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Metabolic thrift and the genetic basis of human obesity.

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Evolution has molded metabolic thrift within humans, a genetic heritage that, when thrust into our modern "obesogenic" environment, creates the current obesity crisis. Modern genetic analysis has identified genetic and epigenetic contributors to obesity, an understanding of which will guide the

Foraging theory and the propensity to be obese: an alternative to thrift.

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The evolutionary origin of obesity is classically believed to be genetic or developmentally induced thrift, as an adaptation to ancestral feast and famine conditions. However, recently the thrift family of hypotheses have attracted serious criticism necessitating alternative thinking. Optimization

The muscle--fat duel or why obese children are taller?

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BACKGROUND Obesity the epidemic of our times appears to be a problem that is easy to resolve: just eat less and move more. However, this very common condition has turned out to be extremely troublesome, and in some cases even irreversible. METHODS The interplay between less muscle and more fat

Low muscle mass--tall and obese children a special genre of obesity.

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The prevalence of over-weight and obesity has increased markedly in the last two decades and vast international resources have been directed toward researching these issues. Obesity would appear to be a problem that is easy to resolve: just eat less and move more. However, this very common condition

Obesity--a disease with many aetiologies disguised in the same oversized phenotype: has the overeating theory failed?

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Evolution has led to metabolic thrift in humans--a genetic heritage that, when exposed to the modern 'obesogenic' milieu with energy-dense food and a sedentary lifestyle, predisposes to obesity. The current paradigm that overeating of easily digestible carbohydrates and the resulting imbalance

Adult-onset obesity reveals prenatal programming of glucose-insulin sensitivity in male sheep nutrient restricted during late gestation.

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BACKGROUND Obesity invokes a range of metabolic disturbances, but the transition from a poor to excessive nutritional environment may exacerbate adult metabolic dysfunction. The current study investigated global maternal nutrient restriction during early or late gestation on glucose tolerance and

The thrifty epigenotype: an acquired and heritable predisposition for obesity and diabetes?

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Obesity and type 2 diabetes arise from a set of complex gene-environment interactions. Explanations for the heritability of these syndromes and the environmental contribution to disease susceptibility are addressed by the "thrifty genotype" and the "thrifty phenotype" hypotheses. Here, the merits of

Thrift: a guide to thrifty genes, thrifty phenotypes and thrifty norms.

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There is a growing interest in evolutionary models of human adiposity. Frequent reference has been made to 'thrifty genes' or 'thrifty phenotypes', referring to a variety of metabolic or behavioural traits that in one or the other way imply frugality in the expenditure or storage of energy. However,

Metabolic risk factors in mice divergently selected for BMR fed high fat and high carb diets.

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Factors affecting contribution of spontaneous physical activity (SPA; activity associated with everyday tasks) to energy balance of humans are not well understood, as it is not clear whether low activity is related to dietary habits, precedes obesity or is a result of thereof. In particular, human

Striatal Dopamine D2 Receptors Regulate Cost Sensitivity and Behavioral Thrift.

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The role of the dopamine D2 receptor (D2R) in regulating appetitive behavior continues to be controversial. Earlier literature suggests that reduced D2R signaling diminishes motivated behavior while more recent theories suggest that reduced D2R, as has been putatively observed in obesity,

Evolutionary neuropathology & congenital mental retardation: environmental cues predictive of maternal deprivation influence the fetus to minimize cerebral metabolism in order to express bioenergetic thrift.

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This article will propose that humans have an adaptive vulnerability to certain forms of mental retardation, specifically, neuropathological disorders that cause decreased energy expenditure in the hippocampus and the cerebral cortex. This hypothesis will be analyzed in terms of the thrifty

Understanding the epigenetics of neurodevelopmental disorders and DOHaD.

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The Developmental Origins of Health and Disease (DOHaD) hypothesis refers to the concept that 'malnutrition during the fetal period induces a nature of thrift in fetuses, such that they have a higher change of developing non-communicable diseases, such as obesity and diabetes, if they grow up in the

The long-term consequences of intra-uterine protein malnutrition for glucose metabolism.

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Our initial observations, in epidemiological studies, linking indices of poor early (fetal and infant) growth to the subsequent development of poor glucose tolerance and the insulin resistance syndrome in adult life, have been confirmed in studies in a wide variety of populations around the world.

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