The thrifty phenotype hypothesis

Hales, C. N.; Barker, D. J. P.

doi:10.1093/bmb/60.1.5

Cited by 2,345 publications

(1,712 citation statements)

References 45 publications

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“…From the point of view of cardiovascular risk, epidemiological studies have demonstrated an association between chronic and degenerative diseases such as diabetes,3, 4 CVDs, and environmental (epigenetic) conditions in the embryonic or foetal phase 5, 6, 7. From the epidemiological studies conducted in England and Wales by Barker et al , The Foetal Programming Hypothesis or ‘Baker's Hypothesis’, finally, important review addressed the various environmental, hereditary, and genetic factors involving the interaction between the parents, placenta, and embryo in the genesis of diseases of adult life, citing epigenetic factors such as nutritional deficiencies and vitamins 8…”

Section: Introductionmentioning

confidence: 99%

Association between vitamin D deficiency and heart failure risk in the elderly

Porto

Silva

Luz³

et al. 2017

ESC Heart Failure

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AimsThe aim of this study was to evaluate the association between vitamin D deficiency and risk of heart failure in elderly patients of cardiology outpatient clinics.Methods and resultsA cross‐sectional study with an analytical approach was employed. Clinical data were collected from the elderly from August 2015 to February 2016. The dependent variable was the risk of heart failure; the independent variable was vitamin D deficiency; and intervening factors were age, gender, education, ethnicity, hypertension, diabetes mellitus, hypothyroidism, renal failure, dementia, stroke, dyslipidaemia, depression, smoking, alcoholism, obesity, andropause, and cardiac arrhythmia. To analyse the association between vitamin D deficiency and risk of heart failure, we used the bivariate logistic analysis, followed by analysis through the multivariate logistic regression model. Of the 137 elderly, the study found the following: women (75.9%); overweight (48.2%); obese (30.6%); increase in the index waist/hip (88.3%); dyslipidaemia (94.2%) and hypertension (91.2%); coronary artery disease (35.0%); and 27.7% with cardiac arrhythmia or left ventricular hypertrophy. Sixty‐five per cent of the elderly were deficient in vitamin D. The risk of heart failure was significantly associated with vitamin D deficiency [odds ratio (OR): 12.19; 95% confidence interval (CI) = 4.23–35.16; P = 0.000], male gender (OR: 15.32; 95% CI = 3.39–69.20, P = 0.000), obesity (OR: 4.17; 95% CI = 1.36–12.81; P = 0.012), and cardiac arrhythmia (OR: 3.69; 95% CI = 1.23–11.11; P = 0.020).ConclusionsThere was a high prevalence of vitamin D deficiency in the elderly, and the evidence shows a strong association between vitamin D deficiency and increased risk of heart failure in this population.

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Section: Introductionmentioning

confidence: 99%

Association between vitamin D deficiency and heart failure risk in the elderly

Porto

Silva

Luz³

et al. 2017

ESC Heart Failure

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“…This process is highly susceptible to changes in the intrauterine environment. Epidemiological studies have suggested an association between poor fetal or infant growth and increased risk of developing glucose intolerance and metabolic syndrome later in life [1,2]. A recent review study suggested that inadequate maternal nutrition might disturb the development of the fetus, which must adopt strategies to ensure survival that will programme its future health [3].…”

Section: Introductionmentioning

confidence: 99%

The intrauterine metabolic environment modulates the gene expression pattern in fetal rat islets: prevention by maternal taurine supplementation

et al. 2008

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Aims/hypothesis Events during fetal life may in critical time windows programme tissue development leading to organ dysfunction with potentially harmful consequences in adulthood such as diabetes. In rats, the beta cell mass of progeny from dams fed with a low-protein (LP) diet during gestation is decreased at birth and metabolic perturbation lasts through adulthood even though a normal diet is given after birth or after weaning. Maternal and fetal plasma taurine levels are suboptimal. Maternal taurine supplementation prevents these induced abnormalities. In this study, we aimed to reveal changes in gene expression in fetal islets affected by the LP diet and how taurine may prevent these changes. Methods Pregnant Wistar rats were fed an LP diet (8% [wt/wt] protein) supplemented or not with taurine in the drinking water or a control diet (20% [wt/wt] protein). At 21.5 days of gestation, fetal pancreases were removed, digested and cultured for 7 days. Neoformed islets were collected and transcriptome analysis was performed. Results Maternal LP diet significantly changed the expression of more than 10% of the genes. Tricarboxylic acid cycle and ATP production were highly targeted, but so too were cell proliferation and defence. Maternal taurine supplementation normalised the expression of all altered genes. Conclusions/interpretation Development of the beta cells and particularly their respiration is modulated by the intrauterine environment, which may epigenetically modify expression of the genome and programme the beta cell towards a pre-diabetic phenotype. This mis-programming by maternal LP diet was prevented by early taurine intervention.Keywords Diabetes . Early programming . Fetal islets . Maternal low-protein diet . Rats . Taurine . Transcriptome Abbreviations EST expressed sequence tag LP low protein LPT low-protein diet supplemented with taurine SAM significance analysis of microarrays TCA tricarboxylic acid Diabetologia (2008) 51:836-845

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“…Insulin resistance (31) and IHD (32) have been associated with low insulin-like growth factor 1 concentrations in observational studies. For the purposes of the present review (10) .) (26) Body composition: Rivera et al (27) Blood pressure: Webb et al (29) Glucose: Conlisk et al (28) Ben-Schlomo et al (30) Blood pressure: Hawkesworth et al (34) Body composition: Hawkesworth et al (35) Date Rivera et al (27) : 1988-9; (subjects exposed during pregnancy until 3 years of age) Webb et al (29) and Conlisk et al (28) 1997-8 (subjects exposed during pregnancy until 7 years of age)…”

Section: Protein-energymentioning

confidence: 98%

“…Evidence that CVD risk may be related to early-life, specifically intrauterine, exposures was initially derived from the inverse association between birth weight and CVD mortality (3)(4)(5) and/or risk factors such as blood pressure (6,7) insulin resistance (8) and the metabolic syndrome (9) . One of the most-widely-cited hypotheses, termed the 'thrifty phenotype' (10) , suggests that when exposed to deprived conditions during development fetal adaptations (metabolic, endocrine and/or anatomical) occur that allow for immediate survival but may be maladapted to cope with the demands of a more-affluent lifestyle in later life (Fig. 1).…”

Section: Developmental Origins Of Health and Disease: Maternal Supplementioning

confidence: 99%

Exploiting dietary supplementation trials to assess the impact of the prenatal environment on CVD risk

Hawkesworth

2008

Proc. Nutr. Soc.

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Animal studies have demonstrated that altering the maternal diet during pregnancy affects offspring disease risk. Data from human subjects on the early-life determinants of disease have been derived primarily from birth-weight associations; studies of the impact of the maternal diet are scarce and inconsistent. Investigating CVD risk factors in the offspring of women who have participated in maternal supplementation trials provides a useful resource in this research field, by virtue of employing an experimental design (as compared with observational studies). To date, follow-up studies have been published only for a small number of trials; these trials include the impact of maternal protein-energy, multiple-micronutrient and Ca supplementation on offspring disease risk. In Nepal maternal micronutrient supplementation has been shown to be associated with lower offspring systolic blood pressure at 2 years of age. Data from Guatemala on a pre-and postnatal protein-energy community intervention have suggested longterm improvements in fasting glucose and body composition but not in blood pressure. In The Gambia no association has been found between prenatal protein-energy supplementation and markers of CVD risk including body composition, blood pressure and fasting glucose and insulin in childhood and adolescence. Little evidence of an effect of maternal Ca supplementation on offspring blood pressure has been demonstrated in four trials, although the risk of high systolic blood pressure was found to be reduced in one trial. The present paper reviews the current evidence relating maternal nutritional supplementation during pregnancy to offspring CVD risk and explores the potential explanations for the lack of association.Developmental origins of health and disease: Maternal supplementation trials: CVD risk

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The thrifty phenotype hypothesis

Cited by 2,345 publications

References 45 publications

Association between vitamin D deficiency and heart failure risk in the elderly

Association between vitamin D deficiency and heart failure risk in the elderly

The intrauterine metabolic environment modulates the gene expression pattern in fetal rat islets: prevention by maternal taurine supplementation

Exploiting dietary supplementation trials to assess the impact of the prenatal environment on CVD risk

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