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Nature Clinical Practice Endocrinology & Metabolism | Childhood obesity: behavioral aberration or biochemical drive? Reinterpreting the First Law of Thermodynamics | Article
The commonly accepted assumption (and it is only an assumption) is that we store excess Fat because we eat too much and/or exercise too little.
This review proposes another way to interpret the exact same observations by turning the assumed cause and effect around... in this scenario we eat more and/or exercise less because the body (under biochemical control) is storing Fat. Or... if the body were not storing Fat, then we would not be overeating or looking for ways to conserve energy
Think of it this way... when a teenager goes through a growth spurt they eat everything in sight (ask any parent)... but in this case we don't suggest that they are "growing because they are eating" but rather that "they are eating because they are growing".
The big difference now becomes that instead of looking for ways to change the "behaviours" of gluttony and sloth -- and we all know how successful that has been -- we can instead ask the question "what controls the biochemistry of Fat storage?" In the expectation that by curtailing the Fat storage you free the person from the need/drive to overeat and promote spontaneous physical activity.
The idea of switching from being in a "Fat storage" mode to a "Fat burning" one, fits my personal experience... I can especially relate to the "normalised" hunger and spontaneous physical activity... and trust me I have tried many different versions of the other model.
In other words...Summary
Childhood obesity has become epidemic over the past 30 years. The First Law of Thermodynamics is routinely interpreted to imply that weight gain is secondary to increased caloric intake and/or decreased energy expenditure, two behaviors that have been documented during this interval; nonetheless, lifestyle interventions are notoriously ineffective at promoting weight loss. Obesity is characterized by hyperinsulinemia. Although hyperinsulinemia is usually thought to be secondary to obesity, it can instead be primary, due to autonomic dysfunction. Obesity is also a state of leptin resistance, in which defective leptin signal transduction promotes excess energy intake, to maintain normal energy expenditure. Insulin and leptin share a common central signaling pathway, and it seems that insulin functions as an endogenous leptin antagonist. Suppressing insulin ameliorates leptin resistance, with ensuing reduction of caloric intake, increased spontaneous activity, and improved quality of life. Hyperinsulinemia also interferes with dopamine clearance in the ventral tegmental area and nucleus accumbens, promoting increased food reward. Accordingly, the First Law of Thermodynamics can be reinterpreted, such that the behaviors of increased caloric intake and decreased energy expenditure are secondary to obligate weight gain. This weight gain is driven by the hyperinsulinemic state, through three mechanisms: energy partitioning into adipose tissue; interference with leptin signal transduction; and interference with extinction of the hedonic response to food.
The commonly accepted assumption (and it is only an assumption) is that we store excess Fat because we eat too much and/or exercise too little.
This review proposes another way to interpret the exact same observations by turning the assumed cause and effect around... in this scenario we eat more and/or exercise less because the body (under biochemical control) is storing Fat. Or... if the body were not storing Fat, then we would not be overeating or looking for ways to conserve energy
Think of it this way... when a teenager goes through a growth spurt they eat everything in sight (ask any parent)... but in this case we don't suggest that they are "growing because they are eating" but rather that "they are eating because they are growing".
The big difference now becomes that instead of looking for ways to change the "behaviours" of gluttony and sloth -- and we all know how successful that has been -- we can instead ask the question "what controls the biochemistry of Fat storage?" In the expectation that by curtailing the Fat storage you free the person from the need/drive to overeat and promote spontaneous physical activity.
The idea of switching from being in a "Fat storage" mode to a "Fat burning" one, fits my personal experience... I can especially relate to the "normalised" hunger and spontaneous physical activity... and trust me I have tried many different versions of the other model.