with the excess generation of reactive oxygen species which may be contributed by the exogenous or the endogenous sources. Glutathione is a unique cellular tripeptide that plays a vital role in maintaining the oxidant/antioxidant balance in the tissue that is essential for normal cellular function. Severe depletion of glutathione is considered as the consequence or the cause of oxidative stress. Boron supplementation could replenish the depleted hepatic glutathione level. It should be noted that oxidative stress is often counteracted by glutathione, resulting in its depletion. Borax partly normalizes the liver and offsets the deleterious effects observed in fulminant hepatic failure by modulating the oxidative stress parameters (Pawa and Ali, 2006). In the present study a high level of lipid peroxidation associated with glutathione depletion was exhibited in group not receiving boron and lipid peroxidation inhibited significantly in experimental groups"
