scholarly journals The thrifty phenotype hypothesis and hearing problems

BMJ ◽  
2003 ◽  
Vol 327 (7425) ◽  
pp. 1199-1200 ◽  
Author(s):  
M.-L. Barrenas
Keyword(s):  
Thrifty Phenotype ◽  
Thrifty Phenotype Hypothesis ◽  
Hearing Problems

scholarly journals Recharacterizing the Metabolic State of Energy Balance in Thrifty and Spendthrift Phenotypes

2020 ◽  
Vol 105 (5) ◽  
pp. 1375-1392 ◽  
Author(s):  
Tim Hollstein ◽  
Alessio Basolo ◽  
Takafumi Ando ◽  
Susanne B Votruba ◽  
Mary Walter ◽  
...  
Keyword(s):  
Energy Balance ◽  
Healthy Subjects ◽  
Liquid Chromatography Mass Spectrometry ◽  
Short Term ◽  
Urinary Catecholamines ◽  
Metabolic Phenotypes ◽  
Thrifty Phenotype ◽  
Thrifty Phenotype Hypothesis ◽  
The Difference ◽  
Prevailing View

Abstract Purpose The human thrifty phenotype hypothesis presupposes that lower 24-hour (24h) energy expenditure (24EE) during famine preserves body mass and promotes survival. The prevailing view defines thrifty individuals as having a lower 24EE during fasting. However, it is also plausible that the greater decline in 24EE during fasting in thrifty individuals is due to higher 24EE during energy balance conditions (ENBAL). Herein, we provide evidence that this is indeed the case. Methods In 108 healthy subjects, 24EE was measured in a whole-room indirect calorimeter both during ENBAL and 24h fasting conditions. Subjects were categorized as thrifty or spendthrift based on the median value (−162 kcal/day) of the difference in 24EE (adjusted for body composition) between fasting and ENBAL conditions. Concomitant 24h urinary catecholamines were assessed by liquid chromatography–mass spectrometry. Results Compared to ENBAL, 24EE decreased during 24h fasting by 172 kcal/day (standard deviation = 93; range, −470 to 122). A greater-than-median decrease in 24EE (“thriftier” phenotype) was due to higher 24EE during ENBAL (+124 kcal/day; P < 0.0001) but not to lower 24EE during fasting (P = 0.35). Greater fasting-induced increase in epinephrine was associated with concomitant lower decrease in 24EE (r = 0.27; P = 0.006). Main Conclusion The greater decrease in 24EE during acute fasting (which characterizes the thrifty phenotype) is not due to reduced metabolic rate during fasting but to a relatively higher 24EE during feeding conditions, and this decrease in 24EE during fasting is accompanied by a smaller increase in epinephrine. These results recharacterize the prevailing view of the short-term 24EE responses that define the human metabolic phenotypes. Clinical Trials: NCT00523627, NCT00687115, NCT02939404

scholarly journals Trade-Offs in Relative Limb Length among Peruvian Children: Extending the Thrifty Phenotype Hypothesis to Limb Proportions

PLoS ONE ◽  
2012 ◽  
Vol 7 (12) ◽  
pp. e51795 ◽  
Author(s):  
Emma Pomeroy ◽  
Jay T. Stock ◽  
Sanja Stanojevic ◽  
J. Jaime Miranda ◽  
Tim J. Cole ◽  
...  
Keyword(s):  
Limb Length ◽  
Thrifty Phenotype ◽  
Thrifty Phenotype Hypothesis ◽  
Trade Offs ◽  
Limb Proportions

scholarly journals Diabetic and Metabolic Programming: Mechanisms Altering the Intrauterine Milieu

2012 ◽  
Vol 2012 ◽  
pp. 1-11 ◽  
Author(s):  
Claudia Eberle ◽  
Christoph Ament
Keyword(s):  
Metabolic Syndrome ◽  
Cardiovascular Diseases ◽  
Maternal Health ◽  
Molecular Mechanisms ◽  
Metabolic Diseases ◽  
Experimental Studies ◽  
Cardiovascular Changes ◽  
Thrifty Phenotype ◽  
The Metabolic Syndrome ◽  
Thrifty Phenotype Hypothesis

A wealth of epidemiological, clinical, and experimental studies have been linked to poor intrauterine conditions as well as metabolic and associated cardiovascular changes postnatal. These are novel perspectives connecting the altered intrauterine milieu to a rising number of metabolic diseases, such as diabetes, obesity, and hypercholesterolemia as well as the Metabolic Syndrome (Met S). Moreover, metabolic associated atherosclerotic diseases are connected to perigestational maternal health. The “Thrifty Phenotype Hypothesis” introduced cross-generational links between poor conditions during gestation and metabolic as well as cardiovascular alterations postnatal. Still, mechanisms altering the intrauterine milieu causing metabolic and associated atherosclerotic diseases are currently poorly understood. This paper will give novel insights in fundamental concepts connected to specific molecular mechanisms “programming” diabetes and associated metabolic as well as cardiovascular diseases.

scholarly journals Obesity epidemic in India: intrauterine origins?

2004 ◽  
Vol 63 (3) ◽  
pp. 387-396 ◽  
Author(s):  
C. S. Yajnik
Keyword(s):  
Genetic Predisposition ◽  
Late Pregnancy ◽  
First Trimester ◽  
Nutrient Concentrations ◽  
Visceral Mass ◽  
Obesity Epidemic ◽  
Thrifty Phenotype ◽  
Thrifty Phenotype Hypothesis ◽  
Obesity And Diabetes ◽  
The Face

The epidemic of ‘obesity’ in India is not appreciated because BMI underestimates the adiposity of Indians. Specific adiposity measurements are necessary for recognition of the adiposity of ‘thin’ Indians. The origin of this adiposity is only beginning to be understood. In addition to a possible genetic predisposition, intrauterine ‘programming’ might be responsible, although in the ‘thrifty phenotype’ hypothesis the adiposity of the ‘thin’ fetus has not been appreciated. Dutch men who faced ‘winter hunger’ during the first trimester of their in utero life have become more obese as adults. Low birth weight predicts central obesity in some studies, including studies in urban children. It has also been shown that small and thin Indian newborns (weight 2·7?kg and ponderal index 2·4?kg\m3) have poor muscle and visceral mass but higher adiposity for a given weight compared with white Caucasian babies. This body composition is influenced by maternal adiposity before pregnancy and by aspects of maternal nutritional intake and circulating nutrient concentrations during pregnancy. There are no strong paternal determinants of adiposity at birth. Adiposity may be an integral part of the orchestrated adjustments made to support ‘brain preservation’ during intrauterine growth, because brain tissue is predominantly fat. Increased nutrition in the face of a genetic predisposition or multigenerational undernutrition increases maternal insulin resistance in late pregnancy and promotes fetal adiposity even in absence of marked hyperglycaemia. Further research is necessary to define the role of specific nutrients and metabolites in the intrauterine processes promoting adiposity before maternal interventions to curtail the epidemic of obesity and diabetes are planned.

scholarly journals The thrifty phenotype hypothesis revisited

Diabetologia ◽  
2012 ◽  
Vol 55 (8) ◽  
pp. 2085-2088 ◽  
Author(s):  
A. A. Vaag ◽  
L. G. Grunnet ◽  
G. P. Arora ◽  
C. Brøns
Keyword(s):  
Thrifty Phenotype ◽  
Thrifty Phenotype Hypothesis
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