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Fetal programming
Published in Hung N. Winn, Frank A. Chervenak, Roberto Romero, Clinical Maternal-Fetal Medicine Online, 2021
Katherine E. Pelch, Jana L. Allison, Susan C. Nagel
Barker further refined his Developmental Origins hypothesis with the introduction of the concept of the thrifty fetus. He hypothesized that the fetal environment could provide a “weather forecast” of the nutritional status outside of the womb. His thrifty phenotype hypothesis suggests that declines in nutritional status while in the womb can program a fetus to be “thrifty” and to store and ration energy accordingly (10). Problems arise, however, when individuals programmed in utero to be “thrifty” are introduced to an environment of plenty during early adolescence and adulthood. Being “thrifty” in development allows a fetus to conserve energy for important tissues like the brain at the expense of other tissues such as muscle and liver. Barker further suggests that the tissues and organs that were sacrificed during development have a diminished ability to properly respond to a “world of plenty” in adulthood. This hypothesis suggests that catch-up growth creates problems for those who were “thrifty” during development.
Energy balance and its regulation
Published in Geoffrey P. Webb, Nutrition, 2019
Alimentary signals are involved in signalling satiety at the end of a meal and signals indicating an absence of food in the gut may help signal the need to eat again. One can alter the energy density of the diets of laboratory rats by the use of an inert bulking agent (e.g. methylcellulose) or by the addition of energy-rich fat. Rats fed diluted diets are able to maintain their body weights and compensate for the dilution by increasing the volume of food they eat. However, long-term feeding with diets of high energy density causes obesity in rats, which suggests that overconcentration of the diet may reduce the effectiveness of feeding control mechanisms, so reducing the energy density of human diets may help to prevent excessive weight. The mechanisms regulating energy balance are generally more effective in preventing under- rather than overconsumption. The term thrifty phenotype has been used in relation to this idea. During our evolutionary history, having so-called thrifty genes that aided survival during periods of food shortage would have been a survival advantage but under conditions of abundant food supply and low need for physical activity they would become disadvantageous and predispose to obesity (discussed further in the next chapter).
Endocrine and reproductive disorders
Published in Angus Clarke, Alex Murray, Julian Sampson, Harper's Practical Genetic Counselling, 2019
T2D is proving to be a major problem in developing countries as they increasingly adopt ‘Western’ dietary habits and sedentary lifestyles. Attempts have been made to replace Neel's ‘thrifty genotype’ hypothesis by a ‘thrifty phenotype’ (Barker's phrase) based on inadequate intrauterine nutrition that marks the body's metabolism so that it is pre-adapted to cope with chronic undernutrition. It has been proposed that this would account for the increase in T2D shown in certain populations, as they are unable to cope well with an unexpectedly generous supply of calories. These ideas of an underlying explanation for such a ‘predictive adaptive response’ remain suggestive and of interest but their place relative to conventional genetic factors has not yet been firmly established. The chronic stresses of unemployment, marginalisation and racism may also add to the causal factors that contribute to the development of T2D and related disorders. Insulin levels are initially increased in someone developing T2D, and insulin resistance is present but the specific genetic determinants remain even less clear than in T1D. Risks to relatives are high (see Table 25.2), especially for monozygotic twins, but are mainly for the same form of diabetes, not for the more severe type I disease.
Seasonality of plasma tryptophan and kynurenine in pregnant mothers with a history of seasonal affective disorder: Vulnerability or adaptation?
Published in The World Journal of Biological Psychiatry, 2020
Robert D. Levitan, Maria Sqapi, Leslie Atkinson, Kellie Murphy, Anthony Levitt, Alan Bocking, Martin Post, Julia A. Knight, Stephen G. Matthews
Distinct seasonal patterns of pregnancy and childbirth have been found in families having a SAD proband (Pjrek et al. 2004, 2007), and the current results extend these findings into the biological realm. Taken together, these two lines of work support the notion that the SAD syndrome may have functional evolutionary significance as it relates to reproduction and foetal development, perhaps by matching the biology of the maternal-placental-foetal system to anticipated needs based on season of conception and anticipated season of birth. While these changes may have been adaptive in ancient times, it is unclear whether they would be adaptive in modern society, particularly given the widespread availability of foods that might lead to tryptophan imbalances and hyperserotonemia in some cases. In this way, the current results are reminiscent of the ‘thrifty phenotype’ described by Hales and Barker (2001) which is adaptive in deprived environments but becomes maladaptive if calories prove readily available.
Sex-dependent effect of post-migration adaptation on height and relative lower leg length in Polish youth
Published in Annals of Human Biology, 2019
Slawomir Koziel, Aleksandra Gomula, Robert M. Malina
The plasticity of growth in segment lengths has been, and continues to be, a topic of interest in human biology. Growth in tibia length, for example, is considered to be more sensitive to environmental stress than overall leg length or estimated thigh length (Cameron et al. 1982; Daly et al. 2000; Lampl et al. 2003). Several studies also indicate that the tibia responds more to hypoxaemia than does the femur, suggesting potentially different underlying adaptive responses (Lampl et al. 2003; Lampl and Jeanty 2004; Bailey et al. 2007). Evidence also suggests that the lower extremities and total stature respond differently to ecological stress (Wadsworth et al. 2002). Such heterogeneity in sensitivity to ecological and environmental stress has also been assumed to underlie the thrifty phenotype hypothesis (Pomeroy et al. 2012).
Family history of diabetes mellitus and long-term endocrine morbidity of the offspring
Published in Gynecological Endocrinology, 2020
Yuval Alon, Tamar Wainstock, Eyal Sheiner, Gali Pariente
A valid causative connection between FHDM and obesity has yet to be established. Studies suggest that maternal diabetes alters the metabolism of sugar via DNA methylation, causing genomic imprinting on fetal metabolism and increasing the risk for obesity and DM later in life [28,29]. Alternatively, the Barker thrifty phenotype hypothesis posits that fetal malnutrition due to maternal malnutrition has an effect on the cellular level, increasing the risk for metabolic disorders [16]. This epigenetic effect may not necessarily result in maternal DM, but can still affect the newborn. However, it should be noted that most of these studies have been conducted on animal models, and the implications in human models are unclear.