Hunger Games - Does Hunger Make You Fat? Every-Other-Day-Fasting Doubles Visceral Fat in 3 Weeks - Despite 60% Reduced Energy Intakes, At Least in Young Mice

Can hunger make you fat even if you're in a caloric deficit?
Ok, let's start with the good news. Even though the provision of food every other day lead to an initial increase in total fat, visceral fat (VAT), retroperitoneal fat (RAT) and epididymal fat / adipose tissue (EAT) in a recent rodent study from the Daejeon University in Korea, this effect was only observed in the young, yet not the old mice, the scientists used in their recent study.

Before we are even trying to make sense of either of these observations, though, I would suggest we take a closer look at the study design.
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The scientists were and still are convinced that the 2.8 million deaths that occur due to obesity-related worldwide would be avoidable, if we were all eating regularly and kept an eye on our total energy intake. Their rationale is that the latter is not the case for people living in affluence, while the former, i.e. a regular eating schedule is absent in "many people in developed countries" who do not follow a regular eating schedule due to a busy lifestyle.

With their latest experiment in the course of which the used a mouse model with both 3-week and 6-week-old mice (10 mice in each group), the Korean researchers wanted to demonstrate that "hunger" is obesogenic, even if it is temporary and occurs in the context of a 60% food restriction.
Figure 1: Relative distribution of body fat and serum ghrelin levels at the end of the study (Han. 2014)
Well, you shouldn't be surprised to see the results in Figure 1, I did, after all, give away most of the findings in the introductory paragraph of this article, already: In spite of the fact that the total food consumption in the FR (eat-every-other-day) group was lower than in the AL group, only the FR group showed a metabolic syndrome-like condition with significant fat accumulation in adipose tissues.

The scientists interpret this results as good evidence that it was the "sense of hunger", which "induced the typical characteristics of metabolic syndrome in an animal model, a distinct visceral obesity, hyperlipidemia, hyperglycemia and hepatic steatosis."
Figure 2: Leptin, liver cholesterol and triglyceride levels at the end of the study period
The researchers also believe that it was the sudden increase in leptin, they observed in the alternate-day fasted group that "played a major role in the development of these pathological disorders," but eventually the increased leptin levels could simply be a result of the increased amount of body fat the 10x by then 11-week old mice were carrying around on their body.
Alternate, better than intermittent fasting? Learn more in a previous article and understand that this single rodent study does not falsify the results of dozens of human studies with highly beneficial results | more
Bottom line: All in all, the results of the study at hand are intriguing - intriguing and confusing and there is little doubt that the idea that it was "hunger" that's responsible for the metabolic mess is as unwarranted / unsustainable as the notion that similar effects would occur in adults who are following my previous advice to fast intermittently in order to lose, not gain body fat (" Alternate Day Fasting: Well-Researched, Proven to Be Effective. So Why Don't You Use It? Plus: Simple Alternate Day Fasting Blueprints to Get You Beach Ready in 2014 " | learn more).

If anything, the study can to tell you that you better don't feed 1-2 year old toddlers on a random every-other-day feeding schedule while cutting their calorie intake by 60% - Why? Well 1-2 human years that's approximately the equivalent age of the young mice and an insufficient energy intake that comes in 2-days intervals can obviously program mice to store more body fat as they grow.
Reference:
  • Han, Jong-Min, et al. "Repeated Sense of Hunger Leads to the Development of Visceral Obesity and Metabolic Syndrome in a Mouse Model." PloS one 9.5 (2014): e98276.
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