Many people think that sugar is sugar. But there are different types, and sugar comes in many forms. Compared with glucose, fructose plays a primary role in the development of metainflammation, obesity, prediabetes, and type 2 diabetes.
Fructose directly increases de novo lipogenesis (the liver making new fat from sugar). It promotes dyslipidemia (unhealthy blood fat levels). It decreases insulin sensitivity. It increases visceral adiposity (fat packed around the organs). And it stimulates the reward center, similar to cocaine.
What is sugar?
Glucose is the sugar we most often talk about and measure in diabetics. Because of that, most people assume their regular table sugar is made of glucose. But common table sugar is actually a disaccharide. It is made of two monosaccharides (single sugars), fructose and glucose, bonded together in a 1:1 ratio.
High fructose corn syrup (HFCS) contains about 5% more fructose than glucose. To make HFCS, corn starch is hydrolyzed (broken down) into glucose. That glucose is then isomerized (rearranged) into fructose. Food and soft drink makers prefer fructose. That is because fructose gives a significantly stronger sense of sweetness, and likely because its production is subsidized. Glucose has a sweetness index of 74, compared to 100 for sucrose or 173 for fructose.
According to the CDC, over 30 million Americans have diabetes, and 1 in every 4 do not know their diagnosis. Fructose is more strongly linked to obesity and diabetes than glucose. There is no biochemical reaction in any eukaryotic organism (any living thing whose cells have a nucleus, such as plants, animals and fungi) that requires fructose.
How does the body process fructose differently from glucose?
Almost every cell in the body can use glucose for energy. Only the liver can metabolize fructose, and it will preferentially turn fructose into stored fat. The body can handle a small amount of fructose at a time without harm to health. Fructose does come naturally from fruits. But it is absorbed slowly due to the large amount of fiber. Sadly, removing the fiber by juicing, or destroying it as a smoothie does, makes fructose absorb dramatically faster. That overwhelms the liver and sends a fructose rush to the brain.
Eating glucose normally causes the pancreas to release insulin. Insulin acts on receptors on the cell surface. These let glucose into the cell, where it is used for energy or turned into fat. High levels of insulin, in the presence of high levels of glucose, cause a liver enzyme [phosphofructokinase PFK] to convert glucose to fructose. That fructose is then quickly turned into stored fat and not used for energy. But if you eat fructose directly, it bypasses the enzyme gateway. Insulin is not released, and the fructose goes straight to fat storage.
The body metabolizes fructose differently than glucose. The liver’s handling of fructose favors de novo lipogenesis [fat production directly from fructose]. Also, fructose does not stimulate insulin secretion or leptin production. Insulin normally controls how sugar gets into cells. Leptin normally tells brain receptors that you are full. Insulin and leptin are key signals in the control of food intake and body weight. Because of this, eating fructose causes yet more hunger and more weight gain. The body is rapidly storing fat, and doesn’t know it’s full.
Does fructose cause insulin resistance?
Fructose can also directly trigger insulin resistance. When mice are fed excessive amounts of fructose, they produce carbohydrate responsive element-binding protein, or ChREBP. This protein blocks the liver from responding to insulin.
Fructose is 20 times more likely to cause fatty liver (the key problem of insulin resistance) than glucose alone. Fructose feeding studies replaced glucose with an equal number of calories from fructose. They document a 5x increase in de novo lipogenesis and a 38% increase in liver fat within eight days.
[The body processes ethanol (alcohol) in a way similar to fructose. Nearly 80% of the ethanol a person drinks goes to the liver. There it is metabolized to acetaldehyde, which also stimulates de novo lipogenesis.]
Fructose overfeeding can provoke insulin resistance. Healthy subjects were overfed 1000 calories per day of fructose. In seven days, their insulin sensitivity got 25 percent worse.
Fructose induces insulin resistance even at typical doses, in less than eight weeks. Subjects got 25 percent of their daily calories as Kool-Aid. It was sweetened with either glucose or fructose. The fructose group increased their insulin resistance and could be clinically classified as pre-diabetic. The glucose group did not.
Fructose engages in the Maillard reaction, or glycation (sugar sticking to proteins), seven times faster than glucose. A metabolite (breakdown product) of fructose does it 250 times faster. For glucose, we commonly measure this as HbA1c. For fructose, the measure is fructosamine. This glycation effect makes the cell walls sticky and keeps the receptors from working. This may explain why patients with high glycation levels need more pain medication. It is because their receptors simply don’t work. It is also part of the explanation for how insulin resistance occurs.
Is fructose addictive?
Fructose stimulates the reward center of the brain, while glucose does not. Data suggests that the fructose molecule in sugar is what makes it addictive.
- Glucose activates the cortex, the basal ganglia and certain other brain parts. But it does not activate the limbic system. Glucose results in a feeling of serotonin-induced happiness. By contrast, fructose stimulates the limbic system. It is associated with more dopamine release in the nucleus accumbens. Other addictive drugs do the same. (Glucose does not stimulate the nucleus accumbens.) Fructose results in a feeling of dopamine-induced pleasure.
Agricultural subsidies
Government subsidies began as a way to support farmers during the Depression and the Dust Bowl in 1933. We had a destitute population in the American southwest, dying of famine. Most of the food and food makers were in the Northeast. In the time it took to ship food by rail to the Southwest, it would go rancid. They had to process it. They removed the fiber from the wheat, packed it in 5-pound bags, shipped it to the Southwest, and then baked it locally. The subsidy was designed to make it worthwhile for the American food industry to invest in a processing and distribution system for a famine-stricken population. That made sense through World War II.
Unfortunately, President Nixon was worried about re-election, and he knew that swinging food prices caused political unrest. Nixon set up a new policy. It used agricultural subsidy to keep consumer food prices low. Until that point, our subsidies were actually designed to pay farmers to not grow certain crops and to keep prices inflated. That policy also let the soil regain nutrients after a harvest. His agriculture secretary, Rusty Butz, changed farming so soil was no longer left fallow (resting). There was no time to restore nutrients after a crop was harvested. It also encouraged monocropping (one crop on the same land) and megafarms. Subsidies have made farmers dependent on government support. The massive overproduction of just a few grain items created a huge surplus that was hard to store long-term. The food stamp system solved the problem of handing out this slowly rotting surplus. That made consumers dependent on government support too. Sadly, these processed staple items are rich in carbohydrates. But most of their fiber has been stripped, and their fat removed to prevent rancidity. They also lack much of the soil-derived micronutrients.
Government subsidies and import tariffs have made corn a much cheaper sweetener than sugar. That trend is not seen in other parts of the world. Consumption of HFCS rose by more than 1000% between 1970 and 1990. That far exceeds the change in intake of any other food or food group. HFCS now makes up more than 40% of the caloric sweeteners added to foods and beverages. That is a daily average of 132 calories per person. The effect of government subsidy is most evident when you compare the same soft drink in the United States to one in Mexico. For example, Coke uses corn syrup as the sweetener in the United States. In Mexico, it uses cane sugar.
High fructose corn syrup is the primary sweetener in soft drinks and other sweetened beverages. Per capita (per person) consumption of it rose from 38.2 pounds in 1980 to 868 pounds in 1998 (Chou et al., 2004). In 1942, annual U.S. production of soft drinks was 90 8 oz. servings per person. In 2000, it was 600 servings (Jacobson, 2005).
What are the other names for sugar on food labels?
Processed foods will most likely have added sugars. Sadly, those sugars can go by any number of names. This list is long, but it is not complete. The more naturally you can eat your foods, the more success you will have in creating a permanent weight loss solution.
Agave Syrup
Amasake
Any name ending in “ose” or “ol” or “syrup”
Barbados Sugar
Barley Malt
Blackstrap Molasses
Black Sugar
Brown Sugar
Cane Juice or Cane Juice Crystals
Cane Sugar
Caramel or Caramel Coloring
Castor Sugar
Confectioner’s Sugar
Corn Sweetener
Corn Syrup – a manufactured syrup of corn starch, containing varying proportions of glucose, maltose, and dextrose
Corn Syrup Solids
Crystallized Cane Juice
D-mannose
Date Sugar
Demerara
Demerara Sugar
Dehydrated Cane Juice or Dehydrated Cane Juice Crystals
Dextran
Dextrin
Dextrine
Dextrose (glucose) – a simple sugar made of only one molecule
Erythritol
Evaporated Cane Juice
Evaporated Cane Juice Sugar
Florida crystals (a trademarked name)
White or Brown Sugars
Fructose – a simple sugar refined from fruit
Fruit Juice Concentrate
Galactose
Glucose or Glucose Syrup
Golden Syrup
Grape Sugar
Grape Juice or Grape Sweetener
High Fructose Corn Syrup (HFCS)
Honey
Hydrolysed or Hydrolyzed Starch
Hydrogenated Glucose Syrup
Hydrogenated Starch Hydrolysates (HSH)
Invert Sugar
Isomalt
Levulose
Lactitol or Lactital
Lactose – a simple sugar from milk
Malt
Malt Extract
Malt Syrup
Maltodextrin
Maltose
Maltitol
Maple Syrup
Molasses
Monosaccharide
Muscovado
Organic Dehydrated Cane Juice
Organic Brown Sugar
Panocha
Polysaccharide
Powdered Sugar
Raw Cane Crystals
Raw Honey
Raw Sugar
Frequently asked questions
Is fructose worse than sugar?
Table sugar is itself half fructose, bonded 1:1 with glucose. Fructose is the half that drives the damage. Only the liver can metabolize fructose, and it preferentially turns it into fat. Fructose is 20 times more likely than glucose to cause fatty liver. And it does not trigger the insulin and leptin signals that tell your brain you are full.
Is fructose bad for you?
In large, fast doses, yes. The body can handle a small amount of fructose at a time. Whole fruit delivers it slowly because of its fiber. Juicing or blending destroys that fiber. That overwhelms the liver and sends a fructose rush to the brain. In feeding studies, replacing glucose with fructose raised liver fat by 38% within eight days.
What foods are high in fructose?
Table sugar, which is half fructose. And high fructose corn syrup, which contains about 5% more fructose than glucose. HFCS is the primary sweetener in US soft drinks. Coke uses corn syrup in the United States and cane sugar in Mexico. HFCS now makes up more than 40% of the caloric sweeteners added to foods and beverages. Fruit juice and smoothies deliver fructose fast because the fiber is gone.
Why is high fructose corn syrup in so many foods?
Government subsidies and import tariffs made corn a much cheaper sweetener than sugar in the United States. And fructose tastes sweeter. It scores 173 on the sweetness index, against 100 for table sugar and 74 for glucose. As a result, HFCS consumption rose more than 1000% between 1970 and 1990, faster than any other food.
Related reading
Sources
- Stanhope KL, Schwarz JM, Keim NL, et al. Consuming fructose-sweetened, not glucose-sweetened, beverages increases visceral adiposity and lipids and decreases insulin sensitivity in overweight/obese humans. Journal of Clinical Investigation. 2009. PMID 19381015
- Jensen T, Abdelmalek MF, Sullivan S, et al. Fructose and sugar: a major mediator of non-alcoholic fatty liver disease. Journal of Hepatology. 2018. PMID 29408694
Medically reviewed by Dr. Gurpreet Singh Padda, MD, MBA, MHP
Interventional pain physician, addiction medicine specialist and obesity medicine diplomate.
Licensed in Missouri and Illinois.
Last reviewed June 17, 2026
