Dispelling Myths
The Toxic Truth
1. How could sugar lead to fat buildup in the liver and arteries?
The liver plays several roles in the body. If the human body were a factory, the liver would be a sorting station for the multiple types of nutrients moving through it. The liver's job is to identify and sort each nutrient, sometimes transforming it into something else the body can use, and then direct those items into the body.
When the body encounters fructose, it will try to use the sugar as energy. But if there is more fructose available than the body needs, the liver stores the excess by converting it into fatty acids, which are then packaged into small fat molecules called triglycerides. Some of those fat globules enter the blood stream and, once there, may end up lining the arteries, increasing the risk of a heart attack. Other triglycerides will build up in the liver, eventually causing damage through a condition called fatty liver. If left unchecked, fatty liver can lead to the more dangerous, life-threatening problem of cirrhosis, just as it does when people consume large amounts of alcohol over long periods of time.
2. Some people question whether the accumulation of fat in the liver, brought about in part by excess fructose consumption, is actually harmful to health.
By and large, there is consensus within the scientific community that the accumulation of fat in the liver is not only harmful to the liver itself, but also signals other health concerns.1 Accumulating fat in the liver leads to scarring and inflammation that produces a condition called "steatosis" which, if left unchecked, can progress to the life-threatening stage of liver cirrhosis. Furthermore, the amount of liver fat is associated with the degree of insulin resistance. Accumulated fat in the liver does not always lead to insulin resistance. But insulin resistance is not associated with fat build up anywhere else in the body, only with fat located inside the liver.2 Insulin resistance is a condition that signals the progression towards Type 2 diabetes, a lifelong chronic condition that can become life threatening.3 Studies have also shown that liver fat is a factor in Type 2 diabetes whether or not a person is obese.4
3. Obese people tend to have lots of fat stored in their livers. Some people contest that the cause of non-alcoholic fatty liver disease (NAFLD) actually may be obesity, suggesting that fructose consumption isn't really the concern.25,6
If obesity were the sole cause of fatty liver disease, we wouldn’t see fatty liver and non-alcoholic fatty liver disease (NAFLD) in thin people. But we do. In fact, doctors have coined the term "TOFI" ("thin on the outside, fat on the inside") to describe such a situation.There is a rare genetic condition in which excessively thin people have an accumulation of fat in the liver.7 But this can't by any means explain all the cases of fatty liver in thin people. Scientists also have questioned whether the source of the fat that builds up in the liver is really from fructose, as opposed to resulting from fat deposited elsewhere on the body that, when broken down, gets transported to the liver.8,9 While some of this may occur, recent studies6 demonstrate that this is not the primary way that fat builds up in the liver to produce fatty liver disease.
4. Perhaps liver fat might be a consequence of excess food intake in general, or other specific food, but not fructose.10,11
It is true that other foods, when consumed in great excess, can promote liver fat accumulation. However, along with fructose, there is really only a handful of other substances that share the special property of being primarily processed in the liver and leading to fat deposits. These include trans-fats, certain proteins ("branched chain amino acids") and alcohol, as well as fructose.12
5. Some scientists have questioned how much fructose must be consumed to produce fatty liver disease. Others have questioned whether animal studies are relevant13 and have said human studies are not always realistic.14 For instance, they argue that study participants should consume fructose and fructose-containing products in similar doses and forms as they typically would.15,16 17
Investigations of how non-alcoholic fatty liver disease (NAFLD) occurs in rats suggest that the process is similar to what occurs in humans.18 Recent studies have focused studying the effects of fructose in healthy human volunteers, where rather moderate amounts of fructose have led to bad health outcomes.19 One study established that the same amount of calories taken in fructose (compared to a different sugar, glucose, which isn’t processed by the liver) increased the amount of liver fat in study participants by 38% within just 2 weeks.20 Another study16 found that people who consumed between 18% and 30% of their daily calories in high-fructose corn syrup experienced increases in liver fat within 10 weeks. Notably, 18% is the average amount of sugar consumed by Americans, and many of us consume much larger amounts.
6. Could the real culprit in fatty liver disease be high-fructose corn syrup, not regular table sugar? After all, it says "high-fructose" right on the label.
Regular table sugar is made up of about 50% fructose, and a common formulation of high-fructose corn syrup (called "HFCS-55") contains 55% fructose. These products are similar enough that there is no evidence of differences in their impact on metabolic health. However, some commercially available formulations of high-fructose corn syrup contain higher proportions of fructose, such as 65% or even higher.21 We do not know whether the health consequences of these products differ from products containing lower concentrations of fructose.
- [1](2013). Redefining metabolic syndrome as a fat storage condition based on studies of comparative physiology. Obesity (Silver Spring) , 21(4), 659-64.
- [2](2010). Obesity and nonalcoholic fatty liver disease: biochemical, metabolic, and clinical implications. Hepatology , 51(2), 679-89.
- [3](2012, February). Relationship between fatty liver and glucose metabolism: A cross-sectional study in 571 obese children. Nutr Metab Cardiovasc Dis , 22 (2), 120-6. doi:10.1016/j.numecd.2010.05.003. Retrieved from http://www.ncbi.nlm.nih.gov/pubmed/20880682
- [4](2011). Interrelationship between fatty liver and insulin resistance in the development of type 2 diabetes. J. Clin. Endocrinol. Metab , 96, 1093-1097.
- [5](2005). Predictors of nonalcoholic steatohepatitis and advanced fibrosis in morbidly obese patients. Obes Surg , 15(3), 310-5.
- [6](2009). Intrahepatic fat, not visceral fat, is linked with metabolic complications of obesity. Proc. Natl. Acad. Sci , 106, 15430-15435.
- [7](2013). Non-alcoholic fatty liver disease (NAFLD) and its connection with insulin resistance, dyslipidemia, atherosclerosis and coronary heart disease. Nutrients , 5(5), 1544-60.
- [8](2005). Sources of fatty acids stored in liver and secreted via lipoproteins in patients with nonalcoholic fatty liver disease. J Clin Invest , 115(5), 1343-51.
- [9](2001). De novo lipogenesis during controlled overfeeding with sucrose or glucose in lean and obese women. Am J Clin Nutr , 74(6), 737-46.
- [10](2009). Aerobic exercise training reduces hepatic and visceral lipids in obese individuals without weight loss. Hepatology , 50(4), 1105-12.
- [11](2012). Sucrose-sweetened beverages increase fat storage in the liver, muscle, and visceral fat depot: a 6-mo randomized intervention study. Am J Clin Nutr , 95(2), 283-9.
- [12](2012, March). Toward a unifying hypothesis of metabolic syndrome. Pediatrics , 129(3), 557-570. doi:10.1542/peds.2011-2912. Retrieved from http://www.ncbi.nlm.nih.gov/pubmed/22351884
- [13](2013). Challenging the fructose hypothesis: new perspectives on fructose consumption and metabolism. , 4(2), 246-56.
- [14](2009). Dietary sweeteners containing fructose: overview of a workshop on the state of the science. , 139(6), 1210S-1213S.
- [15](2009). Fructose ingestion: dose-dependent responses in health research. J Nutr , 139(6), 1246S-1252S. Retrieved from http://www.ncbi.nlm.nih.gov/pubmed/19386821
- [16](2013). Consumption of sucrose and high-fructose corn syrup does not increase liver fat or ectopic fat deposition in muscles. Appl Physiol Nutr Metab , 38(6), 681-8.
- [17](2013). Effects of fructose and glucose overfeeding on hepatic insulin sensitivity and intrahepatic lipids in healthy humans. Obesity (Silver Spring) , 21(4), 782-5.
- [18](2009). Dietary sucrose is essential to the development of liver injury in the MCD model of steatohepatitis. , J. Lipid Res(50), 2072-2082.
- [19](2011, June 15). Low to moderate sugar-sweetened beverage consumption impairs glucose and lipid metabolism and promotes inflammation in healthy young men: a randomized controlled trial. American Journal of Clinical Nutrition , 94(2), 479–485. doi:10.3945/ajcn.111.013540. Retrieved from http://ajcn.nutrition.org/content/94/2/479.long
- [20](2009). Effects of short-term feeding with high- vs low- fructose isoenergetic diets on hepatic de novo lipogenesis, liver fat content and glucose regulation. Diabetes .
- [21](2010). Sugar content of popular sweetened beverages based on objective laboratory analysis: focus on fructose content. Obesity .
non-alcoholic fatty liver disease
(also called NAFLD) Fatty liver that is not caused by drinking too much alcohol. Too much alcohol drinking can cause fatty liver diseases and steatohepatitis. NAFLD happens to people who are overweight, have diabetes, high cholesterol or high triglycerides in their blood. Rapid changes in weight can also cause NAFLD. It can happen to even those without any of the things listed above. It is common, up to 31% of adults in the United States have NAFLD.
SugarScience Glossarynon-alcoholic fatty liver disease
(also called NAFLD) Fatty liver that is not caused by drinking too much alcohol. Too much alcohol drinking can cause fatty liver diseases and steatohepatitis. NAFLD happens to people who are overweight, have diabetes, high cholesterol or high triglycerides in their blood. Rapid changes in weight can also cause NAFLD. It can happen to even those without any of the things listed above. It is common, up to 31% of adults in the United States have NAFLD.
SugarScience GlossaryType 2 Diabetes
Type 2 diabetes mellitus, formerly called Non-Insulin Dependent Diabetes Mellitus (NIDDM) and Adult Onset Diabetes (AODM), is a disease in which our body acts as if it does not have enough insulin to keep our blood sugar levels down at normal levels. This is likely a combined effect of the body not being normally sensitive to the insulin the pancreas does make combined with the pancreas not making enough insulin for the circumstances. There is a genetic component to this disease. The body uses insulin as a signal to store glucose in liver, muscle, and fat cells. High blood glucose causes many changes in the body that lead to damage to many parts of the body over time
SugarScience GlossaryHigh-Fructose Corn Syrup
(HFCS) A concentrated form of liquid sugar which may contain a wide range of fructose concentrations. Most commonly it contains either 42% or 55% fructose, but may contain up to 90% fructose.
SugarScience GlossaryTable sugar
Sucrose, also called granulated sugar, is two simple sugars stuck together in a single molecule. Sucrose is made of one fructose and one glucose molecule. On this website, one level teaspoon of table sugar weighs 4.2 grams and has 16.8 calories.
SugarScience GlossaryLiver disease
A broad term meaning any bodily process in which the liver is injured or does not work as it is supposed to. In this website we focus on liver diseases in which the diet hurts the liver
SugarScience GlossaryDiabetes mellitus
Usually shortened to just diabetes. Sometimes called sugar diabetes. Look at Type 1 Diabetes and Type 2 Diabetes for more information
SugarScience GlossaryFatty acids
A type of fat in our body and our food. Three fatty acids are combined with another chemical called glycerol to form a triglyceride.
SugarScience GlossaryFatty liver
An abnormal condition in which too much fat is stored in the liver. "Too much fat" means more than one tenth of the liver is made of fat.
SugarScience GlossaryTriglycerides
The most common type of fat in our body and in our food. We can eat triglycerides, our bodies can make triglyceride, and our livers can turn excess sugar into triglycerides. If we do not burn triglycerides as fuel, they are stored as fat in the liver and elsewhere in the body.
SugarScience GlossaryCirrhosis
An abnormal condition in which healthy liver is replaced by scar tissue. In cirrhosis, the liver no longer works well to digest food or protect us from toxins. Eventually, liver failure will occur when most normal parts of the liver have been replaced by scar tissue. The only treatment is liver transplant.
SugarScience GlossaryGlucose
Glucose is a sugar we eat. It is found in starch. It is the main fuel for our bodies. It is the sugar measured when we have a blood test to measure the blood sugar.
SugarScience GlossarySteatosis
Abnormal storage of fat in cells of an organ. When this happens, the organ gets bigger and becomes paler in color.
SugarScience GlossaryFat
One of the three major groups of nutrients we eat. Much of this website is related to problems associated with too much fat storage in the body. Each gram of fat produces 9 calories of energy if burned by the body as fuel. Fat can be stored in many places in the body. We generally think of fat as under the skin (subcutaneous), but the fat that may be most damaging to us is the fat stored in the liver and around the organs of the abdomen (intrahepatic and visceral or abdominal or intra-abdominal)
SugarScience GlossaryFructose
A sugar that we eat. Also called fruit sugar. Most fructose comes in sucrose (table sugar, cane sugar, beet sugar), or from high-fructose corn syrup.
SugarScience GlossaryLiver
The largest internal organ. It weighs about three to four pounds and is located under the lower edge of the ribs on the right side. It helps us digest our food and remove toxins from our blood. "Hepat" in a word means liver, so an "hepato-toxin" is a liver poison or something that can cause damage to the liver
SugarScience GlossaryInsulin
Insulin is a messenger released from the pancreas after eating, which shunts energy (glucose or triglycerides) from the blood into fat cells for storage. Insulin is given to some people with diabetes to lower the blood glucose; it leaves the blood and enters the fat cell for storage.
SugarScience GlossaryInflammation
The human body uses special cells and chemicals to fight against injury, poisons or diseases. These cells and chemicals can be seen or measured and when they are present that is called inflammation. Too much inflammation can cause damage to the body and is a part of what happens in many diseases, like cancer and heart disease to name only two.
SugarScience Glossary