Guest guest Posted April 23, 2007 Report Share Posted April 23, 2007 does anyone know if these two items are the same? I know that using glutamine in the presence of neurological deficits can cause further damage. However I think that glutathione is used in detoxification. Does anyone know the differences in these two products or will they both cause damage? thank you. mom to broderick, asd, scd 19 months Quote Link to comment Share on other sites More sharing options...
Guest guest Posted April 23, 2007 Report Share Posted April 23, 2007 They are different. L-glutamine is an amino acid. It only causes neurological damage if it is in excess and converts to glutimate. This is one of those controversial issues. It does help the gut and therefore has also helped many with neurological conditions. Glutathione is an anti-oxidant. It is often better to create more glutathione in the body by giving it's precursers, rather than taking glutathione itself. - lipawe wrote: does anyone know if these two items are the same? I know that using glutamine in the presence of neurological deficits can cause further damage. However I think that glutathione is used in detoxification. Does anyone know the differences in these two products or will they both cause damage? thank you. mom to broderick, asd, scd 19 months --------------------------------- Ahhh...imagining that irresistible " new car " smell? Check outnew cars at Yahoo! Autos. Quote Link to comment Share on other sites More sharing options...
Guest guest Posted April 24, 2007 Report Share Posted April 24, 2007 > > does anyone know if these two items are the same? > I know that using glutamine in the presence of neurological deficits > can cause further damage. However I think that glutathione is used in > detoxification. Does anyone know the differences in these two > products or will they both cause damage? > thank you. , I don't have an answer about " damage " but the two items are different. Glutamine A " conditionally essential " amino acid, glutamine is considered to be a brain fuel. Glutamine has been used therapeutically for alcoholism, mild depression and to reduce the craving for sweets. Glutamine is very important in the functioning of the metabolism and muscle maintenance. Glutamine supplementation can help prevent muscle and other tissue breakdown by providing the body with nitrogen and fuel. Glutathione A natural sulfur-bearing peptide formed from the linking of three amino acids: glutamic acid, cysteine and glycine. Glutathione acts as an antioxidant and detoxicant and is involved with the selenium-containing enzyme glutathione peroxidase. Glutathione is also involved in amino acid transport across cell membranes and is a powerful free radical scavenger and antioxidant that removes unwanted substances from the body. Carol F. Quote Link to comment Share on other sites More sharing options...
Guest guest Posted April 24, 2007 Report Share Posted April 24, 2007 thank you. can you tell me what the precursors are? > does anyone know if these two items are the same? > I know that using glutamine in the presence of neurological deficits > can cause further damage. However I think that glutathione is used in > detoxification. Does anyone know the differences in these two > products or will they both cause damage? > thank you. > > > mom to broderick, asd, scd 19 months > > > > > > > --------------------------------- > Ahhh...imagining that irresistible " new car " smell? > Check outnew cars at Yahoo! Autos. > > Quote Link to comment Share on other sites More sharing options...
Guest guest Posted April 24, 2007 Report Share Posted April 24, 2007 > > > > They are different. L-glutamine is an amino acid. It only causes > neurological damage if it is in excess and converts to glutimate. > This is one of those controversial issues. It does help the gut and > therefore has also helped many with neurological conditions. > > > > Glutathione is an anti-oxidant. It is often better to create > more glutathione in the body by giving it's precursers, rather than > taking glutathione itself. > > > > mom to broderick, asd, scd 19 months I am unable to explain as I am inexperienced with supplements. I got the definitions by doing an Internet search. Carol F. Quote Link to comment Share on other sites More sharing options...
Guest guest Posted April 24, 2007 Report Share Posted April 24, 2007 A natural way to increase glutathione levels is to eliminate the pathogenic bacteria in our guts. LPS, the poison found in pathogenic bacteria decreases glutathione levels. SCD is a great way to eliminate the poisons from gut pathogens and restore the glutathione levels. There is a famous doctor who is an expert in detoxification and he now uses SCD for detoxification. Below is a research article that demonstrates that bacterial poisons decrease the level of glutathione. Mimi http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=Abstra\ ctPlus&list_uids=17291629&query_hl=2&itool=pubmed_docsum 1: Neurochem Int. 2007 Mar;50(4):671-80. Epub 2007 Jan 13. Altered glutathione homeostasis in animals prenatally exposed to lipopolysaccharide. * Zhu Y, * Carvey PM, * Ling Z. Department of Pharmacology, Rush University Medical Center, 1735 West on Street, Chicago, IL 60612, USA. We previously reported that injection of bacterial lipopolysaccharide (LPS) into gravid female rats at embryonic day 10.5 resulted in a birth of offspring with fewer than normal dopamine (DA) neurons along with innate immunity dysfunction and many characteristics seen in Parkinson's disease (PD) patients. The LPS-exposed animals were also more susceptible to secondary toxin exposure as indicated by an accelerated DA neuron loss. Glutathione (GSH) is an important antioxidant in the brain. A disturbance in glutathione homeostasis has been proposed for the pathogenesis of PD. In this study, animals prenatally exposed to LPS were studied along with an acute intranigral LPS injection model for the status of glutathione homeostasis, lipid peroxidation, and related enzyme activities. Both prenatal LPS exposure and acute LPS injection produced a significant GSH reduction and increase in oxidized GSH (GSSG) and lipid peroxide (LPO) production. Activity of gamma-glutamylcysteine synthetase (GCS), the rate-limiting enzyme in de novo GSH synthesis, was up-regulated in acute supranigral LPS model but was reduced in the prenatal LPS model. The GCS light subunit protein expression was also down-regulated in prenatal LPS model. GSH redox recycling enzyme activities (glutathione peroxidase, GPx and glutathione reducdase, GR) and glutathione-S-transferase (GST), gamma-glutamyl transpeptidase (gamma-GT) activities were all increased in prenatal LPS model. Prenatal LPS exposure and aging synergized in GSH level and GSH-related enzyme activities except for those (GR, GST, and gamma-GT) with significant regional variations. Additionally, prenatal LPS exposure produced a reduction of DA neuron count in the substantia nigra (SN). These results suggest that prenatal LPS exposure may cause glutathione homeostasis disturbance in offspring brain and render DA neurons susceptible to the secondary neurotoxin insult. PMID: 17291629 [PubMed - in process] > > > > > > > They are different. L-glutamine is an amino acid. It only causes > > neurological damage if it is in excess and converts to glutimate. > > This is one of those controversial issues. It does help the gut and > > therefore has also helped many with neurological conditions. > > > > > > Glutathione is an anti-oxidant. It is often better to create > > more glutathione in the body by giving it's precursers, rather than > > taking glutathione itself. > > > > > > mom to broderick, asd, scd 19 months > > I am unable to explain as I am inexperienced with supplements. > I got the definitions by doing an Internet search. > > Carol F. > > Quote Link to comment Share on other sites More sharing options...
Guest guest Posted April 25, 2007 Report Share Posted April 25, 2007 Mim, I was just thinking kind of about this in the past couple of weeks since I am expecting again. At first, I was thinking that it would be best for me to go SCD during this pregnancy especially since I already have a child on the spectrum, and I am sure it is at least nutrition wise. I have been so incredibly ill with this pregnancy(which has never happened before) that I just ate whatever I could...which, of course, was definitely no where close to SCD. Then, I started wondering if could make a terrible difference gut wise for the baby because the baby is being fed in utero through the cord which is simply blood. It isn't like breast feeding where sugar and such would come through the milk. Would sugars and starches actually come through the cord blood to feed the baby with harmful bacterial overgrowth? I'm kind of confused about all of that now with this study that you posted. I also was under the impression that babies are born with pretty much a clean slate in the gut. Can you help me understand this whole thing better? Meleah Re: Re: glutamine and Glutathione A natural way to increase glutathione levels is to eliminate the pathogenic bacteria in our guts. LPS, the poison found in pathogenic bacteria decreases glutathione levels. SCD is a great way to eliminate the poisons from gut pathogens and restore the glutathione levels. There is a famous doctor who is an expert in detoxification and he now uses SCD for detoxification. Below is a research article that demonstrates that bacterial poisons decrease the level of glutathione. Mimi http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=Abstra\ ctPlus&list_uids=17291629&query_hl=2&itool=pubmed_docsum 1: Neurochem Int. 2007 Mar;50(4):671-80. Epub 2007 Jan 13. Altered glutathione homeostasis in animals prenatally exposed to lipopolysaccharide. * Zhu Y, * Carvey PM, * Ling Z. Department of Pharmacology, Rush University Medical Center, 1735 West on Street, Chicago, IL 60612, USA. We previously reported that injection of bacterial lipopolysaccharide (LPS) into gravid female rats at embryonic day 10.5 resulted in a birth of offspring with fewer than normal dopamine (DA) neurons along with innate immunity dysfunction and many characteristics seen in Parkinson's disease (PD) patients. The LPS-exposed animals were also more susceptible to secondary toxin exposure as indicated by an accelerated DA neuron loss. Glutathione (GSH) is an important antioxidant in the brain. A disturbance in glutathione homeostasis has been proposed for the pathogenesis of PD. In this study, animals prenatally exposed to LPS were studied along with an acute intranigral LPS injection model for the status of glutathione homeostasis, lipid peroxidation, and related enzyme activities. Both prenatal LPS exposure and acute LPS injection produced a significant GSH reduction and increase in oxidized GSH (GSSG) and lipid peroxide (LPO) production. Activity of gamma-glutamylcysteine synthetase (GCS), the rate-limiting enzyme in de novo GSH synthesis, was up-regulated in acute supranigral LPS model but was reduced in the prenatal LPS model. The GCS light subunit protein expression was also down-regulated in prenatal LPS model. GSH redox recycling enzyme activities (glutathione peroxidase, GPx and glutathione reducdase, GR) and glutathione-S-transferase (GST), gamma-glutamyl transpeptidase (gamma-GT) activities were all increased in prenatal LPS model. Prenatal LPS exposure and aging synergized in GSH level and GSH-related enzyme activities except for those (GR, GST, and gamma-GT) with significant regional variations. Additionally, prenatal LPS exposure produced a reduction of DA neuron count in the substantia nigra (SN). These results suggest that prenatal LPS exposure may cause glutathione homeostasis disturbance in offspring brain and render DA neurons susceptible to the secondary neurotoxin insult. PMID: 17291629 [PubMed - in process] > > > > > > > They are different. L-glutamine is an amino acid. It only causes > > neurological damage if it is in excess and converts to glutimate. > > This is one of those controversial issues. It does help the gut and > > therefore has also helped many with neurological conditions. > > > > > > Glutathione is an anti-oxidant. It is often better to create > > more glutathione in the body by giving it's precursers, rather than > > taking glutathione itself. > > > > > > mom to broderick, asd, scd 19 months > > I am unable to explain as I am inexperienced with supplements. > I got the definitions by doing an Internet search. > > Carol F. > > Quote Link to comment Share on other sites More sharing options...
Guest guest Posted April 25, 2007 Report Share Posted April 25, 2007 THANKS. I was thinking maybe I should investigate chelation, but since he's been on this diet for almost 2 years he may not need it. I ordered from Kirkman Labs, a detox powder, I'll try it. > > > > > > > > They are different. L-glutamine is an amino acid. It only causes > > > neurological damage if it is in excess and converts to glutimate. > > > This is one of those controversial issues. It does help the gut and > > > therefore has also helped many with neurological conditions. > > > > > > > > Glutathione is an anti-oxidant. It is often better to create > > > more glutathione in the body by giving it's precursers, rather than > > > taking glutathione itself. > > > > > > > > mom to broderick, asd, scd 19 months > > > > I am unable to explain as I am inexperienced with supplements. > > I got the definitions by doing an Internet search. > > > > Carol F. > > > > > Quote Link to comment Share on other sites More sharing options...
Guest guest Posted April 25, 2007 Report Share Posted April 25, 2007 > > THANKS. I was thinking maybe I should investigate chelation, but > since he's been on this diet for almost 2 years he may not need it. > I ordered from Kirkman Labs, a detox powder, I'll try it. > > > SCD chelates. What powder did you order? Is it on the list of legal supplements? Otherwise it could cntain starch. Carol F. SCD 7 years, celiac Quote Link to comment Share on other sites More sharing options...
Guest guest Posted April 25, 2007 Report Share Posted April 25, 2007 SCD chelates? My son is needing chelation-where can I find more information? Teena Quote Link to comment Share on other sites More sharing options...
Guest guest Posted April 25, 2007 Report Share Posted April 25, 2007 Elaine opposed chelation. its a big trap for desperate mums becuse it promises the world and they are not exactly truthful about the results on the chelation boards an explanation of the issues http://gutresearch.com/SCDresearch/chelation.htm iv glutathione and nac have similar issues > > SCD chelates? My son is needing chelation-where can I find more information? > > > > Teena > > > > Quote Link to comment Share on other sites More sharing options...
Guest guest Posted April 25, 2007 Report Share Posted April 25, 2007 Not Mimi, But there is a correlation between bad mouth bacteria during pregnancy and the dental health of the children after they are born (ie: if mom has rotting teeth while pregnant, child will likely develop early childhood caries disease), so there must be some way that bacteria gets transferred. Some are now stating that the bacterial exposure in the birth canal is key to the baby's own flora (good bacterial in birth canal equals baby developing good bacteria). - robin wrote: Mim, I was just thinking kind of about this in the past couple of weeks since I am expecting again. At first, I was thinking that it would be best for me to go SCD during this pregnancy especially since I already have a child on the spectrum, and I am sure it is at least nutrition wise. I have been so incredibly ill with this pregnancy(which has never happened before) that I just ate whatever I could...which, of course, was definitely no where close to SCD. Then, I started wondering if could make a terrible difference gut wise for the baby because the baby is being fed in utero through the cord which is simply blood. It isn't like breast feeding where sugar and such would come through the milk. Would sugars and starches actually come through the cord blood to feed the baby with harmful bacterial overgrowth? I'm kind of confused about all of that now with this study that you posted. I also was under the impression that babies are born with pretty much a clean slate in the gut. Can you help me understand this whole thing better? Meleah Re: Re: glutamine and Glutathione A natural way to increase glutathione levels is to eliminate the pathogenic bacteria in our guts. LPS, the poison found in pathogenic bacteria decreases glutathione levels. SCD is a great way to eliminate the poisons from gut pathogens and restore the glutathione levels. There is a famous doctor who is an expert in detoxification and he now uses SCD for detoxification. Below is a research article that demonstrates that bacterial poisons decrease the level of glutathione. Mimi http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=Abstra\ ctPlus&list_uids=17291629&query_hl=2&itool=pubmed_docsum 1: Neurochem Int. 2007 Mar;50(4):671-80. Epub 2007 Jan 13. Altered glutathione homeostasis in animals prenatally exposed to lipopolysaccharide. * Zhu Y, * Carvey PM, * Ling Z. Department of Pharmacology, Rush University Medical Center, 1735 West on Street, Chicago, IL 60612, USA. We previously reported that injection of bacterial lipopolysaccharide (LPS) into gravid female rats at embryonic day 10.5 resulted in a birth of offspring with fewer than normal dopamine (DA) neurons along with innate immunity dysfunction and many characteristics seen in Parkinson's disease (PD) patients. The LPS-exposed animals were also more susceptible to secondary toxin exposure as indicated by an accelerated DA neuron loss. Glutathione (GSH) is an important antioxidant in the brain. A disturbance in glutathione homeostasis has been proposed for the pathogenesis of PD. In this study, animals prenatally exposed to LPS were studied along with an acute intranigral LPS injection model for the status of glutathione homeostasis, lipid peroxidation, and related enzyme activities. Both prenatal LPS exposure and acute LPS injection produced a significant GSH reduction and increase in oxidized GSH (GSSG) and lipid peroxide (LPO) production. Activity of gamma-glutamylcysteine synthetase (GCS), the rate-limiting enzyme in de novo GSH synthesis, was up-regulated in acute supranigral LPS model but was reduced in the prenatal LPS model. The GCS light subunit protein expression was also down-regulated in prenatal LPS model. GSH redox recycling enzyme activities (glutathione peroxidase, GPx and glutathione reducdase, GR) and glutathione-S-transferase (GST), gamma-glutamyl transpeptidase (gamma-GT) activities were all increased in prenatal LPS model. Prenatal LPS exposure and aging synergized in GSH level and GSH-related enzyme activities except for those (GR, GST, and gamma-GT) with significant regional variations. Additionally, prenatal LPS exposure produced a reduction of DA neuron count in the substantia nigra (SN). These results suggest that prenatal LPS exposure may cause glutathione homeostasis disturbance in offspring brain and render DA neurons susceptible to the secondary neurotoxin insult. PMID: 17291629 [PubMed - in process] > > > > > > > They are different. L-glutamine is an amino acid. It only causes > > neurological damage if it is in excess and converts to glutimate. > > This is one of those controversial issues. It does help the gut and > > therefore has also helped many with neurological conditions. > > > > > > Glutathione is an anti-oxidant. It is often better to create > > more glutathione in the body by giving it's precursers, rather than > > taking glutathione itself. > > > > > > mom to broderick, asd, scd 19 months > > I am unable to explain as I am inexperienced with supplements. > I got the definitions by doing an Internet search. > > Carol F. > > Quote Link to comment Share on other sites More sharing options...
Guest guest Posted April 25, 2007 Report Share Posted April 25, 2007 Great. Meleah Re: Re: glutamine and Glutathione A natural way to increase glutathione levels is to eliminate the pathogenic bacteria in our guts. LPS, the poison found in pathogenic bacteria decreases glutathione levels. SCD is a great way to eliminate the poisons from gut pathogens and restore the glutathione levels. There is a famous doctor who is an expert in detoxification and he now uses SCD for detoxification. Below is a research article that demonstrates that bacterial poisons decrease the level of glutathione. Mimi http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=Abstra\ ctPlus&list_uids=17291629&query_hl=2&itool=pubmed_docsum 1: Neurochem Int. 2007 Mar;50(4):671-80. Epub 2007 Jan 13. Altered glutathione homeostasis in animals prenatally exposed to lipopolysaccharide. * Zhu Y, * Carvey PM, * Ling Z. Department of Pharmacology, Rush University Medical Center, 1735 West on Street, Chicago, IL 60612, USA. We previously reported that injection of bacterial lipopolysaccharide (LPS) into gravid female rats at embryonic day 10.5 resulted in a birth of offspring with fewer than normal dopamine (DA) neurons along with innate immunity dysfunction and many characteristics seen in Parkinson's disease (PD) patients. The LPS-exposed animals were also more susceptible to secondary toxin exposure as indicated by an accelerated DA neuron loss. Glutathione (GSH) is an important antioxidant in the brain. A disturbance in glutathione homeostasis has been proposed for the pathogenesis of PD. In this study, animals prenatally exposed to LPS were studied along with an acute intranigral LPS injection model for the status of glutathione homeostasis, lipid peroxidation, and related enzyme activities. Both prenatal LPS exposure and acute LPS injection produced a significant GSH reduction and increase in oxidized GSH (GSSG) and lipid peroxide (LPO) production. Activity of gamma-glutamylcysteine synthetase (GCS), the rate-limiting enzyme in de novo GSH synthesis, was up-regulated in acute supranigral LPS model but was reduced in the prenatal LPS model. The GCS light subunit protein expression was also down-regulated in prenatal LPS model. GSH redox recycling enzyme activities (glutathione peroxidase, GPx and glutathione reducdase, GR) and glutathione-S-transferase (GST), gamma-glutamyl transpeptidase (gamma-GT) activities were all increased in prenatal LPS model. Prenatal LPS exposure and aging synergized in GSH level and GSH-related enzyme activities except for those (GR, GST, and gamma-GT) with significant regional variations. Additionally, prenatal LPS exposure produced a reduction of DA neuron count in the substantia nigra (SN). These results suggest that prenatal LPS exposure may cause glutathione homeostasis disturbance in offspring brain and render DA neurons susceptible to the secondary neurotoxin insult. PMID: 17291629 [PubMed - in process] > > > > > > > They are different. L-glutamine is an amino acid. It only causes > > neurological damage if it is in excess and converts to glutimate. > > This is one of those controversial issues. It does help the gut and > > therefore has also helped many with neurological conditions. > > > > > > Glutathione is an anti-oxidant. It is often better to create > > more glutathione in the body by giving it's precursers, rather than > > taking glutathione itself. > > > > > > mom to broderick, asd, scd 19 months > > I am unable to explain as I am inexperienced with supplements. > I got the definitions by doing an Internet search. > > Carol F. > > Quote Link to comment Share on other sites More sharing options...
Guest guest Posted April 25, 2007 Report Share Posted April 25, 2007 Hi Meleah, There is an endless amount of research articles that point out that injecting LPS into pregnant mice brings autistic like damage to the unborn baby's brain. LPS is one of the toxins from pathogenic bacteria. So if a mother has GI problems and toxins from bacteria, then the toxins could affect her child. I will send you a website that explains the role of LPS in ASD in private email. Mimi Here are two examples: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=Abstra\ ctPlus&list_uids=15829260&query_hl=2&itool=pubmed_docsum 1: Neuropharmacology. 2005 May;48(6):903-17.Click here to read Links Specific neurodevelopmental damage in mice offspring following maternal inflammation during pregnancy. * Golan HM, * Lev V, * Hallak M, * Sorokin Y, * Huleihel M. Department of Developmental Molecular Genetics and Zlotowski Center for Neuroscience, Ben-Gurion University of the Negev, Beer-Sheva, Israel. havag@... Intrauterine inflammation is a major risk for offspring neurodevelopmental brain damage and may result in cognitive limitations and poor cognitive and perceptual outcomes. Pro-inflammatory cytokines, stimulated during inflammatory response, have a pleotrophic effect on neurons and glia cells. They act in a dose-dependent manner, activate cell-death pathways and also act as trophic factors. In the present study, we have examined in mice the effect of short, systemic maternal inflammation on fetal brain development. Maternal inflammation, induced by lipopolysaccharide (LPS) at gestation day 17, did not affect morphogenic parameters and reflex development during the first month of life. However, maternal inflammation specifically increased the number of pyramidal and granular cells in the hippocampus, as well as the shrinkage of pyramidal cells, but not of the granular cells. No additional major morphological differences were observed in the cerebral cortex or cerebellum. In accordance with the morphological effects, maternal inflammation specifically impaired distinct forms of learning and memory, but not motor function or exploration in the adult offspring. The specific deficiency observed, following maternal inflammation, may suggest particular sensitivity of the hippocampus and other associated brain regions to inflammatory factors during late embryonic development. PMID: 15829260 [PubMed - indexed for MEDLINE] http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=Abstra\ ctPlus&list_uids=16793357&query_hl=21&itool=pubmed_docsum 1: Semin Fetal Neonatal Med. 2006 Oct;11(5):343-53. Epub 2006 Jun 21.Click here to read Links Lipopolysaccharide-induced inflammation and perinatal brain injury. * Wang X, * Rousset CI, * Hagberg H, * Mallard C. Perinatal Center, Department of Neuroscience and Physiology, Sahlgrenska Academy, Goteborg University, 40530 Goteborg, Sweden. Both energy failure and infections are important risk factors for brain injury in term and preterm infants. In this review we focus on recent experimental studies that have examined the effects of lipopolysaccharide (LPS) exposure to the fetus or neonate and the interaction of LPS with other events. Intracerebral LPS injections induce a marked cerebral cytokine response and prominent white matter lesions. LPS administered intravenously to the fetus also induces gross lesions, which are mainly localised to the white matter and are accompanied by activation of inflammatory cells. Cerebral effects following fetal LPS exposure via more distant routes, such as intracervical, intrauterine or maternal LPS administration, are characterised by reductions in oligodendrocyte or myelin markers without macroscopic lesions being evident. Both antenatal and neonatal LPS exposures increase the sensitivity of the brain to subsequent hypoxic/ischaemic events, even in adulthood. These studies suggest that fetal inflammation is the strongest predictor of brain lesions. PMID: 16793357 [PubMed - indexed for MEDLINE] > Mim, > I was just thinking kind of about this in the past couple of weeks since I > am expecting again. At first, I was thinking that it would be best for me > to go SCD during this pregnancy especially since I already have a child on > the spectrum, and I am sure it is at least nutrition wise. I have been so > incredibly ill with this pregnancy(which has never happened before) that I > just ate whatever I could...which, of course, was definitely no where close > to SCD. Then, I started wondering if could make a terrible difference gut > wise for the baby because the baby is being fed in utero through the cord > which is simply blood. It isn't like breast feeding where sugar and such > would come through the milk. Would sugars and starches actually come > through the cord blood to feed the baby with harmful bacterial overgrowth? > I'm kind of confused about all of that now with this study that you posted. > I also was under the impression that babies are born with pretty much a > clean slate in the gut. Can you help me understand this whole thing better? > Meleah > Re: Re: glutamine and Glutathione > > > A natural way to increase glutathione levels is to eliminate the > pathogenic bacteria in our guts. LPS, the poison found in pathogenic > bacteria decreases glutathione levels. > SCD is a great way to eliminate the poisons from gut pathogens and > restore the glutathione levels. There is a famous doctor who is an > expert in detoxification and he now uses SCD for detoxification. > > Below is a research article that demonstrates that bacterial poisons > decrease the level of glutathione. > > Mimi > > > http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=Abstra\ ctPlus&list_uids=17291629&query_hl=2&itool=pubmed_docsum > > 1: Neurochem Int. 2007 Mar;50(4):671-80. Epub 2007 Jan 13. > Altered glutathione homeostasis in animals prenatally exposed to > lipopolysaccharide. > > * Zhu Y, > * Carvey PM, > * Ling Z. > > Department of Pharmacology, Rush University Medical Center, 1735 > West on Street, Chicago, IL 60612, USA. > > We previously reported that injection of bacterial > lipopolysaccharide (LPS) into gravid female rats at embryonic day 10.5 > resulted in a birth of offspring with fewer than normal dopamine (DA) > neurons along with innate immunity dysfunction and many > characteristics seen in Parkinson's disease (PD) patients. The > LPS-exposed animals were also more susceptible to secondary toxin > exposure as indicated by an accelerated DA neuron loss. Glutathione > (GSH) is an important antioxidant in the brain. A disturbance in > glutathione homeostasis has been proposed for the pathogenesis of PD. > In this study, animals prenatally exposed to LPS were studied along > with an acute intranigral LPS injection model for the status of > glutathione homeostasis, lipid peroxidation, and related enzyme > activities. Both prenatal LPS exposure and acute LPS injection > produced a significant GSH reduction and increase in oxidized GSH > (GSSG) and lipid peroxide (LPO) production. Activity of > gamma-glutamylcysteine synthetase (GCS), the rate-limiting enzyme in > de novo GSH synthesis, was up-regulated in acute supranigral LPS model > but was reduced in the prenatal LPS model. The GCS light subunit > protein expression was also down-regulated in prenatal LPS model. GSH > redox recycling enzyme activities (glutathione peroxidase, GPx and > glutathione reducdase, GR) and glutathione-S-transferase (GST), > gamma-glutamyl transpeptidase (gamma-GT) activities were all increased > in prenatal LPS model. Prenatal LPS exposure and aging synergized in > GSH level and GSH-related enzyme activities except for those (GR, GST, > and gamma-GT) with significant regional variations. Additionally, > prenatal LPS exposure produced a reduction of DA neuron count in the > substantia nigra (SN). These results suggest that prenatal LPS > exposure may cause glutathione homeostasis disturbance in offspring > brain and render DA neurons susceptible to the secondary neurotoxin > insult. > > PMID: 17291629 [PubMed - in process] > > > > > > > > > > > > They are different. L-glutamine is an amino acid. It only causes > > > neurological damage if it is in excess and converts to glutimate. > > > This is one of those controversial issues. It does help the gut and > > > therefore has also helped many with neurological conditions. > > > > > > > > Glutathione is an anti-oxidant. It is often better to create > > > more glutathione in the body by giving it's precursers, rather than > > > taking glutathione itself. > > > > > > > > mom to broderick, asd, scd 19 months > > > > I am unable to explain as I am inexperienced with supplements. > > I got the definitions by doing an Internet search. > > > > Carol F. > > > > > > > > > Quote Link to comment Share on other sites More sharing options...
Guest guest Posted April 25, 2007 Report Share Posted April 25, 2007 > > SCD chelates? My son is needing chelation-where can I find more information? > > > > Teena http://www.breakingtheviciouscycle.info/testimonies/heavy_metal_toxicity.htm Carol F. SCD 7 years, celiac Quote Link to comment Share on other sites More sharing options...
Guest guest Posted April 25, 2007 Report Share Posted April 25, 2007 Wow! Well that is proof! Who can deny that? Incredible! carolfrilegh wrote: > > >> SCD chelates? My son is needing chelation-where can I find more information? >> >> >> >> Teena >> > > http://www.breakingtheviciouscycle.info/testimonies/heavy_metal_toxicity.htm > > Carol F. > SCD 7 years, celiac > > Quote Link to comment Share on other sites More sharing options...
Guest guest Posted April 25, 2007 Report Share Posted April 25, 2007 I like the sense of humor! Many diets claim to chelate, but usually they mean that they free up the body to do what it is supposed to do (clear out toxins). Is that what people are talking about when they say SCD " chelates? " I personally don't like the over-extended use of the word chelate, so I also would also like clarification. - Will wrote: Wow! Well that is proof! Who can deny that? Incredible! carolfrilegh wrote: > > >> SCD chelates? My son is needing chelation-where can I find more information? >> >> >> >> Teena >> > > http://www.breakingtheviciouscycle.info/testimonies/heavy_metal_toxicity.htm > > Carol F. > SCD 7 years, celiac > > --------------------------------- Ahhh...imagining that irresistible " new car " smell? Check outnew cars at Yahoo! Autos. Quote Link to comment Share on other sites More sharing options...
Guest guest Posted April 25, 2007 Report Share Posted April 25, 2007 Hi , LPS is the toxin produced by many pathogenic bacteria in our gut. The liver is the major detoxifying organ in our body. LPS impairs detoxification by hurting the liver. LPS also impairs detoxification by reducing glutathione. I already sent proof to the list about the reduction of glutathione brought on by LPS. Here are some scientific papers about LPS and liver damage. Hope that they make you realize the importance of getting rid of LPS. HTH, Mimi http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=Abstra\ ctPlus&list_uids=11172429&query_hl=13&itool=pubmed_docsum 1: J Pediatr Surg. 2001 Feb;36(2):338-40.Click here to read Links Effect of lipopolysaccharide and cytokines on oxidative metabolism in neonatal rat hepatocytes. * New KJ, * Eaton S, * Elliott KR, * Spitz L, * Quant PA. Institute of Child Health and Great Ormond Street Hospital for Children, London, England, and the School of Biological Sciences, University of Manchester, Manchester, England. BACKGROUND/PURPOSE: Lipopolysaccharide (LPS) and cytokines produced during neonatal sepsis trigger free radical production, which eventually results in inhibition of liver metabolism. Studies in adults have indicated a hypermetabolic response to sepsis; however, evidence for a hypermetabolic response in neonates is equivocal. This study was carried out to determine whether LPS and cytokines can cause liver hypermetabolism in neonates. METHODS: The initial bacterial insult and cytokine cascade were mimicked by the addition of lipopolysaccharide (Escherichia coli 055:B5), tumour necrosis factor (TNF-alpha), and interleukin-6 (IL6) during the isolation of hepatocytes by collagenase digestion from 11- to 13-day-old Wistar rats. Hepatocyte oxygen consumption was measured polarographically with cells respiring on palmitate (0.5 mmol/L). Myxothiazol, a specific inhibitor of mitochondrial respiration, was used to distinguish extra- and intramitochondrial oxygen consumption. Morphologic changes were assessed by electron microscopy. RESULTS: The addition of LPS, TNF-alpha and IL6 during hepatocyte isolation resulted in a 10% decrease in cell yield (P <.05) compared with untreated controls; however, cell viability was unchanged (n = 31). Both total and extramitochondrial oxygen consumption were significantly greater in treated cells compared with untreated controls (P <.05, Student's t test). Electron microscopy indicated that LPS, TNF-alpha, and IL6 did not cause ultrastructural changes to hepatocytes. CONCLUSIONS: The increase in oxygen consumption was predominantly extramitochondrial and likely to be caused by increased oxygen requirement for cytosolic detoxification and repair purposes. This study shows that liver hypermetabolism metabolism can occur in response to LPS and cytokines. However, during in vivo neonatal sepsis, additional free radical damage may blunt this hypermetabolic response. PMID: 11172429 [PubMed - indexed for MEDLINE] http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=retrieve&db=pubmed&list_uids=9\ 790953&dopt=Abstract 1: Biochem Biophys Res Commun. 1998 Oct 9;251(1):313-9. Related Articles, Links Bacterial lipopolysaccharide induces uncoupling protein-2 expression in hepatocytes by a tumor necrosis factor-alpha-dependent mechanism. Cortez-Pinto H, Yang SQ, Lin HZ, Costa S, Hwang CS, Lane MD, Bagby G, Diehl AM. Department of Medicine, s Hopkins University, Baltimore, land, USA. The liver is a target for bacterial lipopolysaccharide (LPS) and participates in the metabolic response to endotoxemia. Recently published evidence indicates that LPS increases the expression of mitochondrial uncoupling protein-2 (UCP-2) mRNAs in several tissues, including the liver. Because hepatocytes in the healthy liver do not express UCP-2, LPS was thought to induce UCP-2 in liver macrophages, which express UCP-2 constitutively. However, the present studies of cultured peritoneal macrophages indicate that LPS reduces steady state levels of UCP-2 mRNAs in these cells. In contrast, UCP-2 mRNAs are induced in hepatocytes isolated from LPS treated rats and transfection of these hepatocytes with UCP-2 promoter-reporter constructs demonstrates substantial increases in UCP-2 promoter activity. LPS induction of hepatocyte UCP-2 expression is virtually abolished by prior treatment of rats with neutralizing antibodies to tumor necrosis factor alpha (TNF). Futhermore, TNFalpha treatment induces UCP-2 mRNA accumulation in primary cultures of hepatocytes from healthy rats. Thus, hepatocytes are likely to be important contributors to endotoxin-related increases in liver UCP-2 via a mechanism that involves the LPS-inducible cytokine, TNFalpha. Copyright 1998 Academic Press. PMID: 9790953 [PubMed - indexed for MEDLINE] http://ajpgi.physiology.org/cgi/content/full/282/1/G1 [i am quoting somewhere in the middle of the article] ABNORMAL MACROPHAGE PHENOTYPE IN RODENTS WITH DECREASED LEPTIN ACTIVITY TOP ABSTRACT INTRODUCTION ABNORMAL MACROPHAGE PHENOTYPE... MECHANISM FOR MACROPHAGE... HEPATIC CONSEQUENCES OF KC... REFERENCES Studies in obese, Zucker diabetic (fa/fa) rats provided the first clue that KC dysfunction might be involved in the pathogenesis of NAFLD (40). fa/fa Rats have a mutation in the long form of the leptin receptor (obRb) that inhibits leptin-initiated signal transduction (28). Hence, although serum concentrations of leptin are increased in fa/fa rats, these animals resemble ob/ob mice, which are genetically deficient in leptin. Both fa/fa rats and ob/ob mice are obese, insulin-resistant, develop fatty livers, and are unusually vulnerable to liver injury induced by bacterial lipopolysaccharide (LPS). In both strains, a typically innocuous dose of LPS induces severe fatty liver hepatitis (i.e., steatohepatitis) (40). Therefore, these animals provide models that can be used to probe the mechanisms that lead to the development of this type of liver injury. Extensive work by many groups has proven that LPS-liver injury is mediated by tumor necrosis factor- (TNF-). in normal rats and mice. Factors, such as interleukin (IL)-12 and -18 and interferon (IFN), that enhance TNF- activity generally exacerbate LPS liver injury, whereas those that inhibit TNF-, such as IL-10, are hepatoprotective (24). Although many types of cells are capable of producing TNF-, KC are thought to be the principal hepatic source of TNF- after LPS administration, because LPS is a potent KC activator, and various treatments that inhibit KC activation protect rats and mice from LPS-liver injury (34). Baseline serum concentrations of TNF- as well as TNF- gene expression in liver and white adipose tissue are slightly, but significantly, increased in fa/fa rats and ob/ob mice compared with their lean littermates. However, TNF- expression is not induced supranormally following LPS administration in either strain (40). Therefore, enhanced sensitivity to TNF- hepatotoxicity, rather than overproduction of TNF-, must underlie the increased liver damage that occurs in fa/fa rats and ob/ob mice compared with their littermate controls after LPS treatment. Because KC are major producers of the cytokines that modulate TNF- activity, it was logical to screen fa/fa rats and ob/ob mice for evidence of KC alterations. Analysis of the pre- and post-LPS liver samples demonstrated significantly and consistently reduced expression of KCR, a KC-specific gene, in fa/fa livers. In contrast, KCR expression decreased only transiently after LPS administration in control animals. Moreover, fa/fa rats exhibited reduced hepatic clearance of intraperitoneally administered fluorescent-labeled microspheres. Neither of these deficiencies in fa/fa KC function was likely to have been the result of decreased numbers of hepatic macrophages, because the hepatic expression of Pu-1, a myeloid enriched transcription factor that can be used to approximate KC number, was similar in fa/fa rats and controls (40). Further support for the possibility that the phenotype of KC is abnormal in the LPS-sensitive fa/fa rats was provided by subsequent experiments that compared the phagocytic function and cytokine production of cultured peritoneal macrophages and bone marrow cells from control rats and mice with those of ob/ob mice, fa/fa rats, and db/db mice (which also have dysfunctional leptin receptors). Macrophages derived from all of the strains with decreased endogenous leptin activity exhibited reduced phagocytic activity in vitro. In cells with functional leptin receptors, this defect was improved by adding leptin to the culture medium (19). Thus chronic inhibition of leptin signaling reversibly reduces the phagocytic function of macrophages. Macrophages from strains with reduced leptin activity also demonstrated other abnormalities, such as abnormal cytokine production basally and/or after challenge with LPS. For example, LPS induction of IL-6 was enhanced significantly, whereas that of IL-10 was inhibited in fa/fa or ob/ob cells. However, unlike phagocytosis, overnight incubation in leptin-containing medium did little to correct these abnormalities (19). > I like the sense of humor! > > Many diets claim to chelate, but usually they mean that they free up the > body to do what it is supposed to do (clear out toxins). Is that what > people are talking about when they say SCD " chelates? " I personally don't > like the over-extended use of the word chelate, so I also would also like > clarification. > > - > > Will wrote: > > Wow! Well that is proof! Who can deny that? Incredible! > > carolfrilegh wrote: > > > > > >> SCD chelates? My son is needing chelation-where can I find more > information? > >> > >> > >> > >> Teena > >> > > > > > http://www.breakingtheviciouscycle.info/testimonies/heavy_metal_toxicity.htm > > > > Carol F. > > SCD 7 years, celiac > > > > > > > > > > --------------------------------- > Ahhh...imagining that irresistible " new car " smell? > Check outnew cars at Yahoo! Autos. > > Quote Link to comment Share on other sites More sharing options...
Guest guest Posted April 26, 2007 Report Share Posted April 26, 2007 I don't want to get into a big chelation argument here, but I just want to say that's not totally accurate. I'm sure that chelation is a disaster for some kids. In fact, I know of one child that it was just that for. However, my son has made unbelievable progress since chelating, and there's no way around that. I also know a couple of other kids who have had great success with chelation. I think you have to have a knowledgeable physician overseeing what is going on, and one who knows if your child is even a candidate for it. I think that same for IV glutathion and NAC. We have been using glutathion for months, and got the greatest results after switching to the IV form. I'm not opposed to doing natural forms of chelation if one wants to, but I don't think everyone should be slamming the medical chelation procedures either when it does truly work well for some children. I'm not saying that it is helpful for all kids, or that the natural chelation is bad. I don't even belong to a chelation board. I think parents must be very cautious and informed, and make the decision that is best for their child. Meleah Re: glutamine and Glutathione Elaine opposed chelation. its a big trap for desperate mums becuse it promises the world and they are not exactly truthful about the results on the chelation boards an explanation of the issues http://gutresearch.com/SCDresearch/chelation.htm iv glutathione and nac have similar issues > > SCD chelates? My son is needing chelation-where can I find more information? > > > > Teena > > > > Quote Link to comment Share on other sites More sharing options...
Guest guest Posted April 26, 2007 Report Share Posted April 26, 2007 Mimi; You must be kidding, those abstracts say nothing of the sort. I took a look at the full text of the two studies. The first study directly contradicts you. It states that when researchers *simulate sepsis by dripping purified endotoxins and cytokines on cultured liver cells in a dish* there is increased oxygen consumption in cultured rat liver cells, but the cells exhibit no signs of damage. Increased oxygen consumption is what cells normally do in the presence of a " toxin. " Quote: cell viability was unchanged (n = 31). Both total and extramitochondrial oxygen consumption were significantly greater in treated cells compared with untreated controls (P <.05, Student's t test). Electron microscopy indicated that LPS, TNF-alpha, and IL6 did not cause ultrastructural changes to hepatocytes. CONCLUSIONS: The increase in oxygen consumption was predominantly extramitochondrial and likely to be caused by increased oxygen requirement for cytosolic detoxification and repair purposes. And anyway, if a human being was exposed to that level of endotoxin they would within hours experience fever, septic shock and death. It has nothing to do with gut bugs in any realistic scenario. And guess what? The second study says *nothing* about liver damage. In non technical terms it is discussing modulation of fever response through up/downregulation of gene expression for involved proteins relative to various cytokines. Nothing about structural damage to hepatocytes from endotoxemia, rather the fever response and endotoxemia. I just skimmed the third article as this is becoming a waste of time. It states that rats specifically bred to express genetic abnormalities related to leptin receptors are obese, diabetic and have fatty livers. Further, a fatty liver is dysfunctional and they observed an impaired response to TNF alpha featuring over production of IL-6 and under production of IL-10. The fatty liver is due to obesity and diabetes, not endotoxin exposure. I have a suspicion you are just googling technical terms. Credibility? pecan post wrote: > Hi , > > LPS is the toxin produced by many pathogenic bacteria in our gut. The > liver is the major detoxifying organ in our body. LPS impairs > detoxification by hurting the liver. > LPS also impairs detoxification by reducing glutathione. I already > sent proof to the list about the reduction of glutathione brought on > by LPS. > > Here are some scientific papers about LPS and liver damage. Hope that > they make you realize the importance of getting rid of LPS. HTH, Mimi > > > http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=Abstra\ ctPlus&list_uids=11172429&query_hl=13&itool=pubmed_docsum > 1: J Pediatr Surg. 2001 Feb;36(2):338-40.Click here to read Links > Effect of lipopolysaccharide and cytokines on oxidative metabolism > in neonatal rat hepatocytes. > > * New KJ, > * Eaton S, > * Elliott KR, > * Spitz L, > * Quant PA. > > Institute of Child Health and Great Ormond Street Hospital for > Children, London, England, and the School of Biological Sciences, > University of Manchester, Manchester, England. > > BACKGROUND/PURPOSE: Lipopolysaccharide (LPS) and cytokines > produced during neonatal sepsis trigger free radical production, which > eventually results in inhibition of liver metabolism. Studies in > adults have indicated a hypermetabolic response to sepsis; however, > evidence for a hypermetabolic response in neonates is equivocal. This > study was carried out to determine whether LPS and cytokines can cause > liver hypermetabolism in neonates. METHODS: The initial bacterial > insult and cytokine cascade were mimicked by the addition of > lipopolysaccharide (Escherichia coli 055:B5), tumour necrosis factor > (TNF-alpha), and interleukin-6 (IL6) during the isolation of > hepatocytes by collagenase digestion from 11- to 13-day-old Wistar > rats. Hepatocyte oxygen consumption was measured polarographically > with cells respiring on palmitate (0.5 mmol/L). Myxothiazol, a > specific inhibitor of mitochondrial respiration, was used to > distinguish extra- and intramitochondrial oxygen consumption. > Morphologic changes were assessed by electron microscopy. RESULTS: The > addition of LPS, TNF-alpha and IL6 during hepatocyte isolation > resulted in a 10% decrease in cell yield (P <.05) compared with > untreated controls; however, cell viability was unchanged (n = 31). > Both total and extramitochondrial oxygen consumption were > significantly greater in treated cells compared with untreated > controls (P <.05, Student's t test). Electron microscopy indicated > that LPS, TNF-alpha, and IL6 did not cause ultrastructural changes to > hepatocytes. CONCLUSIONS: The increase in oxygen consumption was > predominantly extramitochondrial and likely to be caused by increased > oxygen requirement for cytosolic detoxification and repair purposes. > This study shows that liver hypermetabolism metabolism can occur in > response to LPS and cytokines. However, during in vivo neonatal > sepsis, additional free radical damage may blunt this hypermetabolic > response. > > PMID: 11172429 [PubMed - indexed for MEDLINE] > > http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=retrieve&db=pubmed&list_uids=9\ 790953&dopt=Abstract > 1: Biochem Biophys Res Commun. 1998 Oct 9;251(1):313-9. > Related Articles, Links > > > Bacterial lipopolysaccharide induces uncoupling protein-2 expression > in hepatocytes by a tumor necrosis factor-alpha-dependent mechanism. > > Cortez-Pinto H, Yang SQ, Lin HZ, Costa S, Hwang CS, Lane MD, Bagby G, Diehl AM. > > Department of Medicine, s Hopkins University, Baltimore, land, USA. > > The liver is a target for bacterial lipopolysaccharide (LPS) and > participates in the metabolic response to endotoxemia. Recently > published evidence indicates that LPS increases the expression of > mitochondrial uncoupling protein-2 (UCP-2) mRNAs in several tissues, > including the liver. Because hepatocytes in the healthy liver do not > express UCP-2, LPS was thought to induce UCP-2 in liver macrophages, > which express UCP-2 constitutively. However, the present studies of > cultured peritoneal macrophages indicate that LPS reduces steady state > levels of UCP-2 mRNAs in these cells. In contrast, UCP-2 mRNAs are > induced in hepatocytes isolated from LPS treated rats and transfection > of these hepatocytes with UCP-2 promoter-reporter constructs > demonstrates substantial increases in UCP-2 promoter activity. LPS > induction of hepatocyte UCP-2 expression is virtually abolished by > prior treatment of rats with neutralizing antibodies to tumor necrosis > factor alpha (TNF). Futhermore, TNFalpha treatment induces UCP-2 mRNA > accumulation in primary cultures of hepatocytes from healthy rats. > Thus, hepatocytes are likely to be important contributors to > endotoxin-related increases in liver UCP-2 via a mechanism that > involves the LPS-inducible cytokine, TNFalpha. Copyright 1998 Academic > Press. > > PMID: 9790953 [PubMed - indexed for MEDLINE] > http://ajpgi.physiology.org/cgi/content/full/282/1/G1 > > [i am quoting somewhere in the middle of the article] > ABNORMAL MACROPHAGE PHENOTYPE IN RODENTS WITH DECREASED LEPTIN ACTIVITY > > > TOP > ABSTRACT > INTRODUCTION > ABNORMAL MACROPHAGE PHENOTYPE... > MECHANISM FOR MACROPHAGE... > HEPATIC CONSEQUENCES OF KC... > REFERENCES > > > Studies in obese, Zucker diabetic (fa/fa) rats provided the first clue > that KC dysfunction might be involved in the pathogenesis of NAFLD > (40). fa/fa Rats have a mutation in the long form of the leptin > receptor (obRb) that inhibits leptin-initiated signal transduction > (28). Hence, although serum concentrations of leptin are increased in > fa/fa rats, these animals resemble ob/ob mice, which are genetically > deficient in leptin. Both fa/fa rats and ob/ob mice are obese, > insulin-resistant, develop fatty livers, and are unusually vulnerable > to liver injury induced by bacterial lipopolysaccharide (LPS). In both > strains, a typically innocuous dose of LPS induces severe fatty liver > hepatitis (i.e., steatohepatitis) (40). Therefore, these animals > provide models that can be used to probe the mechanisms that lead to > the development of this type of liver injury. > > > Extensive work by many groups has proven that LPS-liver injury is > mediated by tumor necrosis factor- (TNF-). in normal rats and mice. > Factors, such as interleukin (IL)-12 and -18 and interferon (IFN), > that enhance TNF- activity generally exacerbate LPS liver injury, > whereas those that inhibit TNF-, such as IL-10, are hepatoprotective > (24). Although many types of cells are capable of producing TNF-, KC > are thought to be the principal hepatic source of TNF- after LPS > administration, because LPS is a potent KC activator, and various > treatments that inhibit KC activation protect rats and mice from > LPS-liver injury (34). Baseline serum concentrations of TNF- as well > as TNF- gene expression in liver and white adipose tissue are > slightly, but significantly, increased in fa/fa rats and ob/ob mice > compared with their lean littermates. However, TNF- expression is not > induced supranormally following LPS administration in either strain > (40). Therefore, enhanced sensitivity to TNF- hepatotoxicity, rather > than overproduction of TNF-, must underlie the increased liver damage > that occurs in fa/fa rats and ob/ob mice compared with their > littermate controls after LPS treatment. > > > Because KC are major producers of the cytokines that modulate TNF- > activity, it was logical to screen fa/fa rats and ob/ob mice for > evidence of KC alterations. Analysis of the pre- and post-LPS liver > samples demonstrated significantly and consistently reduced expression > of KCR, a KC-specific gene, in fa/fa livers. In contrast, KCR > expression decreased only transiently after LPS administration in > control animals. Moreover, fa/fa rats exhibited reduced hepatic > clearance of intraperitoneally administered fluorescent-labeled > microspheres. Neither of these deficiencies in fa/fa KC function was > likely to have been the result of decreased numbers of hepatic > macrophages, because the hepatic expression of Pu-1, a myeloid > enriched transcription factor that can be used to approximate KC > number, was similar in fa/fa rats and controls (40). Further support > for the possibility that the phenotype of KC is abnormal in the > LPS-sensitive fa/fa rats was provided by subsequent experiments that > compared the phagocytic function and cytokine production of cultured > peritoneal macrophages and bone marrow cells from control rats and > mice with those of ob/ob mice, fa/fa rats, and db/db mice (which also > have dysfunctional leptin receptors). Macrophages derived from all of > the strains with decreased endogenous leptin activity exhibited > reduced phagocytic activity in vitro. In cells with functional leptin > receptors, this defect was improved by adding leptin to the culture > medium (19). Thus chronic inhibition of leptin signaling reversibly > reduces the phagocytic function of macrophages. Macrophages from > strains with reduced leptin activity also demonstrated other > abnormalities, such as abnormal cytokine production basally and/or > after challenge with LPS. For example, LPS induction of IL-6 was > enhanced significantly, whereas that of IL-10 was inhibited in fa/fa > or ob/ob cells. However, unlike phagocytosis, overnight incubation in > leptin-containing medium did little to correct these abnormalities > (19). > > > Quote Link to comment Share on other sites More sharing options...
Guest guest Posted April 26, 2007 Report Share Posted April 26, 2007 Hi Will, Thank you for checking the full articles. My connection to the full articles is temporarily not working. I was in a great hurry when I wrote my post. I am inviting list members to investigate the role oF LPS, a bacterial toxin, in the causation of ASD. I will soon post a link to the Yahoo Group that will be set up for that purpose. I will soon try answer specific issues that you have made. Thank you again, Mimi Quote Link to comment Share on other sites More sharing options...
Guest guest Posted April 26, 2007 Report Share Posted April 26, 2007 Hi Will, You wrote: >The fatty liver is due to obesity and diabetes, not endotoxin exposure. I just want to point out that LPS does cause insulin resistance and there is discussion that many children with ASD do have some problem with insulin. Some doctors are prescribing Actos, a medication for diaabetes to children with ASD. Mimi http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=retrieve&db=pubmed&list_uids=1\ 1061537&dopt=Abstract 1: J Clin Endocrinol Metab. 2000 Oct;85(10):3770-8. Related Articles, Links Insulin resistance and substrate utilization in human endotoxemia. Agwunobi AO, Reid C, Maycock P, Little RA, Carlson GL. Medical Research Council Trauma Group, North West Injury Research Center, University of Manchester, Hope Hospital, Salford, United Kingdom. Infection results in a state of insulin resistance, but the pathogenesis is poorly understood. Intravenous administration of bacterial lipopolysaccharide (LPS) has been used to mimic the febrile and systemic inflammatory responses to infection, but it is unclear whether LPS induces insulin resistance in man. To investigate the effects of LPS on insulin sensitivity and substrate utilization, we administered, in paired cross-over studies, either 20 U/kg Escherichia coli endotoxin or saline control to healthy volunteers (n = 6) 120 min after the start of a 10-h euglycemic hyperinsulinemic clamp (insulin infusion rate, 80 mU/m2 x min). LPS induced a fever, tachycardia, and mild arterial hypotension. Glucose utilization increased abruptly 120 min after LPS administration (+64.1+/-12.0%; P < 0.003), but then declined progressively, and insulin resistance was evident by 420 min (+1.9+/-3.5%; P < 0.05). The reduction in glucose utilization, like that observed in sepsis, was related to impaired nonoxidative glucose disposal and not abnormal glucose oxidation. The cortisol and GH responses to LPS were of sufficient duration and magnitude to explain the insulin resistance. LPS administration results in metabolic responses very similar to those observed in sepsis and could provide a useful model for the study of insulin resistance in human critical illness. Publication Types: Clinical Trial Randomized Controlled Trial PMID: 11061537 [PubMed - indexed for MEDLINE] > Hi Will, > > Thank you for checking the full articles. My connection to the full > articles is temporarily not working. I was in a great hurry when I > wrote my post. > > I am inviting list members to investigate the role oF LPS, a bacterial > toxin, in the causation of ASD. I will soon post a link to the Yahoo > Group that will be set up for that purpose. > > I will soon try answer specific issues that you have made. > > Thank you again, > Mimi > Quote Link to comment Share on other sites More sharing options...
Guest guest Posted April 26, 2007 Report Share Posted April 26, 2007 I did search on PubMed, the internet library of the National Institute of Health and found that the words " liver dysfunction endotoxemia, " will retrieve 446 citations. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Search&db=PubMed&term=+liver+d\ ysfunction+endotoxemia&tool=QuerySuggestion It does seem that several articles are saying that endotoxemia (LPS poisoning) does cause liver dysfunction. I still believe that I am right but was extremely tired last night when I submitted the wrong articles. Here are two new articles: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=Abstra\ ctPlus&list_uids=17023554&query_hl=3&itool=pubmed_docsum 1: Am J Physiol Gastrointest Liver Physiol. 2007 Feb;292(2):G518-25. Epub 2006 Oct 5.Click here to read Links Increased intestinal permeability in obese mice: new evidence in the pathogenesis of nonalcoholic steatohepatitis. * Brun P, * Castagliuolo I, * Leo VD, * Buda A, * Pinzani M, * Palu G, * es D. Department of Histology, Univ of Padua, Via Gabelli 63, Padova, Italy. A small percentage of pathologically obese subjects with fatty livers develop histological signs of necroinflammation and fibrosis, suggesting a variety of cofactors in the pathogenesis of obesity-related liver diseases including nonalcoholic steatohepatitis. Since several observations have linked bacterial endotoxins to liver damage, the aim of this study was to determine the effect of obesity on intestinal mucosal integrity and portal blood endotoxemia in two strains of obese mice: leptin-deficient (ob/ob) and hyperleptinemic (db/db) mice. Murine intestinal mucosal barrier function was assessed using a Ussing chamber, whereas ileum tight junction proteins were analyzed by immunocytochemistry and Western blot analysis. Circulating proinflammatory cytokines and portal blood endotoxin levels were measured by ELISA and the limulus test, respectively. The inflammatory and fibrogenic phenotype of murine hepatic stellate cells (HSCs) was determined by ELISA and quantitative RT-PCR. Ob/ob and db/db mice showed lower intestinal resistance, profoundly modified distribution of occludin and zonula occludens-1 in the intestinal mucosa, and higher circulating levels of inflammatory cytokines and portal endotoxemia compared with lean control mice. Moreover, HSCs isolated from ob/ob and db/db mice showed higher membrane CD14 mRNA levels and more pronounced lipopolysaccharide-induced proinflammatory and fibrogenic responses than HSCs from lean animals. In conclusion, genetically obese mice display enhanced intestinal permeability leading to increased portal endotoxemia that makes HSCs more sensitive to bacterial endotoxins. We suggest that in metabolic syndrome, patients may likewise have a greater intestinal mucosa permeability and increased lipopolysaccharide levels in portal blood that can contribute to the liver inflammatory damage. PMID: 17023554 [PubMed - indexed for MEDLINE] http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=3\ 692608&dopt=Abstract 1: Infection. 1987;15(5):359-62. Related Articles, Links Presence of endotoxemia and its relationship to liver dysfunction in patients with typhoid fever. Adinolfi LE, Utili R, Gaeta GB, Perna P, Ruggiero G. Clinica delle Malattie Tropicali e Subtropicali, I Facolta di Medicina, Universita di Napoli. Twenty-one patients with typhoid fever were studied to evaluate the presence of endotoxin in peripheral blood and its relationship to the incidence and features of hepatic dysfunction which may occur during this disease. The limulus test for endotoxin was positive in the plasma samples of all patients prior to treatment. Liver dysfunction, as assessed by fasting and postprandial serum bile acid levels and by standard biochemical tests, occurred in 90% of patients. In seven, the injury was purely cholestatic (elevation of postprandial serum bile acid levels, alone); in 12, it was of mixed cholestatic-hepatocellular type (elevation of both serum bile acids and aminotransferase levels). After recovering, the limulus test was negative and liver function tests returned to normal values in all patients. The results demonstrate that endotoxemia is present in patients with typhoid fever. In addition, since endotoxin can impair bile secretion, our results suggest that endotoxin may have a pathogenetic role in the development of liver injury during typhoid fever. Publication Types: * Research Support, Non-U.S. Gov't PMID: 3692608 [PubMed - indexed for MEDLINE] Quote Link to comment Share on other sites More sharing options...
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