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Fatty Liver Disease And Iron
  1. #1
    ironjustice Guest

    Default Fatty Liver Disease And Iron

    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, Craxė A, Cammā 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


    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


  2. #2
    [email protected] Guest

    Default Re: Fatty Liver Disease And Iron

    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.

  3. #3
    ironjustice Guest

    Default Re: Fatty Liver Disease And Iron

    On May 8, 11:34*am, tu...@guy.com wrote:
    This one suffers from the usual flaws of logic as most you post. <<

    You must know logic to speak to logic ..

    You must know science to speak to science ..

    The treatment CURES the person .. USE IT .. and stfu .

    "at NID, there was a 40%-55% improvement
    of both fasting and glucose-stimulated
    plasma insulin concentrations, and near-normalization of
    serum alanine aminotransferase activity"

    Whether YOU 'like it' or not ..the IRON DEFICIENCY.. that iron
    deficiency
    considered to be BAD by .. shtbags like yourself .. CURES the person.

    Now .. cure .. is a word I use alot.

    YOU and your useless nurses and doctors .. don't use it a .. fkg ..
    tall ..

    The people are CURED when they are in a state of iron DEFICIENCY ..

    TOP it .. or .. fk .. off .. understand .. ?
    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, Craxė A, Cammā 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


    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


  4. #4
    Bob Officer Guest

    Default Re: Fatty Liver Disease And Iron

    On Sun, 10 May 2009 22:33:34 -0700 (PDT), in misc.health.alternative,
    ironjustice <[email protected]> wrote:

    >On May 8, 11:34*am, tu...@guy.com wrote:
    >This one suffers from the usual flaws of logic as most you post. <<
    >
    >You must know logic to speak to logic ..
    >
    >You must know science to speak to science ..
    >
    >The treatment CURES the person .. USE IT .. and stfu .


    It doesn't cure the problem, it **MAY** treat a preexisting
    condition. you initial claim was that it would prevent
    >
    >"at NID, there was a 40%-55% improvement
    > of both fasting and glucose-stimulated
    >plasma insulin concentrations, and near-normalization of
    >serum alanine aminotransferase activity"
    >
    >Whether YOU 'like it' or not ..the IRON DEFICIENCY.. that iron
    >deficiency
    >considered to be BAD by .. shtbags like yourself .. CURES the person.


    No it treats a condition. it doesn't sure it. Iron may not even be
    the causal agent which you are claiming, by misconstruing this papers
    findings.

    >Now .. cure .. is a word I use alot.


    But the paper never used the word cure. I wasn't aware you were a MD,
    or could insert finding in to the paper. I read the paper and it
    never mentioned the word cure or preventative. it is a treatment

    >YOU and your useless nurses and doctors .. don't use it a .. fkg ..
    >tall ..


    The Doctors were the ones that wrote the paper, and I am sure they
    would correct your false claims.

    >The people are CURED when they are in a state of iron DEFICIENCY ..


    No,they were not cured.

    >TOP it .. or .. fk .. off .. understand .. ?
    >When the iron is removed the fatty liver is reversed.


    The paper said that? That isn't what this paper said.

    >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, Craxė A, Cammā 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.


    High Ferritin levels not normal levels.

    >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.


    Or maybe High Ferritin levels is an indictor of steatosis? I do know
    that FLD is a risk in Diabetes and Hep-C.

    Note the Study included 124 samples.
    92 had Steatosis
    53 had Hep-c


    >
    >World journal of gastroenterology : WJG [World J Gastroenterol]
    >-------------------
    >
    >
    >Evidenced based medicine ..
    >
    >
    >Low iron equals low fatty liver disease.


    That's a false conclusion. the paper didn't have that conclusion at
    all. It said it should be considered a risk factor.

    >Which would explain somewhat the REVERSAL OF CIRRHOSIS which has been
    >demonstrated by the iron reduction therapy.


    That still isn't what the paper said.
    >
    >"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


    Note: 40-55% improvement is not a cure. it is a treatment.There is no
    mention of long term results.

    Also note: 17 out of 42 show they could not demonstrate supernormal
    levels of body iron.

    This is the problem which happens which poorly educated people reach
    exceeds their grasp of required background knowledge.


    --
    Ak'toh'di

  5. #5
    ironjustice Guest

    Default Fatty Liver Disease And Iron

    On May 12, 4:56*pm, Bob Officer <boboffic...@127.0.0.7> wrote:

    YOU were told to leave .. understand .. ?

    YOU were told you are lucky you ain't in an asylum ..

    YOU shteater were told NOT to try to express yourself .. a .. tall ..

    YOU shteater .. leave .. understand .. ?

    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, Craxė A, Cammā 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


    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


  6. #6
    Rusty the Retard Guest

    Default Re: More of Rusty's CCPed Bullcrap Snipped as a Public Service

    Spamming Moron


  7. #7
    ironjustice Guest

    Default Fatty Liver Disease And Iron

    On May 12, 6:24*pm, Rusty the Retard <flakey...@earthlink.net> wrote:
    snip <<

    You continuously INSIST upon evidencing .. coincidentally .. the
    dysfunctional nature common to a .. shteater ..

    Remember while you cut this post .. shteater .. it is evidence
    OF .. the dysfunctional PREDATORIAL nature of yours common to men
    who prefer .. to have sex with boys ..


    Hit the road you shteating .. disease ridden .. mutated .. freak ..


    http://www.traditionalvalues.org/hom...nd_pedophilia/


    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, Craxė A, Cammā 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


    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

    http://www.talk2action.org/story/2006/10/3/21245/3789


    http://predatorsafety.blogspot.com/2...rooming-of-chi...


    Predator Safety
    Dedicated To The Protection Of Our Children


    ------------------



  8. #8
    Ken Guest

    Default Re: Rusty's BS Deleted

    Spamming Fool


  9. #9
    ironjustice Guest

    Default Fatty Liver Disease And Iron

    On May 12, 8:20*pm, Ken <flakey...@earthlink.net> wrote:snip <<

    You shteater .. have been told to take your shteating somewhere ..
    OTHER .. than my threads ..


    Remember while you cut this post .. shteater .. it is evidence
    OF .. the dysfunctional PREDATORIAL nature of yours common to men
    who prefer .. to have sex with boys ..


    Hit the road you shteating .. disease ridden .. mutated .. freak ..


    http://www.traditionalvalues.org/hom...nd_pedophilia/


    http://www.talk2action.org/story/2006/10/3/21245/3789


    http://predatorsafety.blogspot.com/2...rooming-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, Craxė A, Cammā 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


    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



  10. #10
    Bob Officer Guest

    Default Re: Fatty Liver Disease And Iron

    On Tue, 12 May 2009 17:39:56 -0700 (PDT), in misc.health.alternative,
    ironjustice <[email protected]> wrote:

    >On May 12, 4:56*pm, Bob Officer <boboffic...@127.0.0.7> wrote:
    >
    >YOU were told to leave .. understand .. ?


    Not by anyone with any authority. And you don't have any say. None at
    all.

    >YOU were told you are lucky you ain't in an asylum ..


    It isn't me that his the Huffer, Rusty.

    >YOU shteater were told NOT to try to express yourself .. a .. tall ..


    Sorry, rusty, we have a thing here called free speech.

    >YOU shteater .. leave .. understand .. ?


    Nope, I don't take orders fro people that are Huffers. You know all
    those solvents you cooked off those plastic bottles are affecting you
    ability to think clearly.

    >When the iron is removed the fatty liver is reversed.


    Now, Rusty, I read the articles and not once was that said.

    I don't now what you're doing, but telling lies isn't helping anyone
    >


    --
    Ak'toh'di

  11. #11
    ironjustice Guest

    Default Fatty Liver Disease And Iron

    On May 13, 1:54*pm, Bob Officer <boboffic...@127.0.0.7> wrote: snip
    <<

    You shteater .. have been told to take your shteating somewhere ..
    OTHER .. than my threads ..

    You must think you are some kind of special shteating .. disease
    ridden ..
    mutated .. freak ..

    You are NOT .. a .. special .. shteater .. shteater ..

    You are just a regular disease ridden mutated freak .. shteater ..

    Live with it ..

    http://www.traditionalvalues.org/hom...nd_pedophilia/


    http://www.talk2action.org/story/2006/10/3/21245/3789


    http://predatorsafety.blogspot.com/2...rooming-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, Craxė A, Cammā 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


    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



  12. #12
    Bob Officer Guest

    Default Re: Fatty Liver Disease And Iron

    On Wed, 13 May 2009 17:04:32 -0700 (PDT), in misc.health.alternative,
    ironjustice <[email protected]> wrote:

    >On May 13, 1:54*pm, Bob Officer <boboffic...@127.0.0.7> wrote: snip
    ><<
    >
    >You shteater .. have been told to take your shteating somewhere ..
    >OTHER .. than my threads ..
    >
    >You must think you are some kind of special shteating .. disease
    >ridden ..
    >mutated .. freak ..
    >
    >You are NOT .. a .. special .. shteater .. shteater ..
    >
    >You are just a regular disease ridden mutated freak .. shteater ..
    >
    >Live with it ..
    >
    >http://www.traditionalvalues.org/hom...nd_pedophilia/


    Live you religious beliefs in your church little alter boy. Many
    religious leaders are sexual misfits. At least one large church
    denomination is made up entirely of men that are sexual misfits,
    every last one of them.

    >
    >http://www.talk2action.org/story/2006/10/3/21245/3789



    That doesn't involve me, I am neither Catholic or from Hastert's
    district.

    >http://predatorsafety.blogspot.com/2...rooming-of-chi...


    "Chris McDonough is sought after by law enforcement"

    Too Funny

    >When the iron is removed the fatty liver is reversed.


    Not according to the article you cited. If your reading comprehension
    is poor, try reading simpler works. maybe something with pictures.


    --
    Ak'toh'di

  13. #13
    ironjustice Guest

    Default Fatty Liver Disease And Iron

    On May 13, 6:26*pm, Bob Officer <boboffic...@127.0.0.7> wrote:: snip
    <<

    You braindead shteater ..

    You HAVE been told to take your shteating somewhere .. else ..

    You are evidencing some type of predatory .. nature .. shteater ..

    You do know that is common in homosexual predatorial disease ridden
    mutated shteaters .. do ya .. shteater ..

    You should cease and desist in your predatory propensities ..

    One might think you are .. whacko ..

    Can't have that happen .. a .. gain ..

    Eh .. shteater ..

    Back in the asylum again ..

    Sung to the tune of back in the saddle .. again ..

    Stay off my threads .. 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, Craxė A, Cammā 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


    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

  14. #14
    Bob Officer Guest

    Default Re: Fatty Liver Disease And Iron

    On Wed, 13 May 2009 18:34:39 -0700 (PDT), in misc.health.alternative,
    ironjustice <[email protected]> wrote:

    >On May 13, 6:26*pm, Bob Officer <boboffic...@127.0.0.7> wrote:: snip
    ><<
    >
    >You braindead shteater ..
    >
    >You HAVE been told to take your shteating somewhere .. else ..
    >
    >You are evidencing some type of predatory .. nature .. shteater ..
    >
    >You do know that is common in homosexual predatorial disease ridden
    >mutated shteaters .. do ya .. shteater ..
    >
    >You should cease and desist in your predatory propensities ..
    >
    >One might think you are .. whacko ..
    >
    >Can't have that happen .. a .. gain ..
    >
    >Eh .. shteater ..
    >
    >Back in the asylum again ..
    >
    >Sung to the tune of back in the saddle .. again ..
    >
    >Stay off my threads .. shteater ..
    >
    >------------------
    >
    >
    >When the iron is removed the fatty liver is reversed.


    Stop making stuff up, Rusty. don't you have some plastic bottles to
    cook off some solvents, and huff?



    --
    Ak'toh'di

  15. #15
    ironjustice Guest

    Default Fatty Liver Disease And Iron

    On May 13, 7:00*pm, Bob Officer <boboffic...@127.0.0.7> wrote: snip <<

    You braindead disease ridden shteater ..

    You HAVE been told many times to take your shteating somewhere ..
    else ..

    You continue to evidence that predatory .. nature .. shteater ..

    That predatory nature .. common to .. homosexual predatorial disease
    ridden
    mutated shteaters ..

    Shteater .. you should cease and desist in your predatory
    propensities ..

    People might think you are .. whacko ..

    We can't have that happen .. a .. gain .. can we .. shteater ..

    Stay off my threads .. 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, Craxė A, Cammā 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


    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

  16. #16
    Bob Officer Guest

    Default Re: Fatty Liver Disease And Iron

    On Wed, 13 May 2009 19:04:16 -0700 (PDT), in misc.health.alternative,
    ironjustice <[email protected]> wrote:

    >On May 13, 7:00*pm, Bob Officer <boboffic...@127.0.0.7> wrote: snip <<
    >
    >You braindead disease ridden shteater ..
    >
    >You HAVE been told many times to take your shteating somewhere ..
    >else ..
    >
    >You continue to evidence that predatory .. nature .. shteater ..
    >
    >That predatory nature .. common to .. homosexual predatorial disease
    >ridden
    >mutated shteaters ..
    >
    >Shteater .. you should cease and desist in your predatory
    >propensities ..
    >
    >People might think you are .. whacko ..
    >
    >We can't have that happen .. a .. gain .. can we .. shteater ..
    >
    >Stay off my threads .. shteater ..
    >
    >
    >------------------
    >
    >
    >When the iron is removed the fatty liver is reversed.


    That still isn't what the article says. Even after you full cite the
    articles you still don't understand.


    --
    Ak'toh'di

  17. #17
    ironjustice Guest

    Default Fatty Liver Disease And Iron

    On May 13, 8:30*pm, Bob Officer <boboffic...@127.0.0.7> wrote:: snip
    <<

    You are braindead shteater ..

    You continue to insist upon evidencing the predatory nature of a
    shteater ..

    YOU .. HAVE been told many times to take your shteating somewhere ..
    else ..

    Shteater you continue to evidence that predatory .. nature .. OF a
    shteater ..
    shteater ..

    That predatory nature .. common to .. homosexual predatorial disease
    ridden mutated shteaters .. gives .. shteaters .. away ..

    Along with the face and left-handedness ..

    The cleft-palated lisp sometimes .. tooooo ..

    Hit the road shteater ..

    DOOOOOO .. it .. shteater ..

    You are to cease and desist in your predatory
    propensities ..

    People may begin to think you ALL are .. whacko ..
    once .. again .. shteater ..

    Don't post to my threads .. 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, Craxė A, Cammā 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


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