It’s a familiar image we might attribute to stereotype: a sluggish, maybe portly individual lying prostrate on the couch, his/her front littered with Dorito crumbs. Could there, however, be truth behind the picture? Is there indeed a connection between incessant snacking and chronic slothdom? Or considered another way, is there a connection between fasting and being active? As a long-time fan of intermittent fasting (and a believer in the research behind it), I’m convinced. A study out this month sheds even more light on the relationship between lethargy and continuous eating.

For decades now, conventional wisdom has told us that we should eat regularly throughout the day to keep our blood sugar steady. With three regular meals and at least two snacks, we’re counseled to keep our bodies in a perpetual postprandial state. However, newer research, including this month’s study from ETH Zurich, questions this assumption. Scientists focused on the opposing relationship between a transcription factor, Foxa2, and insulin. Foxa2 is found in both the liver and the hypothalamus, the central command for hunger regulation. It has a hand in the expression of two eating and physical activity related neuropeptides, melanin-concentrating hormone (MCH) and orexin. When insulin is present, as it is during and after eating, Foxa2 and the related MCH and orexin are reduced. However, fasting mice showed consistently high levels of Foxa2, MCH and orexin. The researchers then found that “hyperinsulinemic, obese” mice showed reduced Foxa2, MCH, and orexin, regardless of whether they had eaten or not. When the scientists bred mice with continually active Foxa2 (immune to the counter effect of insulin), these mice showed high levels of MCH and orexin – and a correspondingly high level of physical activity whether they had eaten or not. The specially bred mice had low body fat as well as higher muscle mass.

Consider this study another nail in the coffin of conventional wisdom. (It also goes a long way in explaining the snacking couch potato association.) Fasting, even short, between-meal breaks, promotes the activation of Foxa2 and the resulting formation of MCH and orexin – as well as their activity-inducing effects. A simple survival principle explains this: a hungry animal needs to get up and move to find food. On the other hand, if we are constantly swimming in the insulin of eating and post-eating states, we’re undermining our own motivation (and biochemical stimulus) to get up and burn off what we just ate.

CW encourages us to never skip breakfast, bring along a mid-morning snack, make time for a good lunch, grab a mid-afternoon nibble and then have a good dinner. Oh, and if you can’t sleep, you’re supposed to have warm milk and a banana before bed. Our bodies are either eating or processing what we ate. There’s never a recovery period. Nary a resetting opportunity. We’re so focused on the hobby horse of “stable” blood sugar that we’ve forgotten that there’s more to the biochemical story of balanced energy. We make ourselves feel perpetually full to the exclusion of feeling anything else. (How about light, energized?) We continually raise our blood sugar and insulin levels and, in doing so, turn off the body’s chance to activate or upregulate other key substances that promote energy balance – and as this study shows, the physiological motivation to be active. Simple advice: skip the snack. (Besides, dinner never tasted so good as it does on a healthily empty stomach.)

Let me know your thoughts. IFers – have you found this principle to be apparent in your own experiments? Thanks for reading.

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