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Medical Forum / Diseases and Disorders / Hepatitis / May 2009Iron In Liver Disease
When the iron is removed the fatty liver is reversed. Hyperferritinemia is a risk factor for steatosis in chronic liver disease. Licata A, Nebbia ME, Cabibbo G, Iacono GL, Barbaria F, Brucato V, Alessi N, Porrovecchio S, Di Marco V, Craxì A, Cammà C World J Gastroenterol 2009 May 7; 15(17):2132-8. AIM: To investigate the relationship between ferritin and steatosis in patients with chronically abnormal liver function tests (LFTs) and high ferritin level. METHODS: One hundred and twenty-four consecutive patients with hyperferritinemia (male > 300 ng/mL, female > 200 ng/mL) were evaluated; clinical, biochemical and serological data, iron status parameters, HFE gene mutations and homeostasis model assessment score were obtained. Steatosis was graded by ultrasound as absent or present. Histology was available in 53 patients only. RESULTS: Mean level of ferritin was 881 +/- 77 ng/mL in men and 549 +/- 82 ng/mL in women. The diagnosis was chronic hepatitis C in 53 (42.7%), non-alcoholic fatty liver disease/non-alcoholic steatohepatitis in 57 (45.9%), and cryptogenic liver damage in 14 (11.3%). None was diagnosed as hereditary hemochromatosis (HH). Hepatic siderosis on liver biopsy was present in 17 of 54 (32%) patients; grade 1 in eight and grade 2 in nine. Overall, 92 patients (74.2%) had steatosis. By logistic regression, ferritin and gamma-glutamyltransferase were independent predictors of steatosis. Ferritin levels were significantly related to low platelet count, steatosis and hepatitis C virus infection. CONCLUSION: In a non-obese cohort of non-alcoholic patients with chronically abnormal LFTs without HH, high serum ferritin level is a risk factor for steatosis. World journal of gastroenterology : WJG [World J Gastroenterol] ------------------- Evidenced based medicine .. Low iron equals low fatty liver disease. Which would explain somewhat the REVERSAL OF CIRRHOSIS which has been demonstrated by the iron reduction therapy. "These results reflect the insulin-sparing effect of iron depletion and indicate a key role of iron and hyperinsulinemia in the pathogenesis of NAFLD" Effect of iron depletion in carbohydrate-intolerant patients with clinical evidence of nonalcoholic fatty liver disease. Gastroenterology 2002 Apr;122(4):931-9 Facchini FS, Hua NW, Stoohs RA. Department of Medicine, University of California San Francisco and San Francisco General Hospital, San Francisco, California, USA. ffacch...@ecnea.org BACKGROUND & AIMS: Increased body iron, genetic hemochromatosis (GH) mutations, and nonalcoholic fatty liver disease (NAFLD) tend to cluster in carbohydrate-intolerant patients. In an attempt to further clarify the interrelationships among these conditions, we studied 42 carbohydrate-intolerant patients who were free of the common GH mutations C282Y and H63D, and had a serum iron saturation lower than 50%. METHODS: We measured body iron stores, and induced iron depletion to a level of near-iron deficiency (NID) by quantitative phlebotomy. RESULTS: In the 17 patients with clinical evidence of NAFLD, we could not demonstrate supranormal levels of body iron (1.6 +/- 0.2 vs. 1.4 +/- 0.2 g; P = 0.06). However, at NID, there was a 40%-55% improvement (P = 0.05-0.0001) of both fasting and glucose-stimulated plasma insulin concentrations, and near-normalization of serum alanine aminotransferase activity (from 61 +/- 5 to 32 +/- 2 IU/L; P < 0.001). CONCLUSIONS: These results reflect the insulin-sparing effect of iron depletion and indicate a key role of iron and hyperinsulinemia in the pathogenesis of NAFLD. PMID: 11910345 --------------- http://www.natap.org/2000/jan/fattyliver011700.html Who loves ya. Tom Jesus Was A Vegetarian! http://tinyurl.com/634q5a Man Is A Herbivore! http://tinyurl.com/4rq595 DEAD PEOPLE WALKING http://tinyurl.com/zk9fk This one suffers from the usual flaws of logic as most you post. A quiz, list for us those flaws. You should ace this because those flaws have been presented so often and you are such a goodstudent after all. On May 8, 12:00 pm, tu...@guy.com wrote: snip << Is that an attempt at a smartass .. abusive .. remark .. ? I believe it is .. What maybe you should dooooo .. is .. fkff .. How's that sound .. WHEN the **iron** is REMOVED the fatty liver is REVERSED. Hyperferritinemia is a risk factor for steatosis in chronic liver disease. Licata A, Nebbia ME, Cabibbo G, Iacono GL, Barbaria F, Brucato V, Alessi N, Porrovecchio S, Di Marco V, Craxì A, Cammà C World J Gastroenterol 2009 May 7; 15(17):2132-8. AIM: To investigate the relationship between ferritin and steatosis in patients with chronically abnormal liver function tests (LFTs) and high ferritin level. METHODS: One hundred and twenty-four consecutive patients with hyperferritinemia (male > 300 ng/mL, female > 200 ng/mL) were evaluated; clinical, biochemical and serological data, iron status parameters, HFE gene mutations and homeostasis model assessment score were obtained. Steatosis was graded by ultrasound as absent or present. Histology was available in 53 patients only. RESULTS: Mean level of ferritin was 881 +/- 77 ng/mL in men and 549 +/- 82 ng/mL in women. The diagnosis was chronic hepatitis C in 53 (42.7%), non-alcoholic fatty liver disease/non-alcoholic steatohepatitis in 57 (45.9%), and cryptogenic liver damage in 14 (11.3%). None was diagnosed as hereditary hemochromatosis (HH). Hepatic siderosis on liver biopsy was present in 17 of 54 (32%) patients; grade 1 in eight and grade 2 in nine. Overall, 92 patients (74.2%) had steatosis. By logistic regression, ferritin and gamma-glutamyltransferase were independent predictors of steatosis. Ferritin levels were significantly related to low platelet count, steatosis and hepatitis C virus infection. CONCLUSION: In a non-obese cohort of non-alcoholic patients with chronically abnormal LFTs without HH, high serum ferritin level is a risk factor for steatosis. World journal of gastroenterology : WJG [World J Gastroenterol] ------------------- Evidenced based medicine .. Low iron equals low fatty liver disease. Which would explain somewhat the REVERSAL OF CIRRHOSIS which has been demonstrated by the iron reduction therapy. "These results reflect the insulin-sparing effect of iron depletion and indicate a key role of iron and hyperinsulinemia in the pathogenesis of NAFLD" Effect of iron depletion in carbohydrate-intolerant patients with clinical evidence of nonalcoholic fatty liver disease. Gastroenterology 2002 Apr;122(4):931-9 Facchini FS, Hua NW, Stoohs RA. Department of Medicine, University of California San Francisco and San Francisco General Hospital, San Francisco, California, USA. ffacch...@ecnea.org BACKGROUND & AIMS: Increased body iron, genetic hemochromatosis (GH) mutations, and nonalcoholic fatty liver disease (NAFLD) tend to cluster in carbohydrate-intolerant patients. In an attempt to further clarify the interrelationships among these conditions, we studied 42 carbohydrate-intolerant patients who were free of the common GH mutations C282Y and H63D, and had a serum iron saturation lower than 50%. METHODS: We measured body iron stores, and induced iron depletion to a level of near-iron deficiency (NID) by quantitative phlebotomy. RESULTS: In the 17 patients with clinical evidence of NAFLD, we could not demonstrate supranormal levels of body iron (1.6 +/- 0.2 vs. 1.4 +/- 0.2 g; P = 0.06). However, at NID, there was a 40%-55% improvement (P = 0.05-0.0001) of both fasting and glucose-stimulated plasma insulin concentrations, and near-normalization of serum alanine aminotransferase activity (from 61 +/- 5 to 32 +/- 2 IU/L; P < 0.001). CONCLUSIONS: These results reflect the insulin-sparing effect of iron depletion and indicate a key role of iron and hyperinsulinemia in the pathogenesis of NAFLD. PMID: 11910345 --------------- http://www.natap.org/2000/jan/fattyliver011700.html Who loves ya. Tom Jesus Was A Vegetarian! http://tinyurl.com/634q5a Man Is A Herbivore! http://tinyurl.com/4rq595 DEAD PEOPLE WALKING http://tinyurl.com/zk9fk When pigs fly. And "swine flu" is a different spelling. On May 8, 3:00 pm, tu...@guy.com wrote: > This one suffers from the usual flaws of logic as most you post. > > A quiz, list for us those flaws. > > You should ace this because those flaws have been presented so often and > you are such a goodstudent after all. On May 8, 3:00 pm, Michael B <baugh...@bellsouth.net> wrote::snip << Giiiiit .. you useless mutated disease ridden shteater .. You were told to take your useless mutated disease ridden shteating self somewhere .. else .. You are dysfunctional .. therefore NOT **allowed** in the groups .. Remember all you useless mutated disease ridden shteaters when you cut my posts .. it is evidence of the dysfunctional predatorial nature of yours VERY common in men who prefer to have sex with boys .. http://www.traditionalvalues.org/homosexual_movement_and_pedophilia/ http://www.talk2action.org/story/2006/10/3/21245/3789 http://predatorsafety.blogspot.com/2008/11/homosexual-grooming-of-chi... Predator Safety - Dedicated To The Protection Of Our Children The predatorial posts by the shteaters in this thread .. evidence .. mental instability .. common to homosexuals .. IE: "Dysfunctional Homosexuals" ------------------ WHEN the **iron** is REMOVED the fatty liver is REVERSED. Hyperferritinemia is a risk factor for steatosis in chronic liver disease. Licata A, Nebbia ME, Cabibbo G, Iacono GL, Barbaria F, Brucato V, Alessi N, Porrovecchio S, Di Marco V, Craxì A, Cammà C World J Gastroenterol 2009 May 7; 15(17):2132-8. AIM: To investigate the relationship between ferritin and steatosis in patients with chronically abnormal liver function tests (LFTs) and high ferritin level. METHODS: One hundred and twenty-four consecutive patients with hyperferritinemia (male > 300 ng/mL, female > 200 ng/mL) were evaluated; clinical, biochemical and serological data, iron status parameters, HFE gene mutations and homeostasis model assessment score were obtained. Steatosis was graded by ultrasound as absent or present. Histology was available in 53 patients only. RESULTS: Mean level of ferritin was 881 +/- 77 ng/mL in men and 549 +/- 82 ng/mL in women. The diagnosis was chronic hepatitis C in 53 (42.7%), non-alcoholic fatty liver disease/non-alcoholic steatohepatitis in 57 (45.9%), and cryptogenic liver damage in 14 (11.3%). None was diagnosed as hereditary hemochromatosis (HH). Hepatic siderosis on liver biopsy was present in 17 of 54 (32%) patients; grade 1 in eight and grade 2 in nine. Overall, 92 patients (74.2%) had steatosis. By logistic regression, ferritin and gamma-glutamyltransferase were independent predictors of steatosis. Ferritin levels were significantly related to low platelet count, steatosis and hepatitis C virus infection. CONCLUSION: In a non-obese cohort of non-alcoholic patients with chronically abnormal LFTs without HH, high serum ferritin level is a risk factor for steatosis. World journal of gastroenterology : WJG [World J Gastroenterol] ------------------- Evidenced based medicine .. Low iron equals low fatty liver disease. Which would explain somewhat the REVERSAL OF CIRRHOSIS which has been demonstrated by the iron reduction therapy. "These results reflect the insulin-sparing effect of iron depletion and indicate a key role of iron and hyperinsulinemia in the pathogenesis of NAFLD" Effect of iron depletion in carbohydrate-intolerant patients with clinical evidence of nonalcoholic fatty liver disease. Gastroenterology 2002 Apr;122(4):931-9 Facchini FS, Hua NW, Stoohs RA. Department of Medicine, University of California San Francisco and San Francisco General Hospital, San Francisco, California, USA. ffacch...@ecnea.org BACKGROUND & AIMS: Increased body iron, genetic hemochromatosis (GH) mutations, and nonalcoholic fatty liver disease (NAFLD) tend to cluster in carbohydrate-intolerant patients. In an attempt to further clarify the interrelationships among these conditions, we studied 42 carbohydrate-intolerant patients who were free of the common GH mutations C282Y and H63D, and had a serum iron saturation lower than 50%. METHODS: We measured body iron stores, and induced iron depletion to a level of near-iron deficiency (NID) by quantitative phlebotomy. RESULTS: In the 17 patients with clinical evidence of NAFLD, we could not demonstrate supranormal levels of body iron (1.6 +/- 0.2 vs. 1.4 +/- 0.2 g; P = 0.06). However, at NID, there was a 40%-55% improvement (P = 0.05-0.0001) of both fasting and glucose-stimulated plasma insulin concentrations, and near-normalization of serum alanine aminotransferase activity (from 61 +/- 5 to 32 +/- 2 IU/L; P < 0.001). CONCLUSIONS: These results reflect the insulin-sparing effect of iron depletion and indicate a key role of iron and hyperinsulinemia in the pathogenesis of NAFLD. PMID: 11910345 --------------- http://www.natap.org/2000/jan/fattyliver011700.html Who loves ya. Tom Jesus Was A Vegetarian! http://tinyurl.com/634q5a Man Is A Herbivore! http://tinyurl.com/4rq595 DEAD PEOPLE WALKING http://tinyurl.com/zk9fk Spamming Fuckwit On May 8, 4:46 pm, Rusty the Canuck Dicksucker <flakey...@earthlink.net> wrote:snip << ALL you shteaters were TOLD to stay off my threads .. Understand .. shteater .. ? You shteaters have NO .. input .. ON .. **my** threads .. That must be too hard for you shteaters to understand .. You shteaters ha've been TOLD numerous times .. you are NOT welcome .. You shteaters are a fkg .. looooooons .. STAY .. off .. my .. threads .. you fkg .. loooooon .. Dooooo .. it .. looooon .. ------------------ WHEN the **iron** is REMOVED the fatty liver is REVERSED. Hyperferritinemia is a risk factor for steatosis in chronic liver disease. Licata A, Nebbia ME, Cabibbo G, Iacono GL, Barbaria F, Brucato V, Alessi N, Porrovecchio S, Di Marco V, Craxì A, Cammà C World J Gastroenterol 2009 May 7; 15(17):2132-8. AIM: To investigate the relationship between ferritin and steatosis in patients with chronically abnormal liver function tests (LFTs) and high ferritin level. METHODS: One hundred and twenty-four consecutive patients with hyperferritinemia (male > 300 ng/mL, female > 200 ng/mL) were evaluated; clinical, biochemical and serological data, iron status parameters, HFE gene mutations and homeostasis model assessment score were obtained. Steatosis was graded by ultrasound as absent or present. Histology was available in 53 patients only. RESULTS: Mean level of ferritin was 881 +/- 77 ng/mL in men and 549 +/- 82 ng/mL in women. The diagnosis was chronic hepatitis C in 53 (42.7%), non-alcoholic fatty liver disease/non-alcoholic steatohepatitis in 57 (45.9%), and cryptogenic liver damage in 14 (11.3%). None was diagnosed as hereditary hemochromatosis (HH). Hepatic siderosis on liver biopsy was present in 17 of 54 (32%) patients; grade 1 in eight and grade 2 in nine. Overall, 92 patients (74.2%) had steatosis. By logistic regression, ferritin and gamma-glutamyltransferase were independent predictors of steatosis. Ferritin levels were significantly related to low platelet count, steatosis and hepatitis C virus infection. CONCLUSION: In a non-obese cohort of non-alcoholic patients with chronically abnormal LFTs without HH, high serum ferritin level is a risk factor for steatosis. World journal of gastroenterology : WJG [World J Gastroenterol] ------------------- Evidenced based medicine .. Low iron equals low fatty liver disease. Which would explain somewhat the REVERSAL OF CIRRHOSIS which has been demonstrated by the iron reduction therapy. "These results reflect the insulin-sparing effect of iron depletion and indicate a key role of iron and hyperinsulinemia in the pathogenesis of NAFLD" Effect of iron depletion in carbohydrate-intolerant patients with clinical evidence of nonalcoholic fatty liver disease. Gastroenterology 2002 Apr;122(4):931-9 Facchini FS, Hua NW, Stoohs RA. Department of Medicine, University of California San Francisco and San Francisco General Hospital, San Francisco, California, USA. ffacch...@ecnea.org BACKGROUND & AIMS: Increased body iron, genetic hemochromatosis (GH) mutations, and nonalcoholic fatty liver disease (NAFLD) tend to cluster in carbohydrate-intolerant patients. In an attempt to further clarify the interrelationships among these conditions, we studied 42 carbohydrate-intolerant patients who were free of the common GH mutations C282Y and H63D, and had a serum iron saturation lower than 50%. METHODS: We measured body iron stores, and induced iron depletion to a level of near-iron deficiency (NID) by quantitative phlebotomy. RESULTS: In the 17 patients with clinical evidence of NAFLD, we could not demonstrate supranormal levels of body iron (1.6 +/- 0.2 vs. 1.4 +/- 0.2 g; P = 0.06). However, at NID, there was a 40%-55% improvement (P = 0.05-0.0001) of both fasting and glucose-stimulated plasma insulin concentrations, and near-normalization of serum alanine aminotransferase activity (from 61 +/- 5 to 32 +/- 2 IU/L; P < 0.001). CONCLUSIONS: These results reflect the insulin-sparing effect of iron depletion and indicate a key role of iron and hyperinsulinemia in the pathogenesis of NAFLD. PMID: 11910345 --------------- http://www.natap.org/2000/jan/fattyliver011700.html Who loves ya. Tom Jesus Was A Vegetarian! http://tinyurl.com/634q5a Man Is A Herbivore! http://tinyurl.com/4rq595 DEAD PEOPLE WALKING http://tinyurl.com/zk9fk Get a life, ya fuckin Retard On May 9, 7:38 am, Rusty the OCD Retard <flakey...@earthlink.net> wrote:snip << ALL you shteaters were ALL told to stay off my threads .. That does mean **ALL** you .. shteaters.. NONE of you are special .. shteaters .. ALL you shteaters are to do like you're told .. DOOOOO .. it .. you dysfunctional mutated shteaters .. I told you not to cut these posts .. you dysfunctional mutated shteaters .. ------- WHEN the **iron** is REMOVED the fatty liver is REVERSED. Hyperferritinemia is a risk factor for steatosis in chronic liver disease. Licata A, Nebbia ME, Cabibbo G, Iacono GL, Barbaria F, Brucato V, Alessi N, Porrovecchio S, Di Marco V, Craxì A, Cammà C World J Gastroenterol 2009 May 7; 15(17):2132-8. AIM: To investigate the relationship between ferritin and steatosis in patients with chronically abnormal liver function tests (LFTs) and high ferritin level. METHODS: One hundred and twenty-four consecutive patients with hyperferritinemia (male > 300 ng/mL, female > 200 ng/mL) were evaluated; clinical, biochemical and serological data, iron status parameters, HFE gene mutations and homeostasis model assessment score were obtained. Steatosis was graded by ultrasound as absent or present. Histology was available in 53 patients only. RESULTS: Mean level of ferritin was 881 +/- 77 ng/mL in men and 549 +/- 82 ng/mL in women. The diagnosis was chronic hepatitis C in 53 (42.7%), non-alcoholic fatty liver disease/non-alcoholic steatohepatitis in 57 (45.9%), and cryptogenic liver damage in 14 (11.3%). None was diagnosed as hereditary hemochromatosis (HH). Hepatic siderosis on liver biopsy was present in 17 of 54 (32%) patients; grade 1 in eight and grade 2 in nine. Overall, 92 patients (74.2%) had steatosis. By logistic regression, ferritin and gamma-glutamyltransferase were independent predictors of steatosis. Ferritin levels were significantly related to low platelet count, steatosis and hepatitis C virus infection. CONCLUSION: In a non-obese cohort of non-alcoholic patients with chronically abnormal LFTs without HH, high serum ferritin level is a risk factor for steatosis. World journal of gastroenterology : WJG [World J Gastroenterol] ------------------- Evidenced based medicine .. Low iron equals low fatty liver disease. Which would explain somewhat the REVERSAL OF CIRRHOSIS which has been demonstrated by the iron reduction therapy. "These results reflect the insulin-sparing effect of iron depletion and indicate a key role of iron and hyperinsulinemia in the pathogenesis of NAFLD" Effect of iron depletion in carbohydrate-intolerant patients with clinical evidence of nonalcoholic fatty liver disease. Gastroenterology 2002 Apr;122(4):931-9 Facchini FS, Hua NW, Stoohs RA. Department of Medicine, University of California San Francisco and San Francisco General Hospital, San Francisco, California, USA. ffacch...@ecnea.org BACKGROUND & AIMS: Increased body iron, genetic hemochromatosis (GH) mutations, and nonalcoholic fatty liver disease (NAFLD) tend to cluster in carbohydrate-intolerant patients. In an attempt to further clarify the interrelationships among these conditions, we studied 42 carbohydrate-intolerant patients who were free of the common GH mutations C282Y and H63D, and had a serum iron saturation lower than 50%. METHODS: We measured body iron stores, and induced iron depletion to a level of near-iron deficiency (NID) by quantitative phlebotomy. RESULTS: In the 17 patients with clinical evidence of NAFLD, we could not demonstrate supranormal levels of body iron (1.6 +/- 0.2 vs. 1.4 +/- 0.2 g; P = 0.06). However, at NID, there was a 40%-55% improvement (P = 0.05-0.0001) of both fasting and glucose-stimulated plasma insulin concentrations, and near-normalization of serum alanine aminotransferase activity (from 61 +/- 5 to 32 +/- 2 IU/L; P < 0.001). CONCLUSIONS: These results reflect the insulin-sparing effect of iron depletion and indicate a key role of iron and hyperinsulinemia in the pathogenesis of NAFLD. PMID: 11910345 --------------- http://www.natap.org/2000/jan/fattyliver011700.html Who loves ya. Tom Jesus Was A Vegetarian! http://tinyurl.com/634q5a Man Is A Herbivore! http://tinyurl.com/4rq595 DEAD PEOPLE WALKING http://tinyurl.com/zk9fk What is really your goal here? What is really your goal here?<< Where .. ? How about .. our health care system is in a state of disarray. Eliminating the need for liver transplants will free up plenty of money to treat other diseases .. WHEN the **iron** is REMOVED the fatty liver is REVERSED. Hyperferritinemia is a risk factor for steatosis in chronic liver disease. Licata A, Nebbia ME, Cabibbo G, Iacono GL, Barbaria F, Brucato V, Alessi N, Porrovecchio S, Di Marco V, Craxì A, Cammà C World J Gastroenterol 2009 May 7; 15(17):2132-8. AIM: To investigate the relationship between ferritin and steatosis in patients with chronically abnormal liver function tests (LFTs) and high ferritin level. METHODS: One hundred and twenty-four consecutive patients with hyperferritinemia (male > 300 ng/mL, female > 200 ng/mL) were evaluated; clinical, biochemical and serological data, iron status parameters, HFE gene mutations and homeostasis model assessment score were obtained. Steatosis was graded by ultrasound as absent or present. Histology was available in 53 patients only. RESULTS: Mean level of ferritin was 881 +/- 77 ng/mL in men and 549 +/- 82 ng/mL in women. The diagnosis was chronic hepatitis C in 53 (42.7%), non-alcoholic fatty liver disease/non-alcoholic steatohepatitis in 57 (45.9%), and cryptogenic liver damage in 14 (11.3%). None was diagnosed as hereditary hemochromatosis (HH). Hepatic siderosis on liver biopsy was present in 17 of 54 (32%) patients; grade 1 in eight and grade 2 in nine. Overall, 92 patients (74.2%) had steatosis. By logistic regression, ferritin and gamma-glutamyltransferase were independent predictors of steatosis. Ferritin levels were significantly related to low platelet count, steatosis and hepatitis C virus infection. CONCLUSION: In a non-obese cohort of non-alcoholic patients with chronically abnormal LFTs without HH, high serum ferritin level is a risk factor for steatosis. World journal of gastroenterology : WJG [World J Gastroenterol] ------------------- Evidenced based medicine .. Low iron equals low fatty liver disease. Which would explain somewhat the REVERSAL OF CIRRHOSIS which has been demonstrated by the iron reduction therapy. "These results reflect the insulin-sparing effect of iron depletion and indicate a key role of iron and hyperinsulinemia in the pathogenesis of NAFLD" Effect of iron depletion in carbohydrate-intolerant patients with clinical evidence of nonalcoholic fatty liver disease. Gastroenterology 2002 Apr;122(4):931-9 Facchini FS, Hua NW, Stoohs RA. Department of Medicine, University of California San Francisco and San Francisco General Hospital, San Francisco, California, USA. ffacch...@ecnea.org BACKGROUND & AIMS: Increased body iron, genetic hemochromatosis (GH) mutations, and nonalcoholic fatty liver disease (NAFLD) tend to cluster in carbohydrate-intolerant patients. In an attempt to further clarify the interrelationships among these conditions, we studied 42 carbohydrate-intolerant patients who were free of the common GH mutations C282Y and H63D, and had a serum iron saturation lower than 50%. METHODS: We measured body iron stores, and induced iron depletion to a level of near-iron deficiency (NID) by quantitative phlebotomy. RESULTS: In the 17 patients with clinical evidence of NAFLD, we could not demonstrate supranormal levels of body iron (1.6 +/- 0.2 vs. 1.4 +/- 0.2 g; P = 0.06). However, at NID, there was a 40%-55% improvement (P = 0.05-0.0001) of both fasting and glucose-stimulated plasma insulin concentrations, and near-normalization of serum alanine aminotransferase activity (from 61 +/- 5 to 32 +/- 2 IU/L; P < 0.001). CONCLUSIONS: These results reflect the insulin-sparing effect of iron depletion and indicate a key role of iron and hyperinsulinemia in the pathogenesis of NAFLD. PMID: 11910345 --------------- http://www.natap.org/2000/jan/fattyliver011700.html Who loves ya. Tom Jesus Was A Vegetarian! http://tinyurl.com/634q5a Man Is A Herbivore! http://tinyurl.com/4rq595 DEAD PEOPLE WALKING http://tinyurl.com/zk9fk FOAD Spammer Please, please, you guys, don't feed the troll and spare us from the crossposting. Those of us who have been around for a while know that IJ has "issues" and rational discussion is impossible. Let him be, it's the least annoying to the largest number of people. If you keep this up, you're getting to be as bad as him. Please show where, in the details you provided, the observation is made that when the iron is removed the fatty liver is reversed. Such an observation represents direct causality. Show me. > WHEN the **iron** is REMOVED the fatty liver is REVERSED. > [quoted text clipped - 108 lines] > > DEAD PEOPLE WALKINGhttp://tinyurl.com/zk9fk Each and every .. one .. of you shteaters were taken aside and explained how shteating and loonacy are ground for not posting to my threads .. NOW you have attracted another lunatic .. You .. see .. what did I tell ya .. Like flies to sht .. You were told to stay away from me .. You were told to stay off my posts .. You were told to not display your .. nature .. that predatory nature common to .. predatorial .. homosexuals .. Isn't it .. that nature .. that .. predatory .. nature that gets you shteaters in soooo .. much .. trouble .. ? You shteaters have NO .. input .. ON .. **my** threads .. That must be too hard for you shteaters to understand .. You shteaters ha've been TOLD numerous times .. you are NOT welcome .. You shteaters are a fkg .. looooooons .. STAY .. off .. my .. threads .. you fkg .. loooooon .. Dooooo .. it .. looooon .. WHEN the **iron** is REMOVED the fatty liver is REVERSED. Hyperferritinemia is a risk factor for steatosis in chronic liver disease. Licata A, Nebbia ME, Cabibbo G, Iacono GL, Barbaria F, Brucato V, Alessi N, Porrovecchio S, Di Marco V, Craxì A, Cammà C World J Gastroenterol 2009 May 7; 15(17):2132-8. AIM: To investigate the relationship between ferritin and steatosis in patients with chronically abnormal liver function tests (LFTs) and high ferritin level. METHODS: One hundred and twenty-four consecutive patients with hyperferritinemia (male > 300 ng/mL, female > 200 ng/mL) were evaluated; clinical, biochemical and serological data, iron status parameters, HFE gene mutations and homeostasis model assessment score were obtained. Steatosis was graded by ultrasound as absent or present. Histology was available in 53 patients only. RESULTS: Mean level of ferritin was 881 +/- 77 ng/mL in men and 549 +/- 82 ng/mL in women. The diagnosis was chronic hepatitis C in 53 (42.7%), non-alcoholic fatty liver disease/non-alcoholic steatohepatitis in 57 (45.9%), and cryptogenic liver damage in 14 (11.3%). None was diagnosed as hereditary hemochromatosis (HH). Hepatic siderosis on liver biopsy was present in 17 of 54 (32%) patients; grade 1 in eight and grade 2 in nine. Overall, 92 patients (74.2%) had steatosis. By logistic regression, ferritin and gamma-glutamyltransferase were independent predictors of steatosis. Ferritin levels were significantly related to low platelet count, steatosis and hepatitis C virus infection. CONCLUSION: In a non-obese cohort of non-alcoholic patients with chronically abnormal LFTs without HH, high serum ferritin level is a risk factor for steatosis. World journal of gastroenterology : WJG [World J Gastroenterol] ------------------- Evidenced based medicine .. Low iron equals low fatty liver disease. Which would explain somewhat the REVERSAL OF CIRRHOSIS which has been demonstrated by the iron reduction therapy. "These results reflect the insulin-sparing effect of iron depletion and indicate a key role of iron and hyperinsulinemia in the pathogenesis of NAFLD" Effect of iron depletion in carbohydrate-intolerant patients with clinical evidence of nonalcoholic fatty liver disease. Gastroenterology 2002 Apr;122(4):931-9 Facchini FS, Hua NW, Stoohs RA. Department of Medicine, University of California San Francisco and San Francisco General Hospital, San Francisco, California, USA. ffacch...@ecnea.org BACKGROUND & AIMS: Increased body iron, genetic hemochromatosis (GH) mutations, and nonalcoholic fatty liver disease (NAFLD) tend to cluster in carbohydrate-intolerant patients. In an attempt to further clarify the interrelationships among these conditions, we studied 42 carbohydrate-intolerant patients who were free of the common GH mutations C282Y and H63D, and had a serum iron saturation lower than 50%. METHODS: We measured body iron stores, and induced iron depletion to a level of near-iron deficiency (NID) by quantitative phlebotomy. RESULTS: In the 17 patients with clinical evidence of NAFLD, we could not demonstrate supranormal levels of body iron (1.6 +/- 0.2 vs. 1.4 +/- 0.2 g; P = 0.06). However, at NID, there was a 40%-55% improvement (P = 0.05-0.0001) of both fasting and glucose-stimulated plasma insulin concentrations, and near-normalization of serum alanine aminotransferase activity (from 61 +/- 5 to 32 +/- 2 IU/L; P < 0.001). CONCLUSIONS: These results reflect the insulin-sparing effect of iron depletion and indicate a key role of iron and hyperinsulinemia in the pathogenesis of NAFLD. PMID: 11910345 --------------- http://www.natap.org/2000/jan/fattyliver011700.html Who loves ya. Tom Jesus Was A Vegetarian! http://tinyurl.com/634q5a Man Is A Herbivore! http://tinyurl.com/4rq595 DEAD PEOPLE WALKING http://tinyurl.com/zk9fk Ya know, Tom. It would have been much simpler for you to simply say you were incapable of justifying your observation. But I kinda envy you your ability of seeing the medical world in such simple terms. Not to say that you are stupid. Just...simple-minded. But just a reminder. Presence of a risk factor is not evidence of causation. A diabetic can completely eliminate sugars and still have clinical diabetes. >> On May 9, 9:58 pm, Michael B <baugh...@bellsouth.net> wrote: >> Please show where, in the details you provided, the observation >> is made that when the iron is removed the fatty liver is reversed. >> Such an observation represents direct causality. Show me. > Each and every .. one .. of you shteaters were taken aside and > explained [quoted text clipped - 143 lines] > > DEAD PEOPLE WALKINGhttp://tinyurl.com/zk9fk On May 10, 6:19 am, Michael B <baugh...@bellsouth.net> wrote: snip << Shteater you have been TOLD numerous times .. you are NOT welcome .. Shteaters are a fkg .. looooooons .. understand .. loon .. STAY .. off .. my .. threads .. you fkg .. loooooon .. Dooooo .. it .. you fkg shteating looooon .. WHEN the **iron** is REMOVED the fatty liver is REVERSED. Hyperferritinemia is a risk factor for steatosis in chronic liver disease. Licata A, Nebbia ME, Cabibbo G, Iacono GL, Barbaria F, Brucato V, Alessi N, Porrovecchio S, Di Marco V, Craxì A, Cammà C World J Gastroenterol 2009 May 7; 15(17):2132-8. AIM: To investigate the relationship between ferritin and steatosis in patients with chronically abnormal liver function tests (LFTs) and high ferritin level. METHODS: One hundred and twenty-four consecutive patients with hyperferritinemia (male > 300 ng/mL, female > 200 ng/mL) were evaluated; clinical, biochemical and serological data, iron status parameters, HFE gene mutations and homeostasis model assessment score were obtained. Steatosis was graded by ultrasound as absent or present. Histology was available in 53 patients only. RESULTS: Mean level of ferritin was 881 +/- 77 ng/mL in men and 549 +/- 82 ng/mL in women. The diagnosis was chronic hepatitis C in 53 (42.7%), non-alcoholic fatty liver disease/non-alcoholic steatohepatitis in 57 (45.9%), and cryptogenic liver damage in 14 (11.3%). None was diagnosed as hereditary hemochromatosis (HH). Hepatic siderosis on liver biopsy was present in 17 of 54 (32%) patients; grade 1 in eight and grade 2 in nine. Overall, 92 patients (74.2%) had steatosis. By logistic regression, ferritin and gamma-glutamyltransferase were independent predictors of steatosis. Ferritin levels were significantly related to low platelet count, steatosis and hepatitis C virus infection. CONCLUSION: In a non-obese cohort of non-alcoholic patients with chronically abnormal LFTs without HH, high serum ferritin level is a risk factor for steatosis. World journal of gastroenterology : WJG [World J Gastroenterol] ------------------- Evidenced based medicine .. Low iron equals low fatty liver disease. Which would explain somewhat the REVERSAL OF CIRRHOSIS which has been demonstrated by the iron reduction therapy. "These results reflect the insulin-sparing effect of iron depletion and indicate a key role of iron and hyperinsulinemia in the pathogenesis of NAFLD" Effect of iron depletion in carbohydrate-intolerant patients with clinical evidence of nonalcoholic fatty liver disease. Gastroenterology 2002 Apr;122(4):931-9 Facchini FS, Hua NW, Stoohs RA. Department of Medicine, University of California San Francisco and San Francisco General Hospital, San Francisco, California, USA. ffacch...@ecnea.org BACKGROUND & AIMS: Increased body iron, genetic hemochromatosis (GH) mutations, and nonalcoholic fatty liver disease (NAFLD) tend to cluster in carbohydrate-intolerant patients. In an attempt to further clarify the interrelationships among these conditions, we studied 42 carbohydrate-intolerant patients who were free of the common GH mutations C282Y and H63D, and had a serum iron saturation lower than 50%. METHODS: We measured body iron stores, and induced iron depletion to a level of near-iron deficiency (NID) by quantitative phlebotomy. RESULTS: In the 17 patients with clinical evidence of NAFLD, we could not demonstrate supranormal levels of body iron (1.6 +/- 0.2 vs. 1.4 +/- 0.2 g; P = 0.06). However, at NID, there was a 40%-55% improvement (P = 0.05-0.0001) of both fasting and glucose-stimulated plasma insulin concentrations, and near-normalization of serum alanine aminotransferase activity (from 61 +/- 5 to 32 +/- 2 IU/L; P < 0.001). CONCLUSIONS: These results reflect the insulin-sparing effect of iron depletion and indicate a key role of iron and hyperinsulinemia in the pathogenesis of NAFLD. PMID: 11910345 --------------- http://www.natap.org/2000/jan/fattyliver011700.html Who loves ya. Tom Jesus Was A Vegetarian! http://tinyurl.com/634q5a Man Is A Herbivore! http://tinyurl.com/4rq595 DEAD PEOPLE WALKING http://tinyurl.com/zk9fk Spamming Moron On May 10, 9:24 am, Rusty Canuck Dicksucker <flakey...@aol.com> wrote:snip << Disease ridden shteating freaks cannot post here .. You evidence that dysfunctional nature .. common to you shteaters .. Stay OFF my threads shteater .. Dysfunctional shteating disease ridden mutated freaks are not allowed to post to my threads .. DOOO .. like you are told .. you disease ridden .. shteater .. Remember while you cut this post .. homosexual .. it is evidence OF .. the dysfunctional predatorial nature of yours common to men who prefer .. to have sex with boys .. http://www.traditionalvalues.org/homosexual_movement_and_pedophilia/ http://www.talk2action.org/story/2006/10/3/21245/3789 http://predatorsafety.blogspot.com/2008/11/homosexual-grooming-of-chi... Predator Safety Dedicated To The Protection Of Our Children --------- WHEN the **iron** is REMOVED the fatty liver is REVERSED. Hyperferritinemia is a risk factor for steatosis in chronic liver disease. Licata A, Nebbia ME, Cabibbo G, Iacono GL, Barbaria F, Brucato V, Alessi N, Porrovecchio S, Di Marco V, Craxì A, Cammà C World J Gastroenterol 2009 May 7; 15(17):2132-8. AIM: To investigate the relationship between ferritin and steatosis in patients with chronically abnormal liver function tests (LFTs) and high ferritin level. METHODS: One hundred and twenty-four consecutive patients with hyperferritinemia (male > 300 ng/mL, female > 200 ng/mL) were evaluated; clinical, biochemical and serological data, iron status parameters, HFE gene mutations and homeostasis model assessment score were obtained. Steatosis was graded by ultrasound as absent or present. Histology was available in 53 patients only. RESULTS: Mean level of ferritin was 881 +/- 77 ng/mL in men and 549 +/- 82 ng/mL in women. The diagnosis was chronic hepatitis C in 53 (42.7%), non-alcoholic fatty liver disease/non-alcoholic steatohepatitis in 57 (45.9%), and cryptogenic liver damage in 14 (11.3%). None was diagnosed as hereditary hemochromatosis (HH). Hepatic siderosis on liver biopsy was present in 17 of 54 (32%) patients; grade 1 in eight and grade 2 in nine. Overall, 92 patients (74.2%) had steatosis. By logistic regression, ferritin and gamma-glutamyltransferase were independent predictors of steatosis. Ferritin levels were significantly related to low platelet count, steatosis and hepatitis C virus infection. CONCLUSION: In a non-obese cohort of non-alcoholic patients with chronically abnormal LFTs without HH, high serum ferritin level is a risk factor for steatosis. World journal of gastroenterology : WJG [World J Gastroenterol] ------------------- Evidenced based medicine .. Low iron equals low fatty liver disease. Which would explain somewhat the REVERSAL OF CIRRHOSIS which has been demonstrated by the iron reduction therapy. "These results reflect the insulin-sparing effect of iron depletion and indicate a key role of iron and hyperinsulinemia in the pathogenesis of NAFLD" Effect of iron depletion in carbohydrate-intolerant patients with clinical evidence of nonalcoholic fatty liver disease. Gastroenterology 2002 Apr;122(4):931-9 Facchini FS, Hua NW, Stoohs RA. Department of Medicine, University of California San Francisco and San Francisco General Hospital, San Francisco, California, USA. ffacch...@ecnea.org BACKGROUND & AIMS: Increased body iron, genetic hemochromatosis (GH) mutations, and nonalcoholic fatty liver disease (NAFLD) tend to cluster in carbohydrate-intolerant patients. In an attempt to further clarify the interrelationships among these conditions, we studied 42 carbohydrate-intolerant patients who were free of the common GH mutations C282Y and H63D, and had a serum iron saturation lower than 50%. METHODS: We measured body iron stores, and induced iron depletion to a level of near-iron deficiency (NID) by quantitative phlebotomy. RESULTS: In the 17 patients with clinical evidence of NAFLD, we could not demonstrate supranormal levels of body iron (1.6 +/- 0.2 vs. 1.4 +/- 0.2 g; P = 0.06). However, at NID, there was a 40%-55% improvement (P = 0.05-0.0001) of both fasting and glucose-stimulated plasma insulin concentrations, and near-normalization of serum alanine aminotransferase activity (from 61 +/- 5 to 32 +/- 2 IU/L; P < 0.001). CONCLUSIONS: These results reflect the insulin-sparing effect of iron depletion and indicate a key role of iron and hyperinsulinemia in the pathogenesis of NAFLD. PMID: 11910345 --------------- http://www.natap.org/2000/jan/fattyliver011700.html Who loves ya. Tom Jesus Was A Vegetarian! http://tinyurl.com/634q5a Man Is A Herbivore! http://tinyurl.com/4rq595 DEAD PEOPLE WALKING http://tinyurl.com/zk9fk Spamming Retard Tom, you just can't know how amusing you are. Like flies to sht .. You were told to stay away from me .. > Tom, you just can't know how amusing you are. It would be even more ammusing if he were in an asylum where he belongs. CB but he is! it's called usenet! <G> free admission to all who wish to view the amazing range of human sensibilities ...now be careful children to keep your hands and feet on this side of the fence... >> Tom, you just can't know how amusing you are. > > It would be even more ammusing if he were in an asylum where he > belongs. > CB but flakey! don't you see that tommy is actually conveying a message of concern? no fatty livers, no human foie gras, he's actually trying to protect all of us from epicurian cannibals feman! bane of all flesh eaters - soon to introduce a new product on the market: Dr. Lector's Liver - human flavored tofu > Spamming Fuckwit > but flakey! > [quoted text clipped - 8 lines] > > Dr. Lector's Liver - human flavored tofu Sounds yummy, Does that come with fava beans and Chianti? CB >> Spamming Fuckwit snip << You shteaters .. are congregating again .. You shteaters are to take your congregating somewhere other than the groups phones parks libraries toy sections or bathrooms .. Understand .. you shteating .. freaks .. ? I see you near a toy section .. I'm .. gonna open a can of worms on your a.s .. Understand .. ? .. you shteaters .. ? -------------------- WHEN the **iron** is REMOVED the fatty liver is REVERSED. Hyperferritinemia is a risk factor for steatosis in chronic liver disease. Licata A, Nebbia ME, Cabibbo G, Iacono GL, Barbaria F, Brucato V, Alessi N, Porrovecchio S, Di Marco V, Craxì A, Cammà C World J Gastroenterol 2009 May 7; 15(17):2132-8. AIM: To investigate the relationship between ferritin and steatosis in patients with chronically abnormal liver function tests (LFTs) and high ferritin level. METHODS: One hundred and twenty-four consecutive patients with hyperferritinemia (male > 300 ng/mL, female > 200 ng/mL) were evaluated; clinical, biochemical and serological data, iron status parameters, HFE gene mutations and homeostasis model assessment score were obtained. Steatosis was graded by ultrasound as absent or present. Histology was available in 53 patients only. RESULTS: Mean level of ferritin was 881 +/- 77 ng/mL in men and 549 +/- 82 ng/mL in women. The diagnosis was chronic hepatitis C in 53 (42.7%), non-alcoholic fatty liver disease/non-alcoholic steatohepatitis in 57 (45.9%), and cryptogenic liver damage in 14 (11.3%). None was diagnosed as hereditary hemochromatosis (HH). Hepatic siderosis on liver biopsy was present in 17 of 54 (32%) patients; grade 1 in eight and grade 2 in nine. Overall, 92 patients (74.2%) had steatosis. By logistic regression, ferritin and gamma-glutamyltransferase were independent predictors of steatosis. Ferritin levels were significantly related to low platelet count, steatosis and hepatitis C virus infection. CONCLUSION: In a non-obese cohort of non-alcoholic patients with chronically abnormal LFTs without HH, high serum ferritin level is a risk factor for steatosis. World journal of gastroenterology : WJG [World J Gastroenterol] ------------------- Evidenced based medicine .. Low iron equals low fatty liver disease. Which would explain somewhat the REVERSAL OF CIRRHOSIS which has been demonstrated by the iron reduction therapy. "These results reflect the insulin-sparing effect of iron depletion and indicate a key role of iron and hyperinsulinemia in the pathogenesis of NAFLD" Effect of iron depletion in carbohydrate-intolerant patients with clinical evidence of nonalcoholic fatty liver disease. Gastroenterology 2002 Apr;122(4):931-9 Facchini FS, Hua NW, Stoohs RA. Department of Medicine, University of California San Francisco and San Francisco General Hospital, San Francisco, California, USA. ffacch...@ecnea.org BACKGROUND & AIMS: Increased body iron, genetic hemochromatosis (GH) mutations, and nonalcoholic fatty liver disease (NAFLD) tend to cluster in carbohydrate-intolerant patients. In an attempt to further clarify the interrelationships among these conditions, we studied 42 carbohydrate-intolerant patients who were free of the common GH mutations C282Y and H63D, and had a serum iron saturation lower than 50%. METHODS: We measured body iron stores, and induced iron depletion to a level of near-iron deficiency (NID) by quantitative phlebotomy. RESULTS: In the 17 patients with clinical evidence of NAFLD, we could not demonstrate supranormal levels of body iron (1.6 +/- 0.2 vs. 1.4 +/- 0.2 g; P = 0.06). However, at NID, there was a 40%-55% improvement (P = 0.05-0.0001) of both fasting and glucose-stimulated plasma insulin concentrations, and near-normalization of serum alanine aminotransferase activity (from 61 +/- 5 to 32 +/- 2 IU/L; P < 0.001). CONCLUSIONS: These results reflect the insulin-sparing effect of iron depletion and indicate a key role of iron and hyperinsulinemia in the pathogenesis of NAFLD. PMID: 11910345 --------------- http://www.natap.org/2000/jan/fattyliver011700.html Who loves ya. Tom Jesus Was A Vegetarian! http://tinyurl.com/634q5a Man Is A Herbivore! http://tinyurl.com/4rq595 DEAD PEOPLE WALKING http://tinyurl.com/zk9fk Tom, I have had my iron levels dropped to below normal by going through weekly phlebotomy for anywhere from 10 to 18 weeks in a row. It never helped the Hep-C, Diabetes, or the Hemochromatosis. As a matter of fact the iron levels just went back up. Reducing the iron doesn't cure anything, but it might help in slowing the damage to the liver. Even at that it is temporary. I'm not sure why I'm trying to even reason with you. I do wish you would pick a new hobby and quit fixating on the evils of iron. I don't know if you do this because you honestly think you are helping someone or if you are doing it just to annoy people. I don't remember you being so derogatory towards everyone until you started cross posting. I don't even know if you have any of the diseases/conditions that you have tried so hard to be an expert at. Please find help and I wish you the best of luck. Dwight (Straight, married, three kids and yes, a disease/condition ravaged person) Tom, I have had my iron levels dropped to below normal by going through weekly phlebotomy for anywhere from 10 to 18 weeks in a row. It never helped the Hep-C, Diabetes, or the Hemochromatosis. << Some people have been bloodlet three times a week .. Others have twice a week .. Some people have to go for over a year at a weekly rate .. On May 10, 9:49 pm, Dwight <Dwight@not_real.com> wrote:As a matter of fact the iron levels just went back up. Reducing the iron doesn't cure anything, but it might help in slowing the damage to the liver. << The VERY REASON they say they DON'T use phlebotomy is because they say it doesn't help and the body begins to push for more red blood cells. THAT is the very reason you are doing it. To draw the iron OUT .. Once the body DOESN'T "iron levels just went back up" .. THEN you know the iron is OUT .. On May 10, 9:49 pm, Dwight <Dwight@not_real.com> wrote: I'm not sure why I'm trying to even reason with you. << Especially when you have no idea what you are talking about .. On May 10, 9:49 pm, Dwight <Dwight@not_real.com> wrote:I do wish you would pick a new hobby and quit fixating on the evilsof iron. << You worry about me .. do ya .. On May 10, 9:49 pm, Dwight <Dwight@not_real.com> wrote: don't know if you do this because you honestly think you are helping someone or if you are doing it just to annoy people. << Seems there isn't a whole LOT you are .. really sure about .. and that which you believe you ARE sure of .. you .. are NOT .. sure of .. or more .. you are not .. correct .. on .. On May 10, 9:49 pm, Dwight <Dwight@not_real.com> wrote:I don't remember you being so derogatory towards everyone until you started cross posting. << I've been crossposting for years and it is only NOW you have noticed .. ? On May 10, 9:49 pm, Dwight <Dwight@not_real.com> wrote:I don't even know if you have any of the >diseases/conditions that you have tried so hard to be an expert at. Please find help and I wish you the best of luck. << Actually .. I don't need help .. YOU obviously .. do .. Because .. ? .. you are delusional .. Find a doctor who knows what he is doing .. a hemochromatosis doctor .. and NOT .. a normal GP .. because .. ? Chances are he is a doofus .. Much like yourself .. evidentally .. Who loves ya. Tom Jesus Was A Vegetarian! http://tinyurl.com/634q5a Man Is A Herbivore! http://tinyurl.com/4rq595 DEAD PEOPLE WALKING http://tinyurl.com/zk9fk > Dwight (Straight, married, three kids and yes, a disease/condition > ravaged person) >> but flakey! >> [quoted text clipped - 12 lines] > > Does that come with fava beans and Chianti? well, i think rather a Faustino Rioja Reserva V Spain Rioja Spanish Still Wine > CB > >>> Spamming Fuckwit On May 11, 4:12 pm, "Paul T. Holland" <pholl...@bellatlantic.net> wrote: : snip << snip << You were told to stay off my threads .. DOOOOO .. it .. shteater .. WHEN the **iron** is REMOVED the fatty liver is REVERSED. Hyperferritinemia is a risk factor for steatosis in chronic liver disease. Licata A, Nebbia ME, Cabibbo G, Iacono GL, Barbaria F, Brucato V, Alessi N, Porrovecchio S, Di Marco V, Craxì A, Cammà C World J Gastroenterol 2009 May 7; 15(17):2132-8. AIM: To investigate the relationship between ferritin and steatosis in patients with chronically abnormal liver function tests (LFTs) and high ferritin level. METHODS: One hundred and twenty-four consecutive patients with hyperferritinemia (male > 300 ng/mL, female > 200 ng/mL) were evaluated; clinical, biochemical and serological data, iron status parameters, HFE gene mutations and homeostasis model assessment score were obtained. Steatosis was graded by ultrasound as absent or present. Histology was available in 53 patients only. RESULTS: Mean level of ferritin was 881 +/- 77 ng/mL in men and 549 +/- 82 ng/mL in women. The diagnosis was chronic hepatitis C in 53 (42.7%), non-alcoholic fatty liver disease/non-alcoholic steatohepatitis in 57 (45.9%), and cryptogenic liver damage in 14 (11.3%). None was diagnosed as hereditary hemochromatosis (HH). Hepatic siderosis on liver biopsy was present in 17 of 54 (32%) patients; grade 1 in eight and grade 2 in nine. Overall, 92 patients (74.2%) had steatosis. By logistic regression, ferritin and gamma-glutamyltransferase were independent predictors of steatosis. Ferritin levels were significantly related to low platelet count, steatosis and hepatitis C virus infection. CONCLUSION: In a non-obese cohort of non-alcoholic patients with chronically abnormal LFTs without HH, high serum ferritin level is a risk factor for steatosis. World journal of gastroenterology : WJG [World J Gastroenterol] ------------------- Evidenced based medicine .. Low iron equals low fatty liver disease. Which would explain somewhat the REVERSAL OF CIRRHOSIS which has been demonstrated by the iron reduction therapy. "These results reflect the insulin-sparing effect of iron depletion and indicate a key role of iron and hyperinsulinemia in the pathogenesis of NAFLD" Effect of iron depletion in carbohydrate-intolerant patients with clinical evidence of nonalcoholic fatty liver disease. Gastroenterology 2002 Apr;122(4):931-9 Facchini FS, Hua NW, Stoohs RA. Department of Medicine, University of California San Francisco and San Francisco General Hospital, San Francisco, California, USA. ffacch...@ecnea.org BACKGROUND & AIMS: Increased body iron, genetic hemochromatosis (GH) mutations, and nonalcoholic fatty liver disease (NAFLD) tend to cluster in carbohydrate-intolerant patients. In an attempt to further clarify the interrelationships among these conditions, we studied 42 carbohydrate-intolerant patients who were free of the common GH mutations C282Y and H63D, and had a serum iron saturation lower than 50%. METHODS: We measured body iron stores, and induced iron depletion to a level of near-iron deficiency (NID) by quantitative phlebotomy. RESULTS: In the 17 patients with clinical evidence of NAFLD, we could not demonstrate supranormal levels of body iron (1.6 +/- 0.2 vs. 1.4 +/- 0.2 g; P = 0.06). However, at NID, there was a 40%-55% improvement (P = 0.05-0.0001) of both fasting and glucose-stimulated plasma insulin concentrations, and near-normalization of serum alanine aminotransferase activity (from 61 +/- 5 to 32 +/- 2 IU/L; P < 0.001). CONCLUSIONS: These results reflect the insulin-sparing effect of iron depletion and indicate a key role of iron and hyperinsulinemia in the pathogenesis of NAFLD. PMID: 11910345 --------------- http://www.natap.org/2000/jan/fattyliver011700.html Who loves ya. Tom Jesus Was A Vegetarian! http://tinyurl.com/634q5a Man Is A Herbivore! http://tinyurl.com/4rq595 DEAD PEOPLE WALKING http://tinyurl.com/zk9fk >When the iron is removed the fatty liver is reversed. When ironjustice is removed the bll sht in the newsgroups is reversed. This is an unmoderated newsgroup, so no one "owns" threads. >Hyperferritinemia is a risk factor for steatosis in chronic liver >disease. There's a difference between a risk factor and a cause. For example, giving birth is a risk factor for pregnancy, but it's not a cause of pregnancy. Removing a risk factor is not necessarily a cure. For example, diabetics can remove sugar entirely from their diet and it won't cure diabetes. > >When the iron is removed the fatty liver is reversed. > [quoted text clipped - 7 lines] > For example, giving birth is a risk factor for pregnancy, but it's > not a cause of pregnancy. Sadly, you are talking to a full blown lunatic. Your logic will not penetrate. Someone muct have whacked the guy with an iron weopon. CB Tom, somewhere along the way, you must have wondered why everyone seems to be against you. And it really isn't that way at all. The problem is that you have fixated on a potentially valid issue and presented it as though it were the answer to the ills and illnesses of the world. True, the body has difficulty with excess metals. And existing "normal levels" may well represent problems for some people. Same for mercury, zinc, nickel, and others. But you take it and tell everyone that if they get their iron levels down, the world will be good again. And you eliminate any credibility you may have had by being unwilling or unable to carry on a legitimate discussion. So, the next step is for you to completely strip this out, tell how we surely don't expect you to actually read anything that is printed, and then tell about how disagreeing with you somehow makes everyone homosexual sexual predators. No point in saying it, but thought I would anyway. > When the iron is removed the fatty liver is reversed. > [quoted text clipped - 43 lines] > World journal of gastroenterology : WJG [World J Gastroenterol] > ------------------- On May 10, 5:40 pm, Michael B <baugh...@bellsouth.net> wrote: snip << You shteaters .. were told to stay off my threads .. DOOOOO .. it .. shteater .. Cutting my posts you disease ridden mutated .. shteater .. is evidence of the dysfunctional nature of you shteating .. freaks .. -------------------- WHEN the **iron** is REMOVED the fatty liver is REVERSED. Hyperferritinemia is a risk factor for steatosis in chronic liver disease. Licata A, Nebbia ME, Cabibbo G, Iacono GL, Barbaria F, Brucato V, Alessi N, Porrovecchio S, Di Marco V, Craxì A, Cammà C World J Gastroenterol 2009 May 7; 15(17):2132-8. AIM: To investigate the relationship between ferritin and steatosis in patients with chronically abnormal liver function tests (LFTs) and high ferritin level. METHODS: One hundred and twenty-four consecutive patients with hyperferritinemia (male > 300 ng/mL, female > 200 ng/mL) were evaluated; clinical, biochemical and serological data, iron status parameters, HFE gene mutations and homeostasis model assessment score were obtained. Steatosis was graded by ultrasound as absent or present. Histology was available in 53 patients only. RESULTS: Mean level of ferritin was 881 +/- 77 ng/mL in men and 549 +/- 82 ng/mL in women. The diagnosis was chronic hepatitis C in 53 (42.7%), non-alcoholic fatty liver disease/non-alcoholic steatohepatitis in 57 (45.9%), and cryptogenic liver damage in 14 (11.3%). None was diagnosed as hereditary hemochromatosis (HH). Hepatic siderosis on liver biopsy was present in 17 of 54 (32%) patients; grade 1 in eight and grade 2 in nine. Overall, 92 patients (74.2%) had steatosis. By logistic regression, ferritin and gamma-glutamyltransferase were independent predictors of steatosis. Ferritin levels were significantly related to low platelet count, steatosis and hepatitis C virus infection. CONCLUSION: In a non-obese cohort of non-alcoholic patients with chronically abnormal LFTs without HH, high serum ferritin level is a risk factor for steatosis. World journal of gastroenterology : WJG [World J Gastroenterol] ------------------- Evidenced based medicine .. Low iron equals low fatty liver disease. Which would explain somewhat the REVERSAL OF CIRRHOSIS which has been demonstrated by the iron reduction therapy. "These results reflect the insulin-sparing effect of iron depletion and indicate a key role of iron and hyperinsulinemia in the pathogenesis of NAFLD" Effect of iron depletion in carbohydrate-intolerant patients with clinical evidence of nonalcoholic fatty liver disease. Gastroenterology 2002 Apr;122(4):931-9 Facchini FS, Hua NW, Stoohs RA. Department of Medicine, University of California San Francisco and San Francisco General Hospital, San Francisco, California, USA. ffacch...@ecnea.org BACKGROUND & AIMS: Increased body iron, genetic hemochromatosis (GH) mutations, and nonalcoholic fatty liver disease (NAFLD) tend to cluster in carbohydrate-intolerant patients. In an attempt to further clarify the interrelationships among these conditions, we studied 42 carbohydrate-intolerant patients who were free of the common GH mutations C282Y and H63D, and had a serum iron saturation lower than 50%. METHODS: We measured body iron stores, and induced iron depletion to a level of near-iron deficiency (NID) by quantitative phlebotomy. RESULTS: In the 17 patients with clinical evidence of NAFLD, we could not demonstrate supranormal levels of body iron (1.6 +/- 0.2 vs. 1.4 +/- 0.2 g; P = 0.06). However, at NID, there was a 40%-55% improvement (P = 0.05-0.0001) of both fasting and glucose-stimulated plasma insulin concentrations, and near-normalization of serum alanine aminotransferase activity (from 61 +/- 5 to 32 +/- 2 IU/L; P < 0.001). CONCLUSIONS: These results reflect the insulin-sparing effect of iron depletion and indicate a key role of iron and hyperinsulinemia in the pathogenesis of NAFLD. PMID: 11910345 --------------- http://www.natap.org/2000/jan/fattyliver011700.html Who loves ya. Tom Jesus Was A Vegetarian! http://tinyurl.com/634q5a Man Is A Herbivore! http://tinyurl.com/4rq595 DEAD PEOPLE WALKING http://tinyurl.com/zk9fk Spamming Fuckhead On May 11, 6:49 am, Rusty the Cocksucking Canuck Retard <flakey...@earthlink.net> wrote: snip << ALL you shteaters were TOLD to stay off my threads .. Understand .. shteater .. ? You shteaters have NO .. input .. ON .. **my** threads .. That too hard for you shteaters to understand .. ? You shteaters ha've been TOLD numerous times .. you are NOT welcome .. You shteaters are a fkg .. looooooons .. STAY .. off .. my .. threads .. you fkg .. loooooon .. Dooooo .. it .. looooon .. ------------------ WHEN the **iron** is REMOVED the fatty liver is REVERSED. Hyperferritinemia is a risk factor for steatosis in chronic liver disease. Licata A, Nebbia ME, Cabibbo G, Iacono GL, Barbaria F, Brucato V, Alessi N, Porrovecchio S, Di Marco V, Craxì A, Cammà C World J Gastroenterol 2009 May 7; 15(17):2132-8. AIM: To investigate the relationship between ferritin and steatosis in patients with chronically abnormal liver function tests (LFTs) and high ferritin level. METHODS: One hundred and twenty-four consecutive patients with hyperferritinemia (male > 300 ng/mL, female > 200 ng/mL) were evaluated; clinical, biochemical and serological data, iron status parameters, HFE gene mutations and homeostasis model assessment score were obtained. Steatosis was graded by ultrasound as absent or present. Histology was available in 53 patients only. RESULTS: Mean level of ferritin was 881 +/- 77 ng/mL in men and 549 +/- 82 ng/mL in women. The diagnosis was chronic hepatitis C in 53 (42.7%), non-alcoholic fatty liver disease/non-alcoholic steatohepatitis in 57 (45.9%), and cryptogenic liver damage in 14 (11.3%). None was diagnosed as hereditary hemochromatosis (HH). Hepatic siderosis on liver biopsy was present in 17 of 54 (32%) patients; grade 1 in eight and grade 2 in nine. Overall, 92 patients (74.2%) had steatosis. By logistic regression, ferritin and gamma-glutamyltransferase were independent predictors of steatosis. Ferritin levels were significantly related to low platelet count, steatosis and hepatitis C virus infection. CONCLUSION: In a non-obese cohort of non-alcoholic patients with chronically abnormal LFTs without HH, high serum ferritin level is a risk factor for steatosis. World journal of gastroenterology : WJG [World J Gastroenterol] ------------------- Evidenced based medicine .. Low iron equals low fatty liver disease. Which would explain somewhat the REVERSAL OF CIRRHOSIS which has been demonstrated by the iron reduction therapy. "These results reflect the insulin-sparing effect of iron depletion and indicate a key role of iron and hyperinsulinemia in the pathogenesis of NAFLD" Effect of iron depletion in carbohydrate-intolerant patients with clinical evidence of nonalcoholic fatty liver disease. Gastroenterology 2002 Apr;122(4):931-9 Facchini FS, Hua NW, Stoohs RA. Department of Medicine, University of California San Francisco and San Francisco General Hospital, San Francisco, California, USA. ffacch...@ecnea.org BACKGROUND & AIMS: Increased body iron, genetic hemochromatosis (GH) mutations, and nonalcoholic fatty liver disease (NAFLD) tend to cluster in carbohydrate-intolerant patients. In an attempt to further clarify the interrelationships among these conditions, we studied 42 carbohydrate-intolerant patients who were free of the common GH mutations C282Y and H63D, and had a serum iron saturation lower than 50%. METHODS: We measured body iron stores, and induced iron depletion to a level of near-iron deficiency (NID) by quantitative phlebotomy. RESULTS: In the 17 patients with clinical evidence of NAFLD, we could not demonstrate supranormal levels of body iron (1.6 +/- 0.2 vs. 1.4 +/- 0.2 g; P = 0.06). However, at NID, there was a 40%-55% improvement (P = 0.05-0.0001) of both fasting and glucose-stimulated plasma insulin concentrations, and near-normalization of serum alanine aminotransferase activity (from 61 +/- 5 to 32 +/- 2 IU/L; P < 0.001). CONCLUSIONS: These results reflect the insulin-sparing effect of iron depletion and indicate a key role of iron and hyperinsulinemia in the pathogenesis of NAFLD. PMID: 11910345 --------------- http://www.natap.org/2000/jan/fattyliver011700.html Who loves ya. Tom Jesus Was A Vegetarian! http://tinyurl.com/634q5a Man Is A Herbivore! http://tinyurl.com/4rq595 DEAD PEOPLE WALKING http://tinyurl.com/zk9fk Spamming Dicksucker On May 11, 7:22 am, Rusty the Canuck Cocksucker <flakey...@aol.com> wrote: snip << You shteaters were told to stop trying to express yourselves .. on my threads .. You were told you are are not allowed to post to my threads .. Yet you continue to display that predatorial propensity of yours don't ya shteater .. Remember while you cut this post .. homosexual .. it is evidence OF .. the dysfunctional predatorial nature of yours common to men who prefer .. to have sex with boys .. http://www.traditionalvalues.org/homosexual_movement_and_pedophilia/ http://www.talk2action.org/story/2006/10/3/21245/3789 http://predatorsafety.blogspot.com/2008/11/homosexual-grooming-of-chi... Predator Safety Dedicated To The Protection Of Our Children --------- WHEN the **iron** is REMOVED the fatty liver is REVERSED. Hyperferritinemia is a risk factor for steatosis in chronic liver disease. Licata A, Nebbia ME, Cabibbo G, Iacono GL, Barbaria F, Brucato V, Alessi N, Porrovecchio S, Di Marco V, Craxì A, Cammà C World J Gastroenterol 2009 May 7; 15(17):2132-8. AIM: To investigate the relationship between ferritin and steatosis in patients with chronically abnormal liver function tests (LFTs) and high ferritin level. METHODS: One hundred and twenty-four consecutive patients with hyperferritinemia (male > 300 ng/mL, female > 200 ng/mL) were evaluated; clinical, biochemical and serological data, iron status parameters, HFE gene mutations and homeostasis model assessment score were obtained. Steatosis was graded by ultrasound as absent or present. Histology was available in 53 patients only. RESULTS: Mean level of ferritin was 881 +/- 77 ng/mL in men and 549 +/- 82 ng/mL in women. The diagnosis was chronic hepatitis C in 53 (42.7%), non-alcoholic fatty liver disease/non-alcoholic steatohepatitis in 57 (45.9%), and cryptogenic liver damage in 14 (11.3%). None was diagnosed as hereditary hemochromatosis (HH). Hepatic siderosis on liver biopsy was present in 17 of 54 (32%) patients; grade 1 in eight and grade 2 in nine. Overall, 92 patients (74.2%) had steatosis. By logistic regression, ferritin and gamma-glutamyltransferase were independent predictors of steatosis. Ferritin levels were significantly related to low platelet count, steatosis and hepatitis C virus infection. CONCLUSION: In a non-obese cohort of non-alcoholic patients with chronically abnormal LFTs without HH, high serum ferritin level is a risk factor for steatosis. World journal of gastroenterology : WJG [World J Gastroenterol] ------------------- Evidenced based medicine .. Low iron equals low fatty liver disease. Which would explain somewhat the REVERSAL OF CIRRHOSIS which has been demonstrated by the iron reduction therapy. "These results reflect the insulin-sparing effect of iron depletion and indicate a key role of iron and hyperinsulinemia in the pathogenesis of NAFLD" Effect of iron depletion in carbohydrate-intolerant patients with clinical evidence of nonalcoholic fatty liver disease. Gastroenterology 2002 Apr;122(4):931-9 Facchini FS, Hua NW, Stoohs RA. Department of Medicine, University of California San Francisco and San Francisco General Hospital, San Francisco, California, USA. ffacch...@ecnea.org BACKGROUND & AIMS: Increased body iron, genetic hemochromatosis (GH) mutations, and nonalcoholic fatty liver disease (NAFLD) tend to cluster in carbohydrate-intolerant patients. In an attempt to further clarify the interrelationships among these conditions, we studied 42 carbohydrate-intolerant patients who were free of the common GH mutations C282Y and H63D, and had a serum iron saturation lower than 50%. METHODS: We measured body iron stores, and induced iron depletion to a level of near-iron deficiency (NID) by quantitative phlebotomy. RESULTS: In the 17 patients with clinical evidence of NAFLD, we could not demonstrate supranormal levels of body iron (1.6 +/- 0.2 vs. 1.4 +/- 0.2 g; P = 0.06). However, at NID, there was a 40%-55% improvement (P = 0.05-0.0001) of both fasting and glucose-stimulated plasma insulin concentrations, and near-normalization of serum alanine aminotransferase activity (from 61 +/- 5 to 32 +/- 2 IU/L; P < 0.001). CONCLUSIONS: These results reflect the insulin-sparing effect of iron depletion and indicate a key role of iron and hyperinsulinemia in the pathogenesis of NAFLD. PMID: 11910345 --------------- http://www.natap.org/2000/jan/fattyliver011700.html Who loves ya. Tom Jesus Was A Vegetarian! http://tinyurl.com/634q5a Man Is A Herbivore! http://tinyurl.com/4rq595 DEAD PEOPLE WALKING http://tinyurl.com/zk9fk Spamming Moron On May 11, 2:02 pm, Rusty the OCD Suffering Retard <flakey...@aol.com> wrote: snip << You seem to find .. stay off my threads .. hard to understand .. shteater .. That would be because you are a .. shteating .. **freak** .. http://www.traditionalvalues.org/homosexual_movement_and_pedophilia/ http://www.talk2action.org/story/2006/10/3/21245/3789 http://predatorsafety.blogspot.com/2008/11/homosexual-grooming-of-chi... Predator Safety - Dedicated To The Protection Of Our Children The predatorial posts by the shteaters in this thread .. evidence .. mental instability .. common to homosexuals .. IE: "Dysfunctional Homosexuals" ------------------ WHEN the **iron** is REMOVED the fatty liver is REVERSED. Hyperferritinemia is a risk factor for steatosis in chronic liver disease. Licata A, Nebbia ME, Cabibbo G, Iacono GL, Barbaria F, Brucato V, Alessi N, Porrovecchio S, Di Marco V, Craxì A, Cammà C World J Gastroenterol 2009 May 7; 15(17):2132-8. AIM: To investigate the relationship between ferritin and steatosis in patients with chronically abnormal liver function tests (LFTs) and high ferritin level. METHODS: One hundred and twenty-four consecutive patients with hyperferritinemia (male > 300 ng/mL, female > 200 ng/mL) were evaluated; clinical, biochemical and serological data, iron status parameters, HFE gene mutations and homeostasis model assessment score were obtained. Steatosis was graded by ultrasound as absent or present. Histology was available in 53 patients only. RESULTS: Mean level of ferritin was 881 +/- 77 ng/mL in men and 549 +/- 82 ng/mL in women. The diagnosis was chronic hepatitis C in 53 (42.7%), non-alcoholic fatty liver disease/non-alcoholic steatohepatitis in 57 (45.9%), and cryptogenic liver damage in 14 (11.3%). None was diagnosed as hereditary hemochromatosis (HH). Hepatic siderosis on liver biopsy was present in 17 of 54 (32%) patients; grade 1 in eight and grade 2 in nine. Overall, 92 patients (74.2%) had steatosis. By logistic regression, ferritin and gamma-glutamyltransferase were independent predictors of steatosis. Ferritin levels were significantly related to low platelet count, steatosis and hepatitis C virus infection. CONCLUSION: In a non-obese cohort of non-alcoholic patients with chronically abnormal LFTs without HH, high serum ferritin level is a risk factor for steatosis. World journal of gastroenterology : WJG [World J Gastroenterol] ------------------- Evidenced based medicine .. Low iron equals low fatty liver disease. Which would explain somewhat the REVERSAL OF CIRRHOSIS which has been demonstrated by the iron reduction therapy. "These results reflect the insulin-sparing effect of iron depletion and indicate a key role of iron and hyperinsulinemia in the pathogenesis of NAFLD" Effect of iron depletion in carbohydrate-intolerant patients with clinical evidence of nonalcoholic fatty liver disease. Gastroenterology 2002 Apr;122(4):931-9 Facchini FS, Hua NW, Stoohs RA. Department of Medicine, University of California San Francisco and San Francisco General Hospital, San Francisco, California, USA. ffacch...@ecnea.org BACKGROUND & AIMS: Increased body iron, genetic hemochromatosis (GH) mutations, and nonalcoholic fatty liver disease (NAFLD) tend to cluster in carbohydrate-intolerant patients. In an attempt to further clarify the interrelationships among these conditions, we studied 42 carbohydrate-intolerant patients who were free of the common GH mutations C282Y and H63D, and had a serum iron saturation lower than 50%. METHODS: We measured body iron stores, and induced iron depletion to a level of near-iron deficiency (NID) by quantitative phlebotomy. RESULTS: In the 17 patients with clinical evidence of NAFLD, we could not demonstrate supranormal levels of body iron (1.6 +/- 0.2 vs. 1.4 +/- 0.2 g; P = 0.06). However, at NID, there was a 40%-55% improvement (P = 0.05-0.0001) of both fasting and glucose-stimulated plasma insulin concentrations, and near-normalization of serum alanine aminotransferase activity (from 61 +/- 5 to 32 +/- 2 IU/L; P < 0.001). CONCLUSIONS: These results reflect the insulin-sparing effect of iron depletion and indicate a key role of iron and hyperinsulinemia in the pathogenesis of NAFLD. PMID: 11910345 --------------- http://www.natap.org/2000/jan/fattyliver011700.html Who loves ya. Tom Jesus Was A Vegetarian! http://tinyurl.com/634q5a Man Is A Herbivore! http://tinyurl.com/4rq595 DEAD PEOPLE WALKING http://tinyurl.com/zk9fk "Rusty the Canuck Cocksucker" <flakey714@aol.com> Why don't *you* stop insulting Canadians and gays? --Bill Thompson On May 11, 6:22 pm, ironjustice <teamtan...@hotmail.com> wrote:key role of iron and hyperinsulinemia in the pathogenesis of NAFLD << "The incidence of liver cancer is rising in the developed Western world at a time when obesity is also emerging as a major public health threat" "What is the link between these two phenomena?" Diabetes Link to Liver Disease Karen Barrow Medically Reviewed On: December 19, 2005 Most patients with diabetes know that they have an increased risk of heart disease and stroke, but few realize that their diabetes is also raising their risk of having both liver disease and liver cancer. "There is now growing evidence that some endocrine disorders, in particular diabetes mellitus, may actually cause liver disease," said Dr. Adrian M. DiBisceglie of the division of gastroenterology and hepatology at the Saint Louis University School of Medicine in a response to the new data. A pair of studies reveal that patients with type 2 diabetes have two times the risk of developing liver disease and possibly three times the risk of developing liver cancer as their healthy peers. Because liver disease can go undetected for years, these findings emphasize the importance for those with diabetes to keep a close eye on their liver health. Reviewing the Problem In the first study, published in Gastroenterology, researchers followed over 170,000 patients with type 2 diabetes and over 650,000 patients without diabetes who were admitted to various VA hospitals across the country. Fifteen years after being discharged, the patients with diabetes were almost twice as likely to have chronic liver disease as the patients without diabetes. While it is unclear whether diabetes directly causes liver disease, or if changes in liver function cause diabetes, Dr. Hashem El-Serag, study author from the Houston Veteran Affairs Medical Center, sees this study as an important warning for patients with diabetes. Because liver disease can often go unnoticed, as it causes no discernible symptoms, he recommends "regular testing of liver enzymes for patients with diabetes." In a related study, published in the journal Gut, 2,061 patients with liver cancer were compared to over 6,000 patients without liver cancer from a Medicare database. The researchers found that 43 percent of the patients with liver cancer also had diabetes, while only 19 percent of the cancer-free control group had diabetes. When other factors that contribute to liver cancer risk, like alcoholism, were taken into account, the researchers found that patients with diabetes had three times the risk of developing liver cancer as the general population. "Our results indicate that diabetes is associated with an increased risk of [liver cancer] among people 65 years and older," wrote El-Serag. Chronic liver diseases, caused by hepatitis B, hepatitis C, heavy alcohol consumption and fatty liver disease have previously been shown to be major risk factors for developing liver cancer, but this is the first time that diabetes alone was seen as a risk factor for liver cancer. This correlation may explain why rates of liver cancer have been on the rise in the United States. "The incidence of liver cancer is rising in the developed Western world at a time when obesity is also emerging as a major public health threat," said DiBisceglie. "What is the link between these two phenomena?" Who loves ya. Tom Jesus Was A Vegetarian! http://tinyurl.com/634q5a Man Is A Herbivore! http://tinyurl.com/4rq595 DEAD PEOPLE WALKING http://tinyurl.com/zk9fk > On May 11, 4:12 pm, "Paul T. Holland" <pholl...@bellatlantic.net> > wrote: : snip << [quoted text clipped - 117 lines] > > DEAD PEOPLE WALKINGhttp://tinyurl.com/zk9fk Spammer On May 12, 7:56 am, Ken <flakey...@aol.com> wrote: snip << You were TOLD to take your predatory nature .. somewhere .. else .. That predatory nature common to .. dysfunctional homosexuals .. AND you must remember when you cut my posts .. it is evidence OF .. the dysfunctional predatorial nature of you .. disease ridden mutated .. shteating .. **freaks** .. http://www.traditionalvalues.org/homosexual_movement_and_pedophilia/ http://www.talk2action.org/story/2006/10/3/21245/3789 http://predatorsafety.blogspot.com/2008/11/homosexual-grooming-of-chi... Predator Safety - Dedicated To The Protection Of Our Children The predatorial posts by the shteaters in this thread .. evidence .. mental instability .. common to homosexuals .. IE: "Dysfunctional Homosexuals" ------------------ What is fatty liver ? http://www.natap.org/2000/jan/fattyliver011700.html WHEN the **iron** is REMOVED the fatty liver is REVERSED. Hyperferritinemia is a risk factor for steatosis in chronic liver disease. Licata A, Nebbia ME, Cabibbo G, Iacono GL, Barbaria F, Brucato V, Alessi N, Porrovecchio S, Di Marco V, Craxì A, Cammà C World J Gastroenterol 2009 May 7; 15(17):2132-8. AIM: To investigate the relationship between ferritin and steatosis in patients with chronically abnormal liver function tests (LFTs) and high ferritin level. METHODS: One hundred and twenty-four consecutive patients with hyperferritinemia (male > 300 ng/mL, female > 200 ng/mL) were evaluated; clinical, biochemical and serological data, iron status parameters, HFE gene mutations and homeostasis model assessment score were obtained. Steatosis was graded by ultrasound as absent or present. Histology was available in 53 patients only. RESULTS: Mean level of ferritin was 881 +/- 77 ng/mL in men and 549 +/- 82 ng/mL in women. The diagnosis was chronic hepatitis C in 53 (42.7%), non-alcoholic fatty liver disease/non-alcoholic steatohepatitis in 57 (45.9%), and cryptogenic liver damage in 14 (11.3%). None was diagnosed as hereditary hemochromatosis (HH). Hepatic siderosis on liver biopsy was present in 17 of 54 (32%) patients; grade 1 in eight and grade 2 in nine. Overall, 92 patients (74.2%) had steatosis. By logistic regression, ferritin and gamma-glutamyltransferase were independent predictors of steatosis. Ferritin levels were significantly related to low platelet count, steatosis and hepatitis C virus infection. CONCLUSION: In a non-obese cohort of non-alcoholic patients with chronically abnormal LFTs without HH, high serum ferritin level is a risk factor for steatosis. World journal of gastroenterology : WJG [World J Gastroenterol] ------------------- Evidenced based medicine .. Low iron equals low fatty liver disease. Which would explain somewhat the REVERSAL OF CIRRHOSIS which has been demonstrated by the iron reduction therapy. "These results reflect the insulin-sparing effect of iron depletion and indicate a key role of iron and hyperinsulinemia in the pathogenesis of NAFLD" Effect of iron depletion in carbohydrate-intolerant patients with clinical evidence of nonalcoholic fatty liver disease. Gastroenterology 2002 Apr;122(4):931-9 Facchini FS, Hua NW, Stoohs RA. Department of Medicine, University of California San Francisco and San Francisco General Hospital, San Francisco, California, USA. ffacch...@ecnea.org BACKGROUND & AIMS: Increased body iron, genetic hemochromatosis (GH) mutations, and nonalcoholic fatty liver disease (NAFLD) tend to cluster in carbohydrate-intolerant patients. In an attempt to further clarify the interrelationships among these conditions, we studied 42 carbohydrate-intolerant patients who were free of the common GH mutations C282Y and H63D, and had a serum iron saturation lower than 50%. METHODS: We measured body iron stores, and induced iron depletion to a level of near-iron deficiency (NID) by quantitative phlebotomy. RESULTS: In the 17 patients with clinical evidence of NAFLD, we could not demonstrate supranormal levels of body iron (1.6 +/- 0.2 vs. 1.4 +/- 0.2 g; P = 0.06). However, at NID, there was a 40%-55% improvement (P = 0.05-0.0001) of both fasting and glucose-stimulated plasma insulin concentrations, and near-normalization of serum alanine aminotransferase activity (from 61 +/- 5 to 32 +/- 2 IU/L; P < 0.001). CONCLUSIONS: These results reflect the insulin-sparing effect of iron depletion and indicate a key role of iron and hyperinsulinemia in the pathogenesis of NAFLD. PMID: 11910345 --------------- "The incidence of liver cancer is rising in the developed Western world at a time when obesity is also emerging as a major public health threat" "What is the link between these two phenomena?" Diabetes Link to Liver Disease Karen Barrow Medically Reviewed On: December 19, 2005 Most patients with diabetes know that they have an increased risk of heart disease and stroke, but few realize that their diabetes is also raising their risk of having both liver disease and liver cancer. "There is now growing evidence that some endocrine disorders, in particular diabetes mellitus, may actually cause liver disease," said Dr. Adrian M. DiBisceglie of the division of gastroenterology and hepatology at the Saint Louis University School of Medicine in a response to the new data. A pair of studies reveal that patients with type 2 diabetes have two times the risk of developing liver disease and possibly three times the risk of developing liver cancer as their healthy peers. Because liver disease can go undetected for years, these findings emphasize the importance for those with diabetes to keep a close eye on their liver health. Reviewing the Problem In the first study, published in Gastroenterology, researchers followed over 170,000 patients with type 2 diabetes and over 650,000 patients without diabetes who were admitted to various VA hospitals across the country. Fifteen years after being discharged, the patients with diabetes were almost twice as likely to have chronic liver disease as the patients without diabetes. While it is unclear whether diabetes directly causes liver disease, or if changes in liver function cause diabetes, Dr. Hashem El-Serag, study author from the Houston Veteran Affairs Medical Center, sees this study as an important warning for patients with diabetes. Because liver disease can often go unnoticed, as it causes no discernible symptoms, he recommends "regular testing of liver enzymes for patients with diabetes." In a related study, published in the journal Gut, 2,061 patients with liver cancer were compared to over 6,000 patients without liver cancer from a Medicare database. The researchers found that 43 percent of the patients with liver cancer also had diabetes, while only 19 percent of the cancer-free control group had diabetes. When other factors that contribute to liver cancer risk, like alcoholism, were taken into account, the researchers found that patients with diabetes had three times the risk of developing liver cancer as the general population. "Our results indicate that diabetes is associated with an increased risk of [liver cancer] among people 65 years and older," wrote El-Serag. Chronic liver diseases, caused by hepatitis B, hepatitis C, heavy alcohol consumption and fatty liver disease have previously been shown to be major risk factors for developing liver cancer, but this is the first time that diabetes alone was seen as a risk factor for liver cancer. This correlation may explain why rates of liver cancer have been on the rise in the United States. "The incidence of liver cancer is rising in the developed Western world at a time when obesity is also emerging as a major public health threat," said DiBisceglie. "What is the link between these two phenomena?" Who loves ya. Tom Jesus Was A Vegetarian! http://tinyurl.com/634q5a Man Is A Herbivore! http://tinyurl.com/4rq595 DEAD PEOPLE WALKING http://tinyurl.com/zk9fk |
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