Purpose of review <p>Many physiological models have been put forth to explain the pathogenesis of obesity. All causes must eventually act by altering energy intake, energy expenditure, or the metabolic handling of ingested nutrients to favor storage over oxidation. These mechanisms culminate in two apparently competing models—the Energy Balance Model (EBM) and the Carbohydrate Insulin Model (CIM). In the EBM, eating more precedes increased adiposity, whereas in the CIM, increased adiposity precedes eating more.</p> Recent findings <p>Epidemiological observations on energy intake and obesity prevalence during the last 50&#xa0;years have often become the source of controversy between models. Here, I present a hypothesis, which borrows key elements from the EBM and CIM, and offers a framework that traces the root cause of obesity outside of the modern food environment and aligns with historical, 100-year-long trends in metabolic rate, food intake, physical activity, and adiposity. Body weight has been steadily increasing throughout the previous century, in conjunction with reductions in resting metabolic rate. This, superimposed with varying&#xa0;changes in dietary energy intake and physical activity energy expenditure resulted in an accelerated rise in obesity prevalence after the 1970s.</p> Summary <p>Obesity is a multifactorial disease and alterations in the underlying metabolic pathways that synergize to promote net fat deposition in the body have likely been operating for many decades, if not centuries, and involve both food-related and non-food-related factors.</p>