Amazoniac
Member
Disagree and also disagree.That old hat again. I think of it as the prime example of one of those studies Ray mentioned when he said "they are designed to get the results they want". This study has very little to do with the real world, and if you look at their results, this study actually shows that sucrose is superior to starch with regards to liver inflammation, enzymes, etc. The rats in the sucrose group receiving normal amounts of methionine had lower ALT than starch animals, and significantly lower TNF, CD14, and COX-2 - wait! there is no significance asterix, so these values, eventhough they are twice as large, are of course not significant, at all. Was worried there for a second, but our theory seems to be safe.
Still, the authors of the paper highlight their stupidity when they say absurd things like this:
"Dietary PUFAs also accumulate in the liver, possibly in an effort to reduce SFA-induced lipotoxicity."
They just showed us that liver TG where much higher in the MCS-sucrose group, and that those animals had signif...I meant insignificantly less inflammation than the MCS-starch group, and then they go on and state that it must be the saturated fat causing the inflammation. Every lab rat since the 1970s is aware that corn oil is highly toxic to the liver, but I guess this doesn't neccessarily mean that we should expect Mr. Pickens and his colleagues to be educated so well.
The confounder is that fructose favors saturated fat synthesis and it can mitigate some of the problems from PUFA. Those inflammatory markers would likely disappear if the fat used wasn't rich in them, whereas the accumulation/ballooning aspect would persist (or made worse), along with higher fasting glucose, cholesterol (seems out of mice normal), triglycerides (blood and liver) and Foreign Agricultural Service.
And these are mice that aren't dealing with dysbiosis, because this could put them under extra stress.
The increase in lean weight is interesting, they should've tracked food intake.