Are We Frucked?

“When we eat glucose (say, pasta), we satisfy our hunger enzyme, ghrelin. At the same time, we recruit insulin, which then activates our satiety enzyme, leptin. Consumption of glucose thus initiates a negative feedback mechanism that inhibits further consumption. No such luck with fructose.”—Sanford Rose

Dolors & Sense

By Sanford Rose

KISSIMMEE Florida—(Weekly Hubris)—2/24/2014—Are We “Frucked”? Anti-sugar crusader Dr. Robert Lustig thinks so.

Sugar, in the form of glucose, isn’t half bad, he alleges.

But sugar, in the form of fructose, is the root of nearly all metabolic ills.

That’s in large part because, while glucose is metabolized everywhere in the body, fructose can be digested only by the liver, which just can’t handle the load modern sugarholics routinely impose on it.

In the process of disposing of its sickly-sweet burden, the liver generates too much uric acid, which gives us gout and high blood pressure, and too much fat, which gives us diabetes and heart disease.

Many have suggested that Dr. Lustig has overargued his case. It isn’t that we eat too much sugar; it’s that we eat too much—of everything.

A recent study would seem to bear out that criticism. Researchers put overweight men on diets loaded with either glucose or fructose. Some diets were weight-maintaining and others weight-increasing.

Then the researchers measured the effect on fatty-liver disease.

Those men on the weight-increasing diet suffered incremental liver damage, whether they ate glucose or fructose. By contrast, those on the weight-stabilizing diet suffered no ill effects, regardless of the type of sugar consumed.

But this kind of study may do little to undermine the Lustig thesis.

Consumption of fructose may in fact encourage overeating, whereas consumption of glucose may not.

When we eat glucose (say, pasta), we decrease our hunger enzyme, ghrelin. At the same time, we recruit insulin, which then activates our satiety enzyme, leptin.

Consumption of glucose thus initiates a negative feedback mechanism that inhibits further consumption.

No such luck with fructose.

Its metabolism does not reduce ghrelin, so the consumer may still be hungry.

But that metabolism does activate an inflammatory agent that promotes insulin resistance. And that resistance leads to excess secretion of insulin which, in turn, interferes with leptin signaling.

Too much ghrelin, and we sit down to too many meals. Too little leptin, and we don’t know when to get up

Fructose may indeed qualify as a toxin.

Note: To listen to more of what Dr. Lustig has to say to us about sugar, go to http://www.youtube.com/watch?v=dBnniua6-oM