Fructose is an intermediary in the metabolism of glucose, but there is no biological need for dietary fructose. When ingested by itself, fructose is poorly absorbed from the gastrointestinal tract, and it is almost entirely cleared by the liver—the circulating concentration is ≈0.01 mmol/L in peripheral blood, compared with 5.5 mmol/L for glucose. Fructose is metabolized, primarily in the liver, by phosphorylation on the 1-position, a process that bypasses the rate-limiting phosphofructokinase step. Hepatic metabolism of fructose thus favors lipogenesis, and it is not surprising that several studies have found changes in circulating lipids when subjects eat high-fructose diets.
Fructose differs in several ways from glucose, the other half of the sucrose (sugar) molecule. Fructose is absorbed from the gastrointestinal tract by a different mechanism than that for glucose. Glucose stimulates insulin release from the isolated pancreas, but fructose does not. Most cells have only low amounts of the glut-5 transporter, which transports fructose into cells. Fructose cannot enter most cells, because they lack glut-5, whereas glucose is transported into cells by glut-4, an insulin-dependent transport system. Finally, once inside the liver cell, fructose can enter the pathways that provide glycerol, the backbone for triacylglycerol. The growing dietary amount of fructose that is derived from sucrose or HFCS has raised questions about how children and adults respond to fructose alone or when it is accompanied by glucose. In one study, the consumption of high-fructose meals reduced 24-h plasma insulin and leptin concentrations and increased postprandial fasting triacylglycerols in women, but it did not suppress circulating ghrelin, a major appetite-stimulating hormone. There is evidence that a little bit may help your body process glucose properly. However, consuming too much fructose at once seems to overwhelm the body's capacity to process it. The diets of our ancestors contained only very small amounts of fructose. These days, estimates are that about 10% of the modern diet comes from fructose.
The Harmful Effects of Excess Fructose:
1.) First, it is sweeter than either glucose or sucrose. In fruit, it serves as a marker for foods that are nutritionally rich. However, in soft drinks and other “sweets,” fructose serves to reward sweet taste that provides “calories,” often without much else in the way of nutrition. Second, the intake of soft drinks containing high-fructose corn syrup (HFCS) or sucrose has risen in parallel with the epidemic of obesity, which suggests a relation.
High dietary intake of fructose is problematic because fructose is metabolized differently from glucose. Like fructose, glucose is a simple sugar. Derived from the breakdown of carbohydrates, glucose is a primary source of ready energy. Sucrose (table sugar) comprises one molecule of glucose and one molecule of fructose. Thus, excessive sucrose intake also contributes to the rise in overall daily fructose consumption. Glucose can be metabolized and converted to ATP, which is readily “burned” for energy by the cells’ mitochondria. Alternatively, glucose can be stored in the liver as a carbohydrate for later conversion to energy. Fructose, on the other hand, is more rapidly metabolized in the liver, flooding metabolic pathways and leading to increased triglyceride synthesis and fat storage in the liver. This can cause a rise in serum triglycerides, promoting an atherogenic lipid profile and elevating cardiovascular risk. Increased fat storage in the liver may lead to an increased incidence in non-alcoholic fatty liver disease, and this is one of several links between HFCS consumption and obesity as well as the metabolic syndrome.
2.) Too much fructose may make your liver synthesize fats, which are exported as VLDL cholesterol, which leads to dyslipidemia (blood tryglicerides and cholesterol), fat around the organs and ultimately, heart disease.
3.) Increase blood levels of uric acid, leading to gout and elevated blood pressure.
4.) Cause deposition of fat in the liver, potentially leading to non-alcoholic fatty liver disease.
5.) Insulin resistance leads to elevated insulin and insulin like growth factor (IGF-1) in the entire body, which may ultimately cause cancer.
6.) Fructose may have less impact on appetite than glucose, so processed foods rich in fructose can contribute to weight gain, obesity, and its related consequences by failing to manage appetite (by its insignificant effect on ghrelin).
7.) Excess fructose consumption may cause leptin resistance, throwing body fat regulation off-balance and contributing to obesity. Leptin resistance, elevated insulin and vicious addictive cycles of cravings and binge eating are a recipe for fat gain disaster.
It’s important to realize that all of this does NOT apply to fruit.
Fruits aren’t just watery bags of fructose, they are real foods with a low energy density and lots of fiber.
They’re hard to overeat on and you’d have to eat ridiculous amounts to reach harmful levels of fructose. In general, fruit is a minor source of fructose in the diet compared to added sugars.
The harmful effects of fructose apply to a western diet supplying excess calories and added sugars. It does NOT apply to the natural sugars found in fruits and vegetables.
Research on Fructose Linked With Insulin Resistance and Diabetes:
The high flux of fructose to the liver, the main organ capable of metabolizing this simple carbohydrate, disturbs glucose metabolism and uptake pathways and leads to metabolic disturbances that underlie the induction of insulin resistance, a hallmark of type 2 diabetes. In fact, the effect of HFCS on insulin resistance has been shown to have an impact on the prevalence of diabetes. In 2004, investigators conducted an ecological correlation study, in which they compared the relationship between food consumption of refined carbohydrates and the prevalence of type 2 diabetes in the US from 1909 to 1997. They found that during this period, the use of corn syrup sweeteners, which were almost non-existent at the turn of the century, increased by more than 2,100%. During the same period, the prevalence of diabetes skyrocketed. After controlling for total energy intake from other foods such as fats and proteins, only the increase in corn syrup and a decrease in fiber intake correlated positively with the prevalence of type 2 diabetes.
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