Many of us use body weight or BMI (body mass index) for a quick approximation of our health status. Yet the utility of these metrics is limited because they provide little information about a far more relevant parameter: body composition – and in particular, body fat and its distribution. Body weight and BMI alone do not discriminate between muscle mass (which we want to maintain or increase to promote longevity) and fat mass (which we generally want to keep relatively low). Thus, when we set a goal to “lose weight,” our real aim ought to be losing fat.
Losing fat mass isn’t necessarily easy, but unfortunately, that struggle pales in comparison to the challenge of keeping it off. This is caused in large part by a hormone called leptin, which is secreted by fat cells and plays a critical role in numerous endocrine pathways and functions, including the regulation of energy homeostasis. Leptin is secreted at levels proportional to body fat and acts as a “satiety hormone” in the brain, causing a reduction in food intake. However, as leptin signaling decreases – due to fat loss or to key neurons becoming leptin-resistant – the brain interprets this as a sign of starvation, and drives increased appetite and reduced energy expenditure to counteract the loss.
“Fructose turns out to have been meant to be this wonderful system for survival, but in our culture with the amount of sugar in foods that we are eating (that either provide sugar or can be turned into fructose), this pathway has become hazardous.” —Rick Johnson
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“The function of the mitochondria and mitochondrial health are the ultimate mitigator of neurodegenerative diseases…just by reducing the potential for reactive oxygen species related damage.” — Dom D’Agostino
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