It has been well known that there is a common basis, metabolic disturbances, for many diseases such as type 2 diabetes mellitus, cardiovascular diseases, certain types of cancers, as well as neurodegenerative disorders. Diet has been implicated in the emergence of metabolic syndrome and its most prominent visible symptom, obesity. A recent article (1) broadens our understanding of how mammals acquire this complication over time because of the complex interplay of neuronal circuits in the brain, specifically in the hypothalamus.
Simplistically, two neuronal circuits with opposing effects seem to balance feeling of hunger and satiety. Their actions are based on the state of the system, on energy deficit and excess. Any fault in either of these circuits can lead to the organism over or under consuming nutrients. This opens up possible therapeutic avenues for metabolic syndrome through the central nervous system.
However, what the article does not discuss is the possibility of learning effects in these circuits. In a regime of low or high availability of energy over long periods of time, these circuits may show conditioning effects, necessitating model specific interventions. Further, these circuits could learn the timing of energy arrival or periods of energy deficit (as in the case of fasting), designing optimal countervailing effects. Such optimization may result in rebounds as typically observed in weight loss through dieting and fasting.
The understanding that the hypothalamus could be the initiator of metabolic disturbances certainly advances our thinking in this area.