"The content of the studies makes it appear to me that there is no consenus one way or another. "
And since my position is that fructose isn’t doing anything special or specifically different from any other carbs, how does this not jibe with my position? The claim from the alarmist side, one of them anyway, is that fructose does not ellicit an insulin response or a leptin response. There is contradictory evidence on this matter, with the studies showing an effect tending toward megadosing and/or isolating fructose instead of studing it in context. The study you linked too, as I suspected, has the rats (note: rats are not humans…) eating a diet of 60% fructose.
60%. Pure fructose. The rats were fed ad libidum which means they ate when they felt like it, and according to the study weight gain was basically the same for all the rats for entire length of the study. Then half of each were switched and the rats that ate 60% of their entire ad libidum calorie intake as fructose showed leptin resistance. Then 14 days later they killed 'em all and, well, that kinda screws any chance for a follow up to see if they ever regained a leptin response.
Now to applicability, I admit that if someone took say you, me, and filc, stuck us in a room and fed us a 60% pure fructose diet for 6 months straight and then switched us to a high fat diet for a couple of weeks and then had us tested and then slaughtered and measured for confirmation, our results would likely not indicate ‘good health’. However what’s being hypothesized by the Fuctose Is The Devil crowd is not that a high fructose diet, if suddenly discontinued, would cause you to suck down Ben and Jerry’s Phish Food until you busted. They say the fructose in context (in soda, junk food, etc) is causing these issues. If that’s the case, why did all the rats in both groups self regulate calorie intake at roughly the same levels and show no significant weight gains during the first phase of the study? If anything this study seems to suggest that, surprise surprise, metabolisms adapt to high fructose intake, but when diet intake radically shifts this can cause issues with self regulating calorie intake. Unfortunately the study didn’t continue for a while to see if the rats in the high fructose group ever recovered.
In this study you have both megadosing - no one is eating 60% of calories from pure fructose - and studying fructose in isolation, the latter because as has been mentioned fructose in nature and in HFCS is almost always found in equal proportions to other sugars which do ellicit an insulin/leptin reponse. Then you have a problematic first phase where the supposed results of eating high amounts of fructose don’t happen, both groups gained weight at the same rate. Throughout the first phase of the study all key measures except triglycerides stayed basically the same between both groups except for leptin responsiveness in the high fructose rats, but then one wonders why weren’t they eating more. Then a radical shift in diet make up which shows one of the (now smaller thanks to the subdivision of both initial groups), after which both groups ate more. Yeah, the high fructose group at more; the trend was present in both though. Nopw check out figure 4. The HF and control groups that weren’t switched stayed nearly identical. The HF group showed weight gain, high than but along with the control that switched diet, however food intake in the HF was trending down to meet the control. Not a lot of time to go one, which is why it would have been advisable to let the study play out longer and see if the HF group would have normalized, as what there is of a trend in the data says that’s exactly what their food intake was doing.
In light of the above I don’t see this study showing much of anything except that in rats an abrupt change from a diet ridiculously high in pure fructose to one high in fat can possibly lead to over eating in an unthinking animal without access to a smartphone with a calorie tracking app. It also shows no sign of a continuous HF diet causing significant increases in food intake. The dramatic food intake increase and weight gain happened in the HF group to a significant degree, but it also occurred in both groups that had drastic diet changes to high fat, just not to the same degree. It shows both controls when left alone stayed right in line with each other, showing further that a diet with continuous HF intake is nothing special. It also shows to me at least that researchers should consider repeating the study with a 6 month readjustment time to see if the HF diet has continuing effects or if all groups trend back to normal, because there’s no way of knowing with this study.