![]() The first, Asymmetric Nutrient-Energy Partitioning describes the context-dependent, cell-specific competition for calories that determines the partitioning of nutrient-energy to oxidation, anabolism, and/or storage. Since it is well-established that in utero development and positive energy balance are two such processes ( Greene, 1939 Ingle, 1949 Mayer et al., 1954, 1956 Hill and Peters, 1998 Hill et al., 2003 Hill, 2006 Sun et al., 2011 Archer et al., 2013b, 2018 Archer, 2015a, b, c, 2018 Shook et al., 2015 Archer and McDonald, 2017), in this paper we extend our previous theoretic work, the Maternal Resources Hypothesis ( Archer, 2015a, b, c, d Archer and McDonald, 2017), by introducing two conceptual frameworks. Thus, it is logical and parsimonious to posit that the etiology of obesity is simply the result of physiologic processes that increase fat-cell number, size, or both. William of Occam ( Thorburn, 1918)Īlthough obesity is described as a complex phenomenon of disputed etiology ( Archer et al., 2018), the defining characteristic is an excess of body-fat mass ( Schwartz et al., 2017) attributable to a greater number and/or size of fat-cells (adipocytes) relative to other cell-types ( Brook et al., 1972 Salans et al., 1973 Knittle et al., 1979 Sjostrom and William-Olsson, 1981). “Frustra fit per plura, quod potest fieri per pauciora”. These frameworks, in concert with our previous theoretic work, the Maternal Resources Hypothesis, provide a parsimonious and rigorous explanation for the rapid rise in the global prevalence of increased body and fat mass, and associated metabolic dysfunctions in humans and other mammals inclusive of companion, domesticated, laboratory, and feral animals. ![]() Thus, we posit that the chronic positive energy balance (i.e., over-nutrition) that leads to obesity and metabolic diseases is engendered by apparent deficits (i.e., false signals) driven by the asymmetric inter-cellular competition for calories and concomitant differential partitioning of nutrient-energy to storage. As we demonstrate, if the sensorimotor cells suffer relative caloric deprivation via asymmetric competition from other cell-types (e.g., skeletal muscle- or fat-cells), energy-intake is increased to compensate for both real and merely apparent deficits in energy-homeostasis (i.e., true and false signals, respectively). Inherent in these frameworks is the independence and dissociation of the energetic demands of metabolism and the neuro-muscular pathways that initiate ingestive behaviors and energy intake. Asymmetric Nutrient-Energy Partitioning describes the context-dependent, cell-specific competition for calories that determines the partitioning of nutrient-energy to oxidation, anabolism, and/or storage and Effective Caloric Intake which describes the number of calories available to constrain energy-intake via the inhibition of the sensorimotor appetitive cells in the liver and brain that govern ingestive behaviors. ![]() Accordingly, we introduce two conceptual frameworks. Thus, it is logical and parsimonious to posit that obesity is the competitive advantages of fat-cells (adipocytes) driving a disproportionate acquisition and storage of nutrient-energy. ![]() Axiomatically, cell-types with competitive advantages acquire a greater number of consumed calories, and when possible, increase in size and/or number. The mammalian body is a complex physiologic “ecosystem” in which cells compete for calories (i.e., nutrient-energy).
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