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fructose, aspartame, caramel in soft drinks and nonalcoholic fatty liver disease, W Nseir, F Nassar, N Assy, World J Gastroenterol: Rich Murray 2010.06.07

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  • Rich Murray
    fructose, aspartame, caramel in soft drinks and nonalcoholic fatty liver disease, W Nseir, F Nassar, N Assy, World J Gastroenterol: Rich Murray 2010.06.07
    Message 1 of 1 , Jun 7, 2010
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      fructose, aspartame, caramel in soft drinks and nonalcoholic fatty liver
      disease, W Nseir, F Nassar, N Assy, World J Gastroenterol: Rich Murray
      2010.06.07
      http://rmforall.blogspot.com/2010_06_01_archive.htm
      Monday, June 7, 2010
      [ at end of each long page, click on Older Posts ]
      http://groups.yahoo.com/group/aspartameNM/message/1602
      [ You may have to Copy and Paste URLs into your browser ]
      _______________________________________________


      "During regular soft drinks consumption, fat accumulates in the
      liver by the primary effect of fructose which increases
      lipogenesis, and in the case of diet soft drinks, by the
      additional contribution of aspartame sweetener and
      caramel colorant which are rich in advanced glycation end
      products that potentially increase insulin resistance and
      inflammation." 2010.06.07


      "From our study, it seems that fructose is not the only risk
      factor of liver disease, because 40% of our cohort were
      drinking Diet Coke sweetened with aspartame.

      Aspartame is absorbed from the intestine and metabolized
      by the liver to form phenylalanine, aspartic acid and methanol.
      This process causes mitochondrial dysfunction and ATP
      depletion, which contribute to accumulation of fat (29).

      Also, regarding obesity and aspartame, formaldehyde
      converted from the free methyl alcohol accumulates in the
      cells and damages mitochondrial DNA, with most toxicity
      effects occurring in the liver.

      Finally, the effect of caramel colourant has been incriminated
      as a cause of elevated liver enzymes and may be a potential
      source of advanced glycation end product, which may
      promote insulin resistance and can be proinflammatory
      (5,6,20)." 2008 October

      "29. Trocho C, Pardo R, Rafecas I, et al.
      Formaldehyde derived from dietary aspartame binds to tissue
      components in vivo.
      Life Sci. 1998; 63: 337-49. [PubMed]"

      [ See also:

      Woodrow C Monte, PhD, Emiritus Prof. Nutrition gives
      many PDFs of reseach -- methanol (11% of aspartame) puts
      formaldehyde into brain and body -- multiple sclerosis,
      Alzheimer's, cancers, birth defects, headaches:
      Rich Murray 2010.05.13
      http://rmforall.blogspot.com/2010_05_01_archive.htm
      Thursday, May 13, 2010
      http://groups.yahoo.com/group/aspartameNM/message/1601

      ( Other formaldehyde sources include alcohol drinks and
      tobacco and wood smoke.
      Adequate folic acid levels protect most people from some
      harm, but not for the brain and retinas.) ]


      World J Gastroenterol. 2010 Jun 7; 16(21): 2579-88.
      Soft drinks consumption and nonalcoholic fatty liver disease.
      Nseir W, w.nseir@...;
      Nassar F,
      Assy N. assy.n@...;

      Abstract

      Nonalcoholic fatty liver disease (NAFLD) is a common
      clinical condition which is associated with metabolic syndrome
      in 70% of cases.

      Inappropriate dietary fat intake, excessive intake of soft
      drinks, insulin resistance and increased oxidative stress
      combine to increase free fatty acid delivery to the liver, and
      increased hepatic triglyceride accumulation contributes to
      fatty liver.

      Regular soft drinks have high fructose corn syrup which
      contains basic sugar building blocks, fructose 55% and
      glucose 45%.

      Soft drinks are the leading source of added sugar worldwide,
      and have been linked to obesity, diabetes, and metabolic
      syndrome.

      The consumption of soft drinks can increase the prevalence of
      NAFLD independently of metabolic syndrome.

      During regular soft drinks consumption, fat accumulates in the
      liver by the primary effect of fructose which increases
      lipogenesis, and in the case of diet soft drinks, by the
      additional contribution of aspartame sweetener and caramel
      colorant which are rich in advanced glycation end products
      that potentially increase insulin resistance and inflammation.

      This review emphasizes some hard facts about soft drinks,
      reviews fructose metabolism, and explains how fructose
      contributes to the development of obesity, diabetes,
      metabolic syndrome, and NAFLD. PMID: 2051807


      J Hepatol. 2009 Nov; 51(5): 918-24. Epub 2009 Aug 21.
      Soft drink consumption is associated with fatty liver disease
      independent of metabolic syndrome.
      Abid A,
      Taha O,
      Nseir W,
      Farah R,
      Grosovski M,
      Assy N.
      Liver Unit, Ziv Medical Center, Safed, Israel.
      Comment in:
      J Hepatol. 2010 Jun;52(6):954; author reply 954.

      Abstract

      BACKGROUND/AIMS:
      The independent role of soft drink consumption in
      non-alcoholic fatty liver disease (NAFLD) patients remains
      unclear.
      We aimed to assess the association between consumption of
      soft drinks and fatty liver in patients with or without metabolic
      syndrome.
      METHODS:
      We recruited 31 patients (age: 43+/-12 years) with NAFLD
      and risk factors for metabolic syndrome,
      29 patients with NAFLD and without risk factors for
      metabolic syndrome, and
      30 gender- and age-matched individuals without NAFLD.
      The degree of fatty infiltration was measured by ultrasound.
      Data on physical activity and intake of food and soft drinks
      were collected during two 7-day periods over 6 months
      using a food questionnaire.
      Insulin resistance, inflammation, and oxidant-antioxidant
      markers were measured.
      RESULTS:
      We found that 80% of patients with NAFLD had excessive
      intake of soft drink beverages (>500 cm(3)/day) compared to
      17% of healthy controls (p<0.001).
      The NAFLD group consumed five times more carbohydrates
      from soft drinks compared to healthy controls
      (40% vs. 8%, p<0.001).
      Seven percent of patients consumed one soft drink per day,
      55% consumed two or three soft drinks per day, and
      38% consumed more than four soft drinks per day for most
      days and for the 6-month period.

      The most common soft drinks were Coca-Cola
      (regular: 32%; diet: 21%)
      followed by fruit juices (47%).

      Patients with NAFLD with metabolic syndrome had similar
      malonyldialdehyde, paraoxonase, and C-reactive protein
      (CRP) levels but higher homeostasis model assessment
      (HOMA) and higher ferritin than NAFLD patients without
      metabolic syndrome
      (HOMA: 8.3+/-8 vs. 3.7+/-3.7 mg/dL, p<0.001;
      ferritin: 186+/-192 vs. 87+/-84 mg/dL, p<0.01).
      Logistic regression analysis showed that soft drink
      consumption is a strong predictor of fatty liver
      (odds ratio: 2.0; p<0.04) independent of metabolic syndrome
      and CRP level.
      CONCLUSIONS:
      NAFLD patients display higher soft drink consumption
      independent of metabolic syndrome diagnosis.
      These findings might optimize NAFLD risk stratification.
      PMID: 19765850


      http://www.ncbi.nlm.nih.gov/pubmed/18925303

      Can J Gastroenterol. 2008 Oct; 22(10): 811-6.
      Soft drink consumption linked with fatty liver in the absence
      of traditiona risk factors.
      Assy N, Nasser G, Kamayse I, Nseir W, Beniashvili Z,
      Djibre A, Grosovski M.
      Liver Unit, Ziv Medical Center, Safed, Israel.
      assy.n@...

      Abstract

      BACKGROUND:
      Little is known about dietary habits and their relationships
      with liver disease in nonalcoholic fatty liver disease (NAFLD)
      patients, particularly in the absence of obesity, diabetes or
      hyperlipidemia.
      OBJECTIVE:
      To assess the association between soft drink consumption and
      the presence of fatty liver in NAFLD patients who do not have
      classic risk factors.
      METHODS:
      Three hundred ten patients with NAFLD diagnosed by
      ultrasound were assessed for 36 months in a cross-sectional
      manner.
      Thirty-one patients (10%) who had NAFLD without classic
      risk factors were compared with 30 healthy controls.
      Physical activity was assessed during the preceding week and
      year, and every six months for 36 months.
      Data on daily dietary intake of food and soft drink, and the
      source of added sugar were collected during two seven-day
      periods, at the beginning of the study, and within two weeks
      after the metabolic tests by using a validated
      food questionnaire given by a trained dietician.
      Insulin resistance and lipid peroxidation were assessed by
      homeostasis model assessment-insulin resistance index
      (HOMA-IRI) and malondialdehyde (MDA) levels,
      respectively.
      RESULTS:
      Eighty per cent of patients (25 of 31) consumed an excessive
      amount of soft drink beverages (more than 50 g/day of added
      sugar) for 36 months, compared with
      20% in healthy controls (P<0.001).
      Twenty per cent of patients consumed one drink per day,
      40% consumed two to three drinks per day, and
      40% consumed more than four drinks per day for most days
      during 36 months.

      The most common soft drinks consumed were
      regular Coca-Cola (40% of patients), Diet Coke (40%)
      and flavoured fruit juices (20%).

      Ultrasound findings revealed
      mild fatty liver in 44% of cases (n=14),
      moderate fatty liver in 38% (n=12), and
      severe fatty liver in 18% (n=5).
      HOMA-IRI and MDA levels were significantly higher in
      patients with NAFLD than in healthy controls
      (HOMA-IRI, 3.7 versus 1.7, P<0.001; and
      MDA, 420+/-300 micromol/mL
      versus 200+/-100 micromol/mL; P<0.001).

      When controlled for other factors, including dietary
      composition and physical activity, soft drink beverage
      consumption was the only independent variable that was able
      to predict the presence of fatty liver in 82.5% of cases with a
      sensitivity of 100%, a specificity of 76%, a positive predictive
      value of 57% and a negative predictive value of 100%.

      CONCLUSION:
      The present study may add important insight into the role of
      sugar-sweetened beverage consumption as a cause of fatty
      liver in patients without risk factors.
      Patients are encouraged to change their long-standing
      drinking behaviour. PMID: 18925303

      http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2661299/?tool=pubmed
      free full text

      Nimer Assy, MD, 1,2
      Gattas Nasser, MD, 3
      Iad Kamayse, MD, 4
      William Nseir, MD, 5
      Zaza Beniashvili, MD, 1
      Agness Djibre, MD, 1
      and Maria Grosovski, PhD 6
      1 Liver Unit, Ziv Medical Center, Safed, Israel
      2 Rappaport Faculty of Medicine, Technion -- Israel
      Institute of Technology, Haifa, Israel
      3 Department of Internal Medicine,
      Western Galilee Hospital, Nahariya, Israel
      4 Liver Unit, Rambam Medical Center, Haifa, Israel
      5 Department of Internal Medicine,
      Holy Family Hospital, Nazareth, Israel
      6 Department of Biotechnology,
      ORT Braude College, Karmiel, Israel
      Correspondence: Dr Nimer Assy, Liver Unit,
      Ziv Medical Center, PO Box 1008, Safed 13100, Israel.
      Telephone 9-724-682-8441, fax 9-724-682-8442, e-mail
      assy.n@...; or ; Email: assy.nimer@...;
      Received February 13, 2008; Accepted June 4, 2008.

      [ selections ]

      Normally, less than 5% of the liver is fat by weight, but in
      patients with nonalcoholic steatohepatitis (NASH), as much
      as 50% to 80% of liver weight may be made up of fat,
      mostly in the form of triglycerides (1).
      The clinical implications of NASH are derived mostly from its
      common occurrence in the general population (10% to 24%)
      and its potential to progress to fibrosis (30% to 40%),
      cirrhosis (20% to 30%) and hepatocellular carcinoma (2,3).
      NASH is the most common cause of cryptogenic cirrhosis
      and is an increasingly common indication for liver
      transplantation (3).
      Nonalcoholic fatty liver disease (NAFLD) is one of the most
      important emerging health care issues, and obesity, type 2
      diabetes mellitus and hyperlipidemia are conditions frequently
      associated with NAFLD (1,2).
      However, patients without traditional risk factors have also
      been reported to have fatty infiltration of the liver (3).
      Identifying new risk factors that permit early diagnosis and
      treatment are warranted.

      Soft drinks are the leading cause of added sugar in the diet
      worldwide.
      Recent evidence suggests that sugar-sweetened soft drink
      consumption is associated with the risk of obesity and
      diabetes because they contain large amounts of high-fructose
      corn syrup (HFCS), which raises blood glucose similarly to
      sucrose (4).

      In addition, soft drinks contain caramel colouring, which is rich
      in advanced glycation end products that might increase insulin
      resistance and inflammation (4-6).

      The intake of nutrients (including sweetened beverages) may
      affect insulin resistance, carbohydrate and lipid metabolism,
      and hepatic steatosis, yet many other factors may actually play
      a role (4).

      However, there are few published reports on the intake of
      various nutrients in patients with NAFLD.

      Recently, it has been reported that patients with fatty liver
      consume more simple carbohydrates and less saturated fat
      than those in the general population, suggesting that
      imbalanced diets play important roles in the development and
      progression of NAFLD, and that correction of these diets may
      be necessary (7).
      High-fructose diets have induced fatty liver in rats and
      ducks (8).
      Such diets have also caused increases in hepatic lipid
      peroxidation and activation of inflammatory pathways in the
      liver of rats (9).
      Fructose consumption can cause progressive liver disease in
      humans, which is demonstrated by the inborn error of
      metabolism known as hereditary fructose intolerance.
      Aldolase B is a rare disease that results from a deficiency of
      the fructose metabolizing enzyme (10).
      The extent to which excessive fructose might contribute to the
      high prevalence of NAFLD in western societies has not been
      systematically investigated.

      More recently, soft drink consumption has been linked with
      obesity and has been shown to increase the risk of the
      metabolic syndrome.

      Individuals consuming more than one soft drink per day had
      a higher prevalence of the metabolic syndrome than those
      consuming less than one drink per day.

      Whether soft drink consumption is linked with NAFLD has
      not been assessed (11).

      The aim of the present study was to assess the association
      between soft drink consumption and the presence of fatty
      liver by comparing NAFLD patients with no classic risk
      factors with age-matched, healthy controls.....

      Discussion

      The present study compared dietary constituents, physical
      activity and liver ultrasound in patients with fatty liver.
      We found that NAFLD patients without classic risk factors
      consume more soft drinks and juices than healthy controls.
      The follow-up data, the correlation between severity of fatty
      liver and amount of soft drink consumption, and the fact that
      soft drink consumption was the only independent predictor of
      fatty liver support the association between soft drink
      consumption and fatty liver.
      As expected, insulin resistance (HOMA-IRI) and MDA levels
      were higher in the group with fatty liver.
      However, when controlled for other factors, soft drink
      beverage consumption was the only independent variable that
      correctly predicted the presence of fatty liver.

      The underlying mechanism for this association remains
      unknown.
      Soft drink consumption is the leading cause of added sugar in
      the diet (1 tsp of sugar contains 4.2 g) (17).
      Individuals who consume an excessive amount of soft drinks
      tend to lead a sedentary lifestyle and eat a higher calorie diet
      (an additional 150 kcal/day to 300 kcal/day) that includes
      more fructose (18).

      Because both regular Coca-Cola and Diet Coke consumption
      in our study resulted in an increased risk of fatty liver, factors
      other than calories and sugar content likely contribute to the
      higher risk.

      These factors include the consumption of fructose, aspartame,
      caramel (food colourant) and other covariants.

      These complexes of sugars and colourants may promote
      insulin resistance, lipid peroxidation and hepatic inflammation,
      and are a source of glycation end products (5,19,20).

      The extent to which excessive fructose, aspartame and
      caramel consumption might contribute to the high prevalence
      of liver disease in western societies and to the progression of
      NAFLD to NASH has not been investigated.

      One study of lean women found that four days of overfeeding
      with sucrose (glucose plus fructose) drink increased de novo
      lipogenesis by 200% to 300% (21).

      Another feeding study showed that two days of a
      high-fructose diet (30% of the total energy consumed per day,
      consumed as a sweetened beverage at every meal) resulted
      in decreased postprandial glucose concentration and insulin
      response, and prolonged alimentary lipemia in women (22).

      Another follow-up study indicated that both surplus calories
      and excessive sucrose consumption play a role in the rise of
      liver enzyme levels (23).

      Additional evidence that fructose can cause steatohepatitis is
      that intravenous administration of fructose to healthy volunteers
      has resulted in a 75% decrease in hepatic ATP within 10 min
      because the liver was overwhelmed and could not metabolize
      it (24).

      Fructose can also increase triglyceride levels, de novo
      synthesis of fatty acids, hyperuricemia and insulin resistance
      (25).
      The triglyceride response to fructose ingestion appears to
      depend on whether a person is carbohydrate-sensitive or
      insulin-resistant (26).

      Fructose, especially high-fructose corn syrup, is now used
      extensively in carbonated beverages and other sweetened
      drinks, baked goods, candies, canned fruits, sodas, jams,
      jellies and dairy products (27).

      After absorption in the small bowel, fructose is transported
      via the portal vein to the liver, where it is metabolized by
      fructokinase to fructose-1-phosphate.
      This molecule is cleaved by aldolase to form glycerone
      phosphate and glyceraldehyde-3-phosphate, both of which
      can be further metabolized in the glycolytic pathway (28).
      An increase in serum triglycerides and, ultimately, increased
      low-density lipoprotein cholesterol concentration may result
      from enhanced fatty acid synthesis, increased esterification
      of fatty acids and increased very low-density lipoprotein
      secretion (28).

      A soft drink containing 32.6 g of fructose could increase the
      fasting serum fructose fourfold.
      A 340 g soft drink sweetened with fructose-55 contains
      approximately 40 g of the sweetener (ie, 22 g of fructose and
      17 g of glucose, representing a fructose excess of 5 g per can)
      (20,29).

      Fructose affects each of the three major factors that are
      believed to contribute to the pathogenesis of diabetic end
      organ damage.
      These factors are glycosylation of tissue proteins, intracellular
      accumulation of sorbitol and oxidative stress (4).
      The association between the consumption of beverages
      sweetened with sugars such as HFCS and the risk of diabetes
      has been established by Schultze et al (20).


      From our study, it seems that fructose is not the only risk
      factor of liver disease, because 40% of our cohort were
      drinking Diet Coke sweetened with aspartame.

      Aspartame is absorbed from the intestine and metabolized
      by the liver to form phenylalanine, aspartic acid and methanol.
      This process causes mitochondrial dysfunction and ATP
      depletion, which contribute to accumulation of fat (29).

      Also, regarding obesity and aspartame, formaldehyde
      converted from the free methyl alcohol accumulates in the
      cells and damages mitochondrial DNA, with most toxicity
      effects occurring in the liver.

      Finally, the effect of caramel colourant has been incriminated
      as a cause of elevated liver enzymes and may be a potential
      source of advanced glycation end product, which may
      promote insulin resistance and can be proinflammatory
      (5,6,20).

      The extent to which fructose, aspartame and caramel
      contributed to severe fatty liver could not be concluded
      due to the small size of the cohort.


      When controlled for other factors, including dietary
      composition and physical activity, soft drink beverage
      consumption was the only independent variable that could
      correctly classify the presence of fatty infiltration of the liver.

      A study by Vartanian et al (30) showed a clear association
      among soft drink intake, diabetes and the metabolic
      syndrome, confirming our finding.

      Although we still do not know the most common soft drink
      that induces fatty liver, fructose, caramel and aspartame
      constituents may have a role.
      These coingestants might also increase the risk for fatty
      liver because of their high amount of rapidly absorbable
      carbohydrates (20).

      They contain a large amount of HFCS, which has a similar
      effect on blood glucose as sucrose (31).
      The consumption of sugar-sweetened soft drinks therefore
      induces a fast and dramatic increase in both glucose and
      insulin concentration (32).
      In addition, cola-type soft drink caramel colouring is rich
      in advanced glycation end products, which may increase
      insulin resistance and inflammation (6,33).

      The US Food and Drug Administration has established
      51 mg of aspartame and 200 mg of caramel colouring
      per kg body weight as an acceptable daily intake.

      The natural history of NAFLD is not known.
      The present study may add important insight into the role of
      sugar-sweetened beverage consumption as a cause of fatty
      liver in those without risk factors.
      The time from NAFLD diagnosis to enrolment in the study
      was less than two weeks.
      Therefore, the information obtained for dietary food
      consumption was a good reflection of the patient's dietary
      habits before the diagnosis of NAFLD.....

      CONCLUSIONS

      Although more studies are needed, the findings of the present
      study suggest that soft drink consumption is the most
      common risk factor for fatty infiltration of the liver in
      patients without classic risk factors.
      Patients are encouraged to change their longstanding
      drinking behaviour.
      Whether consumption of soft drinks contributes to the
      progression of simple fatty liver to steatohepatitis in
      patients with metabolic syndrome is yet to be determined.

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      _______________________________________________


      Rich Murray, MA
      Boston University Graduate School 1967 psychology,
      BS MIT 1964, history and physics,
      1943 Otowi Road, Santa Fe, New Mexico 87505
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