Posted: 11 June 2010
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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Monday, June 7, 2010
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"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
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Thursday, May 13, 2010
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(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@yahoo.com; Nassar F, Assy N. assy.n@ziv.health.gov.il
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@ziv.health.gov.il
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@ziv.health.gov.il; or ; Email: assy.nimer@gmail.com;
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.
REFERENCES
Rich Murray, MA
Boston University Graduate School 1967 psychology
BS MIT 1964, history and physics
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