OK, enough politics around here for a while. It's time to talk about fat rats. When I last wrote about fructose around here, it was to highlight a paper that suggested that it had effects on satiety signaling in the brain. The hypothesis was that fructose could lead to an abnormal drop in ATP levels in the hypothalamus, leading to an inappropriate hunger signal. This is partially borne out by the results of infusing various sugars directly into the brains of rats: if you do that trick with glucose, the rats stop eating - their cells have detected abundant glucose, which is a signal that they've been fed recently. On the other hand, if you use fructose, the rodents actually eat more.
Some of the big questions, though, have been whether fructose does this under normal conditions in rats (that is, without the power-drill route of administration into the brain), and whether that result carries over to humans. There's a new paper from a group at Princeton that's sure to add fuel to the debate. They studied the effects on rats of access to high-fructose corn syrup (8% in water) versus 10% sucrose, with unlimited access to normal rat chow, and looked at whether it made a difference if you allowed access for half the day versus the whole 24 hours.
Over an 8-week period, the groups diverged significantly. The half-day corn syrup rats put on significantly more weight than the half-day sucrose rats did, even though (most interestingly) the corn syrup group turned out to be ingesting fewer calories from the added corn syrup than the sucrose rats were getting from their sugar water. That is, the difference in caloric intake (and thus the excess weight) was all coming from eating more chow.
When the study was extended to six months, it turned out that it didn't matter much if the rats had 12-hour or 24-hour access to the high-fructose corn syrup - by week 3, the weights of both groups had diverged from the controls. (Looking at the graphs, it appears that the 24-hour group may have done somewhat worse, but I don't think they reached statistical significance versus the 12-hours). But that result is in male rats. The females showed what seems to be a much less dramatic effect. Only the 24-hour-HFCS group showed a significant weight difference from the controls.
Looking at the fat deposits the rats had laid down during this time shows another gender difference, although it doesn't help clear things up any. The males show a tendency for more fat pad mass, although the only measurement that reached significance was the abdominal fat for the 12-hour-a-day group. The females, although they didn't show nearly as wide a difference in weight gain, had much more significant differences in their fat mass (but only for the 24-hour-a-day HFCS group). Finally, in blood chemistry, none of the groups showed differences in insulin levels. But the both the male HFCS groups had elevated triglycerides, as did the 24-hour-HFCS females.
Taken together, it appears that rats (especially males) are able to adjust their caloric intake when given access to small amounts of sucrose, but not so much when given equivalent amounts of HFCS. Earlier work has shown that access to higher levels of sucrose or other sugars, though, will indeed cause rats to gain weight. But not everyone, it seems, even sees these effects. A study from last December looked at a variety of sweetened waters, given to rats 12 hours/day for ten weeks, but only three days out of each week. No differences in weight were seen, although it should be noted that in head-to-head tests, the rats preferred HFCS to agave or Stevia sweeteners. (I wish this group had run sucrose in this experiment, too).
So does this effect even apply across the board in rodents? And if it does, is it operating in humans as well? Short term, no one has been able to find any short-term differences in satiety or blood chemistry when comparing HFCS with sucrose in humans. That alone (as mentioned in the earlier post here linked in the first paragraph) makes you wonder if that fructose/brain hypothesis can hold up in people. But what about long-term effects, which may or may not have anything to do with that CNS-based mechanism?
As far as I can tell, we have no controlled data for that, which isn't surprising, considering the sort of experiment you'd have to run. Most people aren't in a position to have their food and liquid intake completely monitored for two or three months. But short of that, I'm not sure how we're ever going to straighten all this out.