Date and Time
April 25, 2007
1:30 PM - 3:00 PM

Availability
Open to the public
No RSVP required

Speaker
Robert Lustig - University of California, San Francisco

The Western diet has become a primary focus of the etiology of the current obesity epidemic. Various aspects of our diet have been promoted (or demoted) as culprits. One particularly egregious component is fructose. Thanks to its abundance, sweetness, and low price, high-fructose corn syrup (HFCS) has become the most common sweetener used in processed foods. It's not that HFCS is biologically more ominous than sucrose (table sugar); it's that its low cost has made it available to everyone, especially low socioeconomic groups.

After all, there weren't 2-liter bottles of soda before the advent of HFCS in 1980. HFCS is found in processed foods ranging from soft drinks and candy bars to crackers to hot dog buns to ketchup. Average daily fructose consumption from all its sources (HFCS, sucrose, juice) has increased by over 50% over the past 30 years. There is abundant correlative evidence that the growing dependence on fructose in the Western diet is fueling the obesity and T2DM epidemics. In addition, mechanistic models in both animals and humans demonstrate that high-fructose diets lead to increased energy intake, decreased resting energy expenditure, excess fat deposition, and insulin resistance, which suggest that fructose consumption is playing a direct role in the epidemics of insulin resistance and obesity and T2DM in humans.

The metabolism of fructose differs significantly from that of glucose, the carbohydrate found in starch. Fructose is absorbed in the intestine and enters the liver without insulin regulation. Once there, fructose enters the glycolytic (energy breakdown) pathway without regulation. This leads to an excess accumulation of citrate outside the mitochondria (the fuel burning factories in cells), which then undergoes de novo lipogenesis (fat buildup) and is reassembled into free fatty acids (which promote insulin resistance), very low density lipoproteins (which promote atherosclerosis and serve as a substrate for obesity), and triglycerides (some of which precipitate in the liver, and cause non-alcoholic steatohepatitis). Indeed, fructose alone causes all of the manifestations of what is referred to as the "Metabolic Syndrome".

Fructose also does not suppress secretion of the "hunger hormone" ghrelin from the stomach, levels of which correlate with perceived hunger. Lastly, fructose is 7 times more likely than glucose to form advanced glycosylation endproducts (AGEs), which promote atherosclerosis. In sum, fructose consumption has metabolic and hormonal consequences that facilitate development of obesity and the Metabolic Syndrome. The highest fructose loads are soda (1.7 gm/oz) and juice (1.8 gm/oz). Although soda has received most of the attention, high fruit juice intake is also associated with childhood obesity, especially by lower income families. Therefore, it's not HFCS; rather, it's fructose from any source, including sucrose, that needs to be reduced.

Altering fructose consumption will take physician and patient education, school participation, community will, food industry regulation, and a new agricultural policy. This lecture is presented in order to start this dialog.